p stat5  (Cell Signaling Technology Inc)


Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 86

    Structured Review

    Cell Signaling Technology Inc p stat5
    The primary antibodies used in this study
    P Stat5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p stat5/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p stat5 - by Bioz Stars, 2024-07
    86/100 stars

    Images

    1) Product Images from "Growth hormone promotes the reconstruction of injured axons in the hypothalamo-neurohypophyseal system"

    Article Title: Growth hormone promotes the reconstruction of injured axons in the hypothalamo-neurohypophyseal system

    Journal: Neural Regeneration Research

    doi: 10.4103/1673-5374.389358

    The primary antibodies used in this study
    Figure Legend Snippet: The primary antibodies used in this study

    Techniques Used:

    Normal condition of growth hormone-reactive nucleus and cell types. (A) p-STAT5 (green, Alexa Fluor™ 488)-positive cells were mainly located near the third ventricle and ventral side of the hypothalamus, including SON, PVN, SCN, ARC, and TU. Signal was minimal in AHP, VMH, LH, and DMH. Scale bars: 200 μm (left) and 100 μm (right). Slice thickness, 30 μm. (B) Images of p-STAT5 (green, Alexa Fluor TM 488) co-stained with AVP (red, Alexa Fluor TM 594), OXT (red, Alexa Fluor TM 594), or GFAP (red, Alexa Fluor TM 594); and AVP (green, Alexa Fluor TM 488) with OXT (red, Alexa Fluor TM 594) by IF in the SON. Scale bars: 50 μm (left) and 10 μm (right). Slice thickness: 3 μm. (C) The proportion of co-stained cells in p-STAT5-positive cells in the SON. (D) The proportion of co-stained cells in AVP-, OXT- and GFAP-positive SON cells. Data are expressed as mean ± SEM ( n = 5). * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparison test). AHP: Anterior hypothalamic posterior; ARC: arcuate nucleus; AVP: arginine vasopressin; DAPI: 4′,6-diamidino-2-phenylindole; DMH: dorsomedial hypothalamus; GFAP: glial fibrillary acidic protein; GH: growth hormone; IF: immunofluorescence staining; LH: lateral hypothalamic nucleus; ns: not significant; OC: optic chiasm; OXT: oxytocin; p-STAT5: signal transducer and activator of transcription 5 phosphorylation; PVN: paraventricular nucleus; SCN: suprachiasmatic nucleus; SON: supraoptic nucleus; TU: tuberal nucleus; VMH: Ventromedial hypothalamus.
    Figure Legend Snippet: Normal condition of growth hormone-reactive nucleus and cell types. (A) p-STAT5 (green, Alexa Fluor™ 488)-positive cells were mainly located near the third ventricle and ventral side of the hypothalamus, including SON, PVN, SCN, ARC, and TU. Signal was minimal in AHP, VMH, LH, and DMH. Scale bars: 200 μm (left) and 100 μm (right). Slice thickness, 30 μm. (B) Images of p-STAT5 (green, Alexa Fluor TM 488) co-stained with AVP (red, Alexa Fluor TM 594), OXT (red, Alexa Fluor TM 594), or GFAP (red, Alexa Fluor TM 594); and AVP (green, Alexa Fluor TM 488) with OXT (red, Alexa Fluor TM 594) by IF in the SON. Scale bars: 50 μm (left) and 10 μm (right). Slice thickness: 3 μm. (C) The proportion of co-stained cells in p-STAT5-positive cells in the SON. (D) The proportion of co-stained cells in AVP-, OXT- and GFAP-positive SON cells. Data are expressed as mean ± SEM ( n = 5). * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparison test). AHP: Anterior hypothalamic posterior; ARC: arcuate nucleus; AVP: arginine vasopressin; DAPI: 4′,6-diamidino-2-phenylindole; DMH: dorsomedial hypothalamus; GFAP: glial fibrillary acidic protein; GH: growth hormone; IF: immunofluorescence staining; LH: lateral hypothalamic nucleus; ns: not significant; OC: optic chiasm; OXT: oxytocin; p-STAT5: signal transducer and activator of transcription 5 phosphorylation; PVN: paraventricular nucleus; SCN: suprachiasmatic nucleus; SON: supraoptic nucleus; TU: tuberal nucleus; VMH: Ventromedial hypothalamus.

    Techniques Used: Staining, Comparison, Immunofluorescence

    Expression pattern of p-STAT5 post-pituitary stalk electrical lesion in the supraoptic nucleus. (A) IF of p-STAT5 (red, Alexa Fluor TM 594) in AVP neurons (green, Alexa Fluor TM 488) in the SON at 3 and 7 days post-surgery in normal saline- or GH-treated groups. (B) Quantification results of A. In the GH-treated group, more AVP neurons survived at 3 days post-PEL, while the percentage of p-STAT5 cells in AVP neurons was less. (C) IF of p-STAT5 (red, Alexa Fluor TM 594) in OXT neurons (green, Alexa Fluor TM 488) in the SON at 3 and 7 days post-surgery in normal saline- or GH-treated groups. (D) Quantification results of C. In the GH-treated group, survival of OXT neurons was not different compared with normal saline, but the percentage of p-STAT5 cells in OXT neurons was greater at 7 days post-PEL. (E) IF of p-STAT5 (red, Alexa Fluor TM 594) in c-fos cells (green, Alexa Fluor TM 488) in the SON at 3 and 7 days post-surgery in normal saline- or GH-treated groups. (F) Quantification results of E. GH treatment promoted c-fos expression in the SON. (G) IF of p-STAT5 (red, Alexa Fluor TM 594) in GFAP cells (green, Alexa Fluor TM 488) in the SON at 3 and 7 days post-surgery in normal saline- or GH-treated groups. (H) Quantification results of G. GH treatment reduced the number of astrocytes post-PEL. Scale bars: 50 μm (left) and 10 μm (right). Slice thickness: 3 μm. Data are expressed as mean ± SEM ( n = 5). * P < 0.05 (two-tailed unpaired t -test). AVP: Arginine vasopressin; DAPI: 4′,6-diamidino-2-phenylindole; GFAP: glial fibrillary acidic protein; GH: growth hormone; IF: immunofluorescence staining; ns: not significant; OC: optic chiasm; OXT: oxytocin; PEL: pituitary stalk electrical lesion; PEL_3d GH: 3 days post-PEL with GH treated; PEL_3d: 3 days post-PEL; PEL_7d GH: 7 days post-PEL with GH treated; PEL_7d: 7 days post-PEL; p-STAT5: signal transducer and activator of transcription 5 phosphorylation; SON: supraoptic nucleus.
    Figure Legend Snippet: Expression pattern of p-STAT5 post-pituitary stalk electrical lesion in the supraoptic nucleus. (A) IF of p-STAT5 (red, Alexa Fluor TM 594) in AVP neurons (green, Alexa Fluor TM 488) in the SON at 3 and 7 days post-surgery in normal saline- or GH-treated groups. (B) Quantification results of A. In the GH-treated group, more AVP neurons survived at 3 days post-PEL, while the percentage of p-STAT5 cells in AVP neurons was less. (C) IF of p-STAT5 (red, Alexa Fluor TM 594) in OXT neurons (green, Alexa Fluor TM 488) in the SON at 3 and 7 days post-surgery in normal saline- or GH-treated groups. (D) Quantification results of C. In the GH-treated group, survival of OXT neurons was not different compared with normal saline, but the percentage of p-STAT5 cells in OXT neurons was greater at 7 days post-PEL. (E) IF of p-STAT5 (red, Alexa Fluor TM 594) in c-fos cells (green, Alexa Fluor TM 488) in the SON at 3 and 7 days post-surgery in normal saline- or GH-treated groups. (F) Quantification results of E. GH treatment promoted c-fos expression in the SON. (G) IF of p-STAT5 (red, Alexa Fluor TM 594) in GFAP cells (green, Alexa Fluor TM 488) in the SON at 3 and 7 days post-surgery in normal saline- or GH-treated groups. (H) Quantification results of G. GH treatment reduced the number of astrocytes post-PEL. Scale bars: 50 μm (left) and 10 μm (right). Slice thickness: 3 μm. Data are expressed as mean ± SEM ( n = 5). * P < 0.05 (two-tailed unpaired t -test). AVP: Arginine vasopressin; DAPI: 4′,6-diamidino-2-phenylindole; GFAP: glial fibrillary acidic protein; GH: growth hormone; IF: immunofluorescence staining; ns: not significant; OC: optic chiasm; OXT: oxytocin; PEL: pituitary stalk electrical lesion; PEL_3d GH: 3 days post-PEL with GH treated; PEL_3d: 3 days post-PEL; PEL_7d GH: 7 days post-PEL with GH treated; PEL_7d: 7 days post-PEL; p-STAT5: signal transducer and activator of transcription 5 phosphorylation; SON: supraoptic nucleus.

    Techniques Used: Expressing, IF-P, Saline, Two Tailed Test, Immunofluorescence, Staining

    anti phospho stat5 antibody  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 86

    Structured Review

    Cell Signaling Technology Inc anti phospho stat5 antibody
    Anti Phospho Stat5 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti phospho stat5 antibody/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti phospho stat5 antibody - by Bioz Stars, 2024-07
    86/100 stars

    Images

    anti stat5 antibody  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 86

    Structured Review

    Cell Signaling Technology Inc anti stat5 antibody
    Anti Stat5 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti stat5 antibody/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti stat5 antibody - by Bioz Stars, 2024-07
    86/100 stars

    Images

    anti phospho stat5 antibody  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 86

    Structured Review

    Cell Signaling Technology Inc anti phospho stat5 antibody
    Anti Phospho Stat5 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti phospho stat5 antibody/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti phospho stat5 antibody - by Bioz Stars, 2024-07
    86/100 stars

    Images

    anti stat5  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 86

    Structured Review

    Cell Signaling Technology Inc anti stat5
    Ningetinib inhibits FLT3 phosphorylation and exhibits antitumor activity against FLT3-ITD mutation in vivo. A, B, C. Western blot analysis of p-FLT3, FLT3, <t>p-STAT5,</t> STAT5, p-AKT, AKT, p-ERK and ERK in the MV4-11 and MOLM13 cells after treatment with ningetinib at the indicated doses for 2 h or 6 h. D. Schematic representation of the leukemic mouse model induced by Ba/F3-FLT3-ITD cells. E. Schematic representation of xenograft experiments using human MOLM13 cells. F. Proportion of GFP-positive cells in the BM and SP of mice, measured by flow cytometry on Day 12 ( n = 3 mice per group). G. The survival curves of BaF3-FLT3-ITD-diseased mice treated with the vehicle ( n = 7), ningetinib ( n = 7), gilteritinib ( n = 7) or quizartinib ( n = 7). H. The percentage of human CD45 positive cells in BM and SP of MOLM13-diseased NSG mice detected by flow cytometry on day 22 ( n = 3 mice per group). Error bars indicate mean ± standard error, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001
    Anti Stat5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti stat5/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti stat5 - by Bioz Stars, 2024-07
    86/100 stars

    Images

    1) Product Images from "Ningetinib, a novel FLT3 inhibitor, overcomes secondary drug resistance in acute myeloid leukemia"

    Article Title: Ningetinib, a novel FLT3 inhibitor, overcomes secondary drug resistance in acute myeloid leukemia

    Journal: Cell Communication and Signaling : CCS

    doi: 10.1186/s12964-024-01729-0

    Ningetinib inhibits FLT3 phosphorylation and exhibits antitumor activity against FLT3-ITD mutation in vivo. A, B, C. Western blot analysis of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK in the MV4-11 and MOLM13 cells after treatment with ningetinib at the indicated doses for 2 h or 6 h. D. Schematic representation of the leukemic mouse model induced by Ba/F3-FLT3-ITD cells. E. Schematic representation of xenograft experiments using human MOLM13 cells. F. Proportion of GFP-positive cells in the BM and SP of mice, measured by flow cytometry on Day 12 ( n = 3 mice per group). G. The survival curves of BaF3-FLT3-ITD-diseased mice treated with the vehicle ( n = 7), ningetinib ( n = 7), gilteritinib ( n = 7) or quizartinib ( n = 7). H. The percentage of human CD45 positive cells in BM and SP of MOLM13-diseased NSG mice detected by flow cytometry on day 22 ( n = 3 mice per group). Error bars indicate mean ± standard error, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001
    Figure Legend Snippet: Ningetinib inhibits FLT3 phosphorylation and exhibits antitumor activity against FLT3-ITD mutation in vivo. A, B, C. Western blot analysis of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK in the MV4-11 and MOLM13 cells after treatment with ningetinib at the indicated doses for 2 h or 6 h. D. Schematic representation of the leukemic mouse model induced by Ba/F3-FLT3-ITD cells. E. Schematic representation of xenograft experiments using human MOLM13 cells. F. Proportion of GFP-positive cells in the BM and SP of mice, measured by flow cytometry on Day 12 ( n = 3 mice per group). G. The survival curves of BaF3-FLT3-ITD-diseased mice treated with the vehicle ( n = 7), ningetinib ( n = 7), gilteritinib ( n = 7) or quizartinib ( n = 7). H. The percentage of human CD45 positive cells in BM and SP of MOLM13-diseased NSG mice detected by flow cytometry on day 22 ( n = 3 mice per group). Error bars indicate mean ± standard error, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Techniques Used: Activity Assay, Mutagenesis, In Vivo, Western Blot, Flow Cytometry

    Ningetinib inhibits secondary resistant TKD mutations in vitro. A. Dose‒response curve for cells with secondary mutations (FLT3-ITD-D835Y/D835V/Y842C/N676D/F691L) after treatment with ningetinib for 48 h. The mean viability of triplicate at concentration 0 was normalized as 100% as control. Error bars indicate the mean ± standard error, n = 3 independent experiments. B, C, D, E. Western blot analysis of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK expression in the FLT3-ITD-D835Y/D835V/Y842C/F691L cells treated with ningetinib for 6 h. Tubulin was used as a loading control
    Figure Legend Snippet: Ningetinib inhibits secondary resistant TKD mutations in vitro. A. Dose‒response curve for cells with secondary mutations (FLT3-ITD-D835Y/D835V/Y842C/N676D/F691L) after treatment with ningetinib for 48 h. The mean viability of triplicate at concentration 0 was normalized as 100% as control. Error bars indicate the mean ± standard error, n = 3 independent experiments. B, C, D, E. Western blot analysis of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK expression in the FLT3-ITD-D835Y/D835V/Y842C/F691L cells treated with ningetinib for 6 h. Tubulin was used as a loading control

    Techniques Used: In Vitro, Concentration Assay, Control, Western Blot, Expressing

    Ningetinib exhibits therapeutic potential in primary cells derived from patients with FLT3-ITD mutations. A, B, C, D. Cell viability values for primary BM cells from AML patients with FLT-ITD or FLT3-WT after treatment with different concentrations of ningetinib. The data are representative of three experiments. E. Cell viability values for PBMCs from healthy donors after treatment with different concentrations of ningetinib. F, G. Primary cells from FLT3-ITD-positive AML patients were cultured with ningetinib for 12 h. Proteins were extracted, and the expression of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK was assessed by western blot analysis. Data are presented as the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001
    Figure Legend Snippet: Ningetinib exhibits therapeutic potential in primary cells derived from patients with FLT3-ITD mutations. A, B, C, D. Cell viability values for primary BM cells from AML patients with FLT-ITD or FLT3-WT after treatment with different concentrations of ningetinib. The data are representative of three experiments. E. Cell viability values for PBMCs from healthy donors after treatment with different concentrations of ningetinib. F, G. Primary cells from FLT3-ITD-positive AML patients were cultured with ningetinib for 12 h. Proteins were extracted, and the expression of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK was assessed by western blot analysis. Data are presented as the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Techniques Used: Derivative Assay, Cell Culture, Expressing, Western Blot

    anti p stat5  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 86

    Structured Review

    Cell Signaling Technology Inc anti p stat5
    Ningetinib inhibits FLT3 phosphorylation and exhibits antitumor activity against FLT3-ITD mutation in vivo. A, B, C. Western blot analysis of p-FLT3, FLT3, <t>p-STAT5,</t> STAT5, p-AKT, AKT, p-ERK and ERK in the MV4-11 and MOLM13 cells after treatment with ningetinib at the indicated doses for 2 h or 6 h. D. Schematic representation of the leukemic mouse model induced by Ba/F3-FLT3-ITD cells. E. Schematic representation of xenograft experiments using human MOLM13 cells. F. Proportion of GFP-positive cells in the BM and SP of mice, measured by flow cytometry on Day 12 ( n = 3 mice per group). G. The survival curves of BaF3-FLT3-ITD-diseased mice treated with the vehicle ( n = 7), ningetinib ( n = 7), gilteritinib ( n = 7) or quizartinib ( n = 7). H. The percentage of human CD45 positive cells in BM and SP of MOLM13-diseased NSG mice detected by flow cytometry on day 22 ( n = 3 mice per group). Error bars indicate mean ± standard error, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001
    Anti P Stat5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti p stat5/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti p stat5 - by Bioz Stars, 2024-07
    86/100 stars

    Images

    1) Product Images from "Ningetinib, a novel FLT3 inhibitor, overcomes secondary drug resistance in acute myeloid leukemia"

    Article Title: Ningetinib, a novel FLT3 inhibitor, overcomes secondary drug resistance in acute myeloid leukemia

    Journal: Cell Communication and Signaling : CCS

    doi: 10.1186/s12964-024-01729-0

    Ningetinib inhibits FLT3 phosphorylation and exhibits antitumor activity against FLT3-ITD mutation in vivo. A, B, C. Western blot analysis of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK in the MV4-11 and MOLM13 cells after treatment with ningetinib at the indicated doses for 2 h or 6 h. D. Schematic representation of the leukemic mouse model induced by Ba/F3-FLT3-ITD cells. E. Schematic representation of xenograft experiments using human MOLM13 cells. F. Proportion of GFP-positive cells in the BM and SP of mice, measured by flow cytometry on Day 12 ( n = 3 mice per group). G. The survival curves of BaF3-FLT3-ITD-diseased mice treated with the vehicle ( n = 7), ningetinib ( n = 7), gilteritinib ( n = 7) or quizartinib ( n = 7). H. The percentage of human CD45 positive cells in BM and SP of MOLM13-diseased NSG mice detected by flow cytometry on day 22 ( n = 3 mice per group). Error bars indicate mean ± standard error, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001
    Figure Legend Snippet: Ningetinib inhibits FLT3 phosphorylation and exhibits antitumor activity against FLT3-ITD mutation in vivo. A, B, C. Western blot analysis of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK in the MV4-11 and MOLM13 cells after treatment with ningetinib at the indicated doses for 2 h or 6 h. D. Schematic representation of the leukemic mouse model induced by Ba/F3-FLT3-ITD cells. E. Schematic representation of xenograft experiments using human MOLM13 cells. F. Proportion of GFP-positive cells in the BM and SP of mice, measured by flow cytometry on Day 12 ( n = 3 mice per group). G. The survival curves of BaF3-FLT3-ITD-diseased mice treated with the vehicle ( n = 7), ningetinib ( n = 7), gilteritinib ( n = 7) or quizartinib ( n = 7). H. The percentage of human CD45 positive cells in BM and SP of MOLM13-diseased NSG mice detected by flow cytometry on day 22 ( n = 3 mice per group). Error bars indicate mean ± standard error, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Techniques Used: Activity Assay, Mutagenesis, In Vivo, Western Blot, Flow Cytometry

    Ningetinib inhibits secondary resistant TKD mutations in vitro. A. Dose‒response curve for cells with secondary mutations (FLT3-ITD-D835Y/D835V/Y842C/N676D/F691L) after treatment with ningetinib for 48 h. The mean viability of triplicate at concentration 0 was normalized as 100% as control. Error bars indicate the mean ± standard error, n = 3 independent experiments. B, C, D, E. Western blot analysis of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK expression in the FLT3-ITD-D835Y/D835V/Y842C/F691L cells treated with ningetinib for 6 h. Tubulin was used as a loading control
    Figure Legend Snippet: Ningetinib inhibits secondary resistant TKD mutations in vitro. A. Dose‒response curve for cells with secondary mutations (FLT3-ITD-D835Y/D835V/Y842C/N676D/F691L) after treatment with ningetinib for 48 h. The mean viability of triplicate at concentration 0 was normalized as 100% as control. Error bars indicate the mean ± standard error, n = 3 independent experiments. B, C, D, E. Western blot analysis of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK expression in the FLT3-ITD-D835Y/D835V/Y842C/F691L cells treated with ningetinib for 6 h. Tubulin was used as a loading control

    Techniques Used: In Vitro, Concentration Assay, Control, Western Blot, Expressing

    Ningetinib exhibits therapeutic potential in primary cells derived from patients with FLT3-ITD mutations. A, B, C, D. Cell viability values for primary BM cells from AML patients with FLT-ITD or FLT3-WT after treatment with different concentrations of ningetinib. The data are representative of three experiments. E. Cell viability values for PBMCs from healthy donors after treatment with different concentrations of ningetinib. F, G. Primary cells from FLT3-ITD-positive AML patients were cultured with ningetinib for 12 h. Proteins were extracted, and the expression of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK was assessed by western blot analysis. Data are presented as the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001
    Figure Legend Snippet: Ningetinib exhibits therapeutic potential in primary cells derived from patients with FLT3-ITD mutations. A, B, C, D. Cell viability values for primary BM cells from AML patients with FLT-ITD or FLT3-WT after treatment with different concentrations of ningetinib. The data are representative of three experiments. E. Cell viability values for PBMCs from healthy donors after treatment with different concentrations of ningetinib. F, G. Primary cells from FLT3-ITD-positive AML patients were cultured with ningetinib for 12 h. Proteins were extracted, and the expression of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK was assessed by western blot analysis. Data are presented as the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Techniques Used: Derivative Assay, Cell Culture, Expressing, Western Blot

    anti stat5  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 86

    Structured Review

    Cell Signaling Technology Inc anti stat5
    Anti Stat5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti stat5/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti stat5 - by Bioz Stars, 2024-07
    86/100 stars

    Images

    anti stat5  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 86

    Structured Review

    Cell Signaling Technology Inc anti stat5
    Anti Stat5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti stat5/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti stat5 - by Bioz Stars, 2024-07
    86/100 stars

    Images

    p stat5  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 86

    Structured Review

    Cell Signaling Technology Inc p stat5
    DAMPs-driven reprogramming of peri-necroptotic microenvironment facilitate tumor-cell EMT and invasiveness. A Schematic of the RNA-seq analysis. B Hierarchical clustering analysis showing differential expression patterns of SCC25 cells treated by apoptotic (TS), necrotic (FT) and necroptotic (TSZ) DAMPs. C GSEA results of signal alterations in TSZ group comparing to Control group (TS + FT). D SCC25 and FaDu were treated by different CM for 24 h. The activation of NF-κB, STAT3 and <t>STAT5</t> signaling and the expression of EMT markers were detected by Western blotting. E IHC of p-p65 and p-STAT3 were performed to the xenograft tissue sections from the Dox-induced necroptosis model. The overall IHC score were compared by one-way ANOVA and Turkey’s multiple comparisons test. F Representative image of p-p65 and p-STAT3 staining around MLKL high necroptosis in Dox-induced group and MLKL low necrosis in uninduced group. The necrotic and necroptotic clusters were outlined by dotted line, respectively. G Multi-immunofluorescent staining was performed to the three groups of xenograft tissue sections from the Dox-induced necroptosis model. Representative image of E-cad and N-cad staining in non-necrotic, necrotic and necroptotic microenvironment were shown. Necrotic clusters in MLKL-FD tumor sections were outlined by dotted line (scale bar = 100μm). H – J Primary HNSCC tissues were divided into high-necroptosis (p-MLKL high) and low-necroptosis (p-MLKL low) group based on p-MLKL staining. Then the IHC staining of p-p65, and p-STAT3 were conducted on the serial sections of each group. The IHC score was quantified and compared ( H , I ). Representative image of p-p65, p-STAT3 activation in peri-necroptotic cells were shown in (J). P-MLKL + necroptotic clusters were outlined by dotted line. K – M SCC25 and FaDu were pre-treated with BAY 11-7082 or Stattic for 1 h and then treated with necroptotic DAMPs for 24 h. Protein expression and tumor-cell migration and invasion were analyzed by K western blotting and L , M Transwell assays respectively (Scale bar = 200μm, n = 5). * p < 0.05, ** p < 0.01, *** p < 0.001
    P Stat5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p stat5/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p stat5 - by Bioz Stars, 2024-07
    86/100 stars

    Images

    1) Product Images from "cGAS-ISG15-RAGE axis reprogram necroptotic microenvironment and promote lymphatic metastasis in head and neck cancer"

    Article Title: cGAS-ISG15-RAGE axis reprogram necroptotic microenvironment and promote lymphatic metastasis in head and neck cancer

    Journal: Experimental Hematology & Oncology

    doi: 10.1186/s40164-024-00531-5

    DAMPs-driven reprogramming of peri-necroptotic microenvironment facilitate tumor-cell EMT and invasiveness. A Schematic of the RNA-seq analysis. B Hierarchical clustering analysis showing differential expression patterns of SCC25 cells treated by apoptotic (TS), necrotic (FT) and necroptotic (TSZ) DAMPs. C GSEA results of signal alterations in TSZ group comparing to Control group (TS + FT). D SCC25 and FaDu were treated by different CM for 24 h. The activation of NF-κB, STAT3 and STAT5 signaling and the expression of EMT markers were detected by Western blotting. E IHC of p-p65 and p-STAT3 were performed to the xenograft tissue sections from the Dox-induced necroptosis model. The overall IHC score were compared by one-way ANOVA and Turkey’s multiple comparisons test. F Representative image of p-p65 and p-STAT3 staining around MLKL high necroptosis in Dox-induced group and MLKL low necrosis in uninduced group. The necrotic and necroptotic clusters were outlined by dotted line, respectively. G Multi-immunofluorescent staining was performed to the three groups of xenograft tissue sections from the Dox-induced necroptosis model. Representative image of E-cad and N-cad staining in non-necrotic, necrotic and necroptotic microenvironment were shown. Necrotic clusters in MLKL-FD tumor sections were outlined by dotted line (scale bar = 100μm). H – J Primary HNSCC tissues were divided into high-necroptosis (p-MLKL high) and low-necroptosis (p-MLKL low) group based on p-MLKL staining. Then the IHC staining of p-p65, and p-STAT3 were conducted on the serial sections of each group. The IHC score was quantified and compared ( H , I ). Representative image of p-p65, p-STAT3 activation in peri-necroptotic cells were shown in (J). P-MLKL + necroptotic clusters were outlined by dotted line. K – M SCC25 and FaDu were pre-treated with BAY 11-7082 or Stattic for 1 h and then treated with necroptotic DAMPs for 24 h. Protein expression and tumor-cell migration and invasion were analyzed by K western blotting and L , M Transwell assays respectively (Scale bar = 200μm, n = 5). * p < 0.05, ** p < 0.01, *** p < 0.001
    Figure Legend Snippet: DAMPs-driven reprogramming of peri-necroptotic microenvironment facilitate tumor-cell EMT and invasiveness. A Schematic of the RNA-seq analysis. B Hierarchical clustering analysis showing differential expression patterns of SCC25 cells treated by apoptotic (TS), necrotic (FT) and necroptotic (TSZ) DAMPs. C GSEA results of signal alterations in TSZ group comparing to Control group (TS + FT). D SCC25 and FaDu were treated by different CM for 24 h. The activation of NF-κB, STAT3 and STAT5 signaling and the expression of EMT markers were detected by Western blotting. E IHC of p-p65 and p-STAT3 were performed to the xenograft tissue sections from the Dox-induced necroptosis model. The overall IHC score were compared by one-way ANOVA and Turkey’s multiple comparisons test. F Representative image of p-p65 and p-STAT3 staining around MLKL high necroptosis in Dox-induced group and MLKL low necrosis in uninduced group. The necrotic and necroptotic clusters were outlined by dotted line, respectively. G Multi-immunofluorescent staining was performed to the three groups of xenograft tissue sections from the Dox-induced necroptosis model. Representative image of E-cad and N-cad staining in non-necrotic, necrotic and necroptotic microenvironment were shown. Necrotic clusters in MLKL-FD tumor sections were outlined by dotted line (scale bar = 100μm). H – J Primary HNSCC tissues were divided into high-necroptosis (p-MLKL high) and low-necroptosis (p-MLKL low) group based on p-MLKL staining. Then the IHC staining of p-p65, and p-STAT3 were conducted on the serial sections of each group. The IHC score was quantified and compared ( H , I ). Representative image of p-p65, p-STAT3 activation in peri-necroptotic cells were shown in (J). P-MLKL + necroptotic clusters were outlined by dotted line. K – M SCC25 and FaDu were pre-treated with BAY 11-7082 or Stattic for 1 h and then treated with necroptotic DAMPs for 24 h. Protein expression and tumor-cell migration and invasion were analyzed by K western blotting and L , M Transwell assays respectively (Scale bar = 200μm, n = 5). * p < 0.05, ** p < 0.01, *** p < 0.001

    Techniques Used: RNA Sequencing Assay, Expressing, Control, Activation Assay, Western Blot, Paraffin-embedded Immunohistochemistry, Staining, Immunohistochemistry, Migration

    phospho stat5 tyr694  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 86

    Structured Review

    Cell Signaling Technology Inc phospho stat5 tyr694
    A , B Flow cytometry analysis (left) and MFI intensity (right) demonstrate the expression levels of <t>p-STAT5,</t> p-S6, p-AKT473 and p-Erk in NK cells from Mst1/2 fl/fl and Mst1/2 fl/fl CD122 Cre mice upon stimulation with or without IL-15 (50 ng/mL) for 30 min ( n ≥ 4). C Gene-set enrichment analysis of RNA-seq data shows the enrichment of hallmark-IL6-JAK-STAT3-signaling related genes in Mst1/2-deficient NK cells compared to WT NK cells. D Flow cytometry analysis (left) and MFI intensity (right) reveals the expression level of p-STAT3 (Ser727) in NK cells from Mst1/2 fl/fl and Mst1/2 fl/fl CD122 Cre mice upon stimulation with or without IL-15 (50 ng/mL) for 30 min ( n = 4). E ChIP-qPCR analysis demonstrated binding of p-STAT3 conserved motifs in the Tcf7 5′ regulatory region (−17.5 kb), while no binding was observed in a region without p-STAT3-binding motifs (+0.2 kb), serving as a negative control. The experiments were using sorted NK cells from WT mice with anti-p-STAT3 antibody or isotype-matched IgG. F – I WT splenocytes were treated with DMSO, Mst1 inhibitor XMU-MP-1 (1 mM, MedChemExpress) or p-STAT3 inhibitor Stattic (1 mM, MedChemExpress) for 24 h, followed by flow cytometry analysis. The representative plots (left) and summary data (right) show the expression level of p-STAT3 (F), TCF1 ( G ), total cellular ROS ( H ) and the percentage of 7AAD + NK cells ( I ) ( n = 4). J Schematic illustration of Mst1/2 regulate NK cell survival and function via controlling metabolic state and transcriptional activity. Data A , B and D – I are representative of three independent experiments with similar results.
    Phospho Stat5 Tyr694, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/phospho stat5 tyr694/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    phospho stat5 tyr694 - by Bioz Stars, 2024-07
    86/100 stars

    Images

    1) Product Images from "Hippo kinases Mst1 and Mst2 maintain NK cell homeostasis by orchestrating metabolic state and transcriptional activity"

    Article Title: Hippo kinases Mst1 and Mst2 maintain NK cell homeostasis by orchestrating metabolic state and transcriptional activity

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-024-06828-x

    A , B Flow cytometry analysis (left) and MFI intensity (right) demonstrate the expression levels of p-STAT5, p-S6, p-AKT473 and p-Erk in NK cells from Mst1/2 fl/fl and Mst1/2 fl/fl CD122 Cre mice upon stimulation with or without IL-15 (50 ng/mL) for 30 min ( n ≥ 4). C Gene-set enrichment analysis of RNA-seq data shows the enrichment of hallmark-IL6-JAK-STAT3-signaling related genes in Mst1/2-deficient NK cells compared to WT NK cells. D Flow cytometry analysis (left) and MFI intensity (right) reveals the expression level of p-STAT3 (Ser727) in NK cells from Mst1/2 fl/fl and Mst1/2 fl/fl CD122 Cre mice upon stimulation with or without IL-15 (50 ng/mL) for 30 min ( n = 4). E ChIP-qPCR analysis demonstrated binding of p-STAT3 conserved motifs in the Tcf7 5′ regulatory region (−17.5 kb), while no binding was observed in a region without p-STAT3-binding motifs (+0.2 kb), serving as a negative control. The experiments were using sorted NK cells from WT mice with anti-p-STAT3 antibody or isotype-matched IgG. F – I WT splenocytes were treated with DMSO, Mst1 inhibitor XMU-MP-1 (1 mM, MedChemExpress) or p-STAT3 inhibitor Stattic (1 mM, MedChemExpress) for 24 h, followed by flow cytometry analysis. The representative plots (left) and summary data (right) show the expression level of p-STAT3 (F), TCF1 ( G ), total cellular ROS ( H ) and the percentage of 7AAD + NK cells ( I ) ( n = 4). J Schematic illustration of Mst1/2 regulate NK cell survival and function via controlling metabolic state and transcriptional activity. Data A , B and D – I are representative of three independent experiments with similar results.
    Figure Legend Snippet: A , B Flow cytometry analysis (left) and MFI intensity (right) demonstrate the expression levels of p-STAT5, p-S6, p-AKT473 and p-Erk in NK cells from Mst1/2 fl/fl and Mst1/2 fl/fl CD122 Cre mice upon stimulation with or without IL-15 (50 ng/mL) for 30 min ( n ≥ 4). C Gene-set enrichment analysis of RNA-seq data shows the enrichment of hallmark-IL6-JAK-STAT3-signaling related genes in Mst1/2-deficient NK cells compared to WT NK cells. D Flow cytometry analysis (left) and MFI intensity (right) reveals the expression level of p-STAT3 (Ser727) in NK cells from Mst1/2 fl/fl and Mst1/2 fl/fl CD122 Cre mice upon stimulation with or without IL-15 (50 ng/mL) for 30 min ( n = 4). E ChIP-qPCR analysis demonstrated binding of p-STAT3 conserved motifs in the Tcf7 5′ regulatory region (−17.5 kb), while no binding was observed in a region without p-STAT3-binding motifs (+0.2 kb), serving as a negative control. The experiments were using sorted NK cells from WT mice with anti-p-STAT3 antibody or isotype-matched IgG. F – I WT splenocytes were treated with DMSO, Mst1 inhibitor XMU-MP-1 (1 mM, MedChemExpress) or p-STAT3 inhibitor Stattic (1 mM, MedChemExpress) for 24 h, followed by flow cytometry analysis. The representative plots (left) and summary data (right) show the expression level of p-STAT3 (F), TCF1 ( G ), total cellular ROS ( H ) and the percentage of 7AAD + NK cells ( I ) ( n = 4). J Schematic illustration of Mst1/2 regulate NK cell survival and function via controlling metabolic state and transcriptional activity. Data A , B and D – I are representative of three independent experiments with similar results.

    Techniques Used: Flow Cytometry, Expressing, RNA Sequencing Assay, Binding Assay, Negative Control, Activity Assay

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 86
    Cell Signaling Technology Inc p stat5
    The primary antibodies used in this study
    P Stat5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p stat5/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p stat5 - by Bioz Stars, 2024-07
    86/100 stars
      Buy from Supplier

    86
    Cell Signaling Technology Inc anti phospho stat5 antibody
    The primary antibodies used in this study
    Anti Phospho Stat5 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti phospho stat5 antibody/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti phospho stat5 antibody - by Bioz Stars, 2024-07
    86/100 stars
      Buy from Supplier

    86
    Cell Signaling Technology Inc anti stat5 antibody
    The primary antibodies used in this study
    Anti Stat5 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti stat5 antibody/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti stat5 antibody - by Bioz Stars, 2024-07
    86/100 stars
      Buy from Supplier

    86
    Cell Signaling Technology Inc anti stat5
    Ningetinib inhibits FLT3 phosphorylation and exhibits antitumor activity against FLT3-ITD mutation in vivo. A, B, C. Western blot analysis of p-FLT3, FLT3, <t>p-STAT5,</t> STAT5, p-AKT, AKT, p-ERK and ERK in the MV4-11 and MOLM13 cells after treatment with ningetinib at the indicated doses for 2 h or 6 h. D. Schematic representation of the leukemic mouse model induced by Ba/F3-FLT3-ITD cells. E. Schematic representation of xenograft experiments using human MOLM13 cells. F. Proportion of GFP-positive cells in the BM and SP of mice, measured by flow cytometry on Day 12 ( n = 3 mice per group). G. The survival curves of BaF3-FLT3-ITD-diseased mice treated with the vehicle ( n = 7), ningetinib ( n = 7), gilteritinib ( n = 7) or quizartinib ( n = 7). H. The percentage of human CD45 positive cells in BM and SP of MOLM13-diseased NSG mice detected by flow cytometry on day 22 ( n = 3 mice per group). Error bars indicate mean ± standard error, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001
    Anti Stat5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti stat5/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti stat5 - by Bioz Stars, 2024-07
    86/100 stars
      Buy from Supplier

    86
    Cell Signaling Technology Inc anti p stat5
    Ningetinib inhibits FLT3 phosphorylation and exhibits antitumor activity against FLT3-ITD mutation in vivo. A, B, C. Western blot analysis of p-FLT3, FLT3, <t>p-STAT5,</t> STAT5, p-AKT, AKT, p-ERK and ERK in the MV4-11 and MOLM13 cells after treatment with ningetinib at the indicated doses for 2 h or 6 h. D. Schematic representation of the leukemic mouse model induced by Ba/F3-FLT3-ITD cells. E. Schematic representation of xenograft experiments using human MOLM13 cells. F. Proportion of GFP-positive cells in the BM and SP of mice, measured by flow cytometry on Day 12 ( n = 3 mice per group). G. The survival curves of BaF3-FLT3-ITD-diseased mice treated with the vehicle ( n = 7), ningetinib ( n = 7), gilteritinib ( n = 7) or quizartinib ( n = 7). H. The percentage of human CD45 positive cells in BM and SP of MOLM13-diseased NSG mice detected by flow cytometry on day 22 ( n = 3 mice per group). Error bars indicate mean ± standard error, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001
    Anti P Stat5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti p stat5/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti p stat5 - by Bioz Stars, 2024-07
    86/100 stars
      Buy from Supplier

    86
    Cell Signaling Technology Inc phospho stat5 tyr694
    A , B Flow cytometry analysis (left) and MFI intensity (right) demonstrate the expression levels of <t>p-STAT5,</t> p-S6, p-AKT473 and p-Erk in NK cells from Mst1/2 fl/fl and Mst1/2 fl/fl CD122 Cre mice upon stimulation with or without IL-15 (50 ng/mL) for 30 min ( n ≥ 4). C Gene-set enrichment analysis of RNA-seq data shows the enrichment of hallmark-IL6-JAK-STAT3-signaling related genes in Mst1/2-deficient NK cells compared to WT NK cells. D Flow cytometry analysis (left) and MFI intensity (right) reveals the expression level of p-STAT3 (Ser727) in NK cells from Mst1/2 fl/fl and Mst1/2 fl/fl CD122 Cre mice upon stimulation with or without IL-15 (50 ng/mL) for 30 min ( n = 4). E ChIP-qPCR analysis demonstrated binding of p-STAT3 conserved motifs in the Tcf7 5′ regulatory region (−17.5 kb), while no binding was observed in a region without p-STAT3-binding motifs (+0.2 kb), serving as a negative control. The experiments were using sorted NK cells from WT mice with anti-p-STAT3 antibody or isotype-matched IgG. F – I WT splenocytes were treated with DMSO, Mst1 inhibitor XMU-MP-1 (1 mM, MedChemExpress) or p-STAT3 inhibitor Stattic (1 mM, MedChemExpress) for 24 h, followed by flow cytometry analysis. The representative plots (left) and summary data (right) show the expression level of p-STAT3 (F), TCF1 ( G ), total cellular ROS ( H ) and the percentage of 7AAD + NK cells ( I ) ( n = 4). J Schematic illustration of Mst1/2 regulate NK cell survival and function via controlling metabolic state and transcriptional activity. Data A , B and D – I are representative of three independent experiments with similar results.
    Phospho Stat5 Tyr694, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/phospho stat5 tyr694/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    phospho stat5 tyr694 - by Bioz Stars, 2024-07
    86/100 stars
      Buy from Supplier

    Image Search Results


    The primary antibodies used in this study

    Journal: Neural Regeneration Research

    Article Title: Growth hormone promotes the reconstruction of injured axons in the hypothalamo-neurohypophyseal system

    doi: 10.4103/1673-5374.389358

    Figure Lengend Snippet: The primary antibodies used in this study

    Article Snippet: P-STAT5 , Rabbit , 1:1000 , Cell Signaling Technology , Boston, MA, USA , 9351 , AB_2315225.

    Techniques:

    Normal condition of growth hormone-reactive nucleus and cell types. (A) p-STAT5 (green, Alexa Fluor™ 488)-positive cells were mainly located near the third ventricle and ventral side of the hypothalamus, including SON, PVN, SCN, ARC, and TU. Signal was minimal in AHP, VMH, LH, and DMH. Scale bars: 200 μm (left) and 100 μm (right). Slice thickness, 30 μm. (B) Images of p-STAT5 (green, Alexa Fluor TM 488) co-stained with AVP (red, Alexa Fluor TM 594), OXT (red, Alexa Fluor TM 594), or GFAP (red, Alexa Fluor TM 594); and AVP (green, Alexa Fluor TM 488) with OXT (red, Alexa Fluor TM 594) by IF in the SON. Scale bars: 50 μm (left) and 10 μm (right). Slice thickness: 3 μm. (C) The proportion of co-stained cells in p-STAT5-positive cells in the SON. (D) The proportion of co-stained cells in AVP-, OXT- and GFAP-positive SON cells. Data are expressed as mean ± SEM ( n = 5). * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparison test). AHP: Anterior hypothalamic posterior; ARC: arcuate nucleus; AVP: arginine vasopressin; DAPI: 4′,6-diamidino-2-phenylindole; DMH: dorsomedial hypothalamus; GFAP: glial fibrillary acidic protein; GH: growth hormone; IF: immunofluorescence staining; LH: lateral hypothalamic nucleus; ns: not significant; OC: optic chiasm; OXT: oxytocin; p-STAT5: signal transducer and activator of transcription 5 phosphorylation; PVN: paraventricular nucleus; SCN: suprachiasmatic nucleus; SON: supraoptic nucleus; TU: tuberal nucleus; VMH: Ventromedial hypothalamus.

    Journal: Neural Regeneration Research

    Article Title: Growth hormone promotes the reconstruction of injured axons in the hypothalamo-neurohypophyseal system

    doi: 10.4103/1673-5374.389358

    Figure Lengend Snippet: Normal condition of growth hormone-reactive nucleus and cell types. (A) p-STAT5 (green, Alexa Fluor™ 488)-positive cells were mainly located near the third ventricle and ventral side of the hypothalamus, including SON, PVN, SCN, ARC, and TU. Signal was minimal in AHP, VMH, LH, and DMH. Scale bars: 200 μm (left) and 100 μm (right). Slice thickness, 30 μm. (B) Images of p-STAT5 (green, Alexa Fluor TM 488) co-stained with AVP (red, Alexa Fluor TM 594), OXT (red, Alexa Fluor TM 594), or GFAP (red, Alexa Fluor TM 594); and AVP (green, Alexa Fluor TM 488) with OXT (red, Alexa Fluor TM 594) by IF in the SON. Scale bars: 50 μm (left) and 10 μm (right). Slice thickness: 3 μm. (C) The proportion of co-stained cells in p-STAT5-positive cells in the SON. (D) The proportion of co-stained cells in AVP-, OXT- and GFAP-positive SON cells. Data are expressed as mean ± SEM ( n = 5). * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparison test). AHP: Anterior hypothalamic posterior; ARC: arcuate nucleus; AVP: arginine vasopressin; DAPI: 4′,6-diamidino-2-phenylindole; DMH: dorsomedial hypothalamus; GFAP: glial fibrillary acidic protein; GH: growth hormone; IF: immunofluorescence staining; LH: lateral hypothalamic nucleus; ns: not significant; OC: optic chiasm; OXT: oxytocin; p-STAT5: signal transducer and activator of transcription 5 phosphorylation; PVN: paraventricular nucleus; SCN: suprachiasmatic nucleus; SON: supraoptic nucleus; TU: tuberal nucleus; VMH: Ventromedial hypothalamus.

    Article Snippet: P-STAT5 , Rabbit , 1:1000 , Cell Signaling Technology , Boston, MA, USA , 9351 , AB_2315225.

    Techniques: Staining, Comparison, Immunofluorescence

    Expression pattern of p-STAT5 post-pituitary stalk electrical lesion in the supraoptic nucleus. (A) IF of p-STAT5 (red, Alexa Fluor TM 594) in AVP neurons (green, Alexa Fluor TM 488) in the SON at 3 and 7 days post-surgery in normal saline- or GH-treated groups. (B) Quantification results of A. In the GH-treated group, more AVP neurons survived at 3 days post-PEL, while the percentage of p-STAT5 cells in AVP neurons was less. (C) IF of p-STAT5 (red, Alexa Fluor TM 594) in OXT neurons (green, Alexa Fluor TM 488) in the SON at 3 and 7 days post-surgery in normal saline- or GH-treated groups. (D) Quantification results of C. In the GH-treated group, survival of OXT neurons was not different compared with normal saline, but the percentage of p-STAT5 cells in OXT neurons was greater at 7 days post-PEL. (E) IF of p-STAT5 (red, Alexa Fluor TM 594) in c-fos cells (green, Alexa Fluor TM 488) in the SON at 3 and 7 days post-surgery in normal saline- or GH-treated groups. (F) Quantification results of E. GH treatment promoted c-fos expression in the SON. (G) IF of p-STAT5 (red, Alexa Fluor TM 594) in GFAP cells (green, Alexa Fluor TM 488) in the SON at 3 and 7 days post-surgery in normal saline- or GH-treated groups. (H) Quantification results of G. GH treatment reduced the number of astrocytes post-PEL. Scale bars: 50 μm (left) and 10 μm (right). Slice thickness: 3 μm. Data are expressed as mean ± SEM ( n = 5). * P < 0.05 (two-tailed unpaired t -test). AVP: Arginine vasopressin; DAPI: 4′,6-diamidino-2-phenylindole; GFAP: glial fibrillary acidic protein; GH: growth hormone; IF: immunofluorescence staining; ns: not significant; OC: optic chiasm; OXT: oxytocin; PEL: pituitary stalk electrical lesion; PEL_3d GH: 3 days post-PEL with GH treated; PEL_3d: 3 days post-PEL; PEL_7d GH: 7 days post-PEL with GH treated; PEL_7d: 7 days post-PEL; p-STAT5: signal transducer and activator of transcription 5 phosphorylation; SON: supraoptic nucleus.

    Journal: Neural Regeneration Research

    Article Title: Growth hormone promotes the reconstruction of injured axons in the hypothalamo-neurohypophyseal system

    doi: 10.4103/1673-5374.389358

    Figure Lengend Snippet: Expression pattern of p-STAT5 post-pituitary stalk electrical lesion in the supraoptic nucleus. (A) IF of p-STAT5 (red, Alexa Fluor TM 594) in AVP neurons (green, Alexa Fluor TM 488) in the SON at 3 and 7 days post-surgery in normal saline- or GH-treated groups. (B) Quantification results of A. In the GH-treated group, more AVP neurons survived at 3 days post-PEL, while the percentage of p-STAT5 cells in AVP neurons was less. (C) IF of p-STAT5 (red, Alexa Fluor TM 594) in OXT neurons (green, Alexa Fluor TM 488) in the SON at 3 and 7 days post-surgery in normal saline- or GH-treated groups. (D) Quantification results of C. In the GH-treated group, survival of OXT neurons was not different compared with normal saline, but the percentage of p-STAT5 cells in OXT neurons was greater at 7 days post-PEL. (E) IF of p-STAT5 (red, Alexa Fluor TM 594) in c-fos cells (green, Alexa Fluor TM 488) in the SON at 3 and 7 days post-surgery in normal saline- or GH-treated groups. (F) Quantification results of E. GH treatment promoted c-fos expression in the SON. (G) IF of p-STAT5 (red, Alexa Fluor TM 594) in GFAP cells (green, Alexa Fluor TM 488) in the SON at 3 and 7 days post-surgery in normal saline- or GH-treated groups. (H) Quantification results of G. GH treatment reduced the number of astrocytes post-PEL. Scale bars: 50 μm (left) and 10 μm (right). Slice thickness: 3 μm. Data are expressed as mean ± SEM ( n = 5). * P < 0.05 (two-tailed unpaired t -test). AVP: Arginine vasopressin; DAPI: 4′,6-diamidino-2-phenylindole; GFAP: glial fibrillary acidic protein; GH: growth hormone; IF: immunofluorescence staining; ns: not significant; OC: optic chiasm; OXT: oxytocin; PEL: pituitary stalk electrical lesion; PEL_3d GH: 3 days post-PEL with GH treated; PEL_3d: 3 days post-PEL; PEL_7d GH: 7 days post-PEL with GH treated; PEL_7d: 7 days post-PEL; p-STAT5: signal transducer and activator of transcription 5 phosphorylation; SON: supraoptic nucleus.

    Article Snippet: P-STAT5 , Rabbit , 1:1000 , Cell Signaling Technology , Boston, MA, USA , 9351 , AB_2315225.

    Techniques: Expressing, IF-P, Saline, Two Tailed Test, Immunofluorescence, Staining

    Ningetinib inhibits FLT3 phosphorylation and exhibits antitumor activity against FLT3-ITD mutation in vivo. A, B, C. Western blot analysis of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK in the MV4-11 and MOLM13 cells after treatment with ningetinib at the indicated doses for 2 h or 6 h. D. Schematic representation of the leukemic mouse model induced by Ba/F3-FLT3-ITD cells. E. Schematic representation of xenograft experiments using human MOLM13 cells. F. Proportion of GFP-positive cells in the BM and SP of mice, measured by flow cytometry on Day 12 ( n = 3 mice per group). G. The survival curves of BaF3-FLT3-ITD-diseased mice treated with the vehicle ( n = 7), ningetinib ( n = 7), gilteritinib ( n = 7) or quizartinib ( n = 7). H. The percentage of human CD45 positive cells in BM and SP of MOLM13-diseased NSG mice detected by flow cytometry on day 22 ( n = 3 mice per group). Error bars indicate mean ± standard error, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Journal: Cell Communication and Signaling : CCS

    Article Title: Ningetinib, a novel FLT3 inhibitor, overcomes secondary drug resistance in acute myeloid leukemia

    doi: 10.1186/s12964-024-01729-0

    Figure Lengend Snippet: Ningetinib inhibits FLT3 phosphorylation and exhibits antitumor activity against FLT3-ITD mutation in vivo. A, B, C. Western blot analysis of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK in the MV4-11 and MOLM13 cells after treatment with ningetinib at the indicated doses for 2 h or 6 h. D. Schematic representation of the leukemic mouse model induced by Ba/F3-FLT3-ITD cells. E. Schematic representation of xenograft experiments using human MOLM13 cells. F. Proportion of GFP-positive cells in the BM and SP of mice, measured by flow cytometry on Day 12 ( n = 3 mice per group). G. The survival curves of BaF3-FLT3-ITD-diseased mice treated with the vehicle ( n = 7), ningetinib ( n = 7), gilteritinib ( n = 7) or quizartinib ( n = 7). H. The percentage of human CD45 positive cells in BM and SP of MOLM13-diseased NSG mice detected by flow cytometry on day 22 ( n = 3 mice per group). Error bars indicate mean ± standard error, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Article Snippet: The following antibodies were used: anti-p-FLT3 (#3464, CST), anti-FLT3 (#3462, CST), anti-p-STAT5 (#9351, CST), anti-STAT5 (#9363, CST), anti-ERK (#4695, CST), anti-p-ERK (#4370, CST), anti-AKT (#9272, CST), anti-p-AKT (#4060, CST), anti-tubulin-HRP (#HRP-66,031, Proteintech), anti-PARP1 (#13371-1-AP, Proteintech) and anti-caspase8 (#13423-1-AP, Proteintech).

    Techniques: Activity Assay, Mutagenesis, In Vivo, Western Blot, Flow Cytometry

    Ningetinib inhibits secondary resistant TKD mutations in vitro. A. Dose‒response curve for cells with secondary mutations (FLT3-ITD-D835Y/D835V/Y842C/N676D/F691L) after treatment with ningetinib for 48 h. The mean viability of triplicate at concentration 0 was normalized as 100% as control. Error bars indicate the mean ± standard error, n = 3 independent experiments. B, C, D, E. Western blot analysis of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK expression in the FLT3-ITD-D835Y/D835V/Y842C/F691L cells treated with ningetinib for 6 h. Tubulin was used as a loading control

    Journal: Cell Communication and Signaling : CCS

    Article Title: Ningetinib, a novel FLT3 inhibitor, overcomes secondary drug resistance in acute myeloid leukemia

    doi: 10.1186/s12964-024-01729-0

    Figure Lengend Snippet: Ningetinib inhibits secondary resistant TKD mutations in vitro. A. Dose‒response curve for cells with secondary mutations (FLT3-ITD-D835Y/D835V/Y842C/N676D/F691L) after treatment with ningetinib for 48 h. The mean viability of triplicate at concentration 0 was normalized as 100% as control. Error bars indicate the mean ± standard error, n = 3 independent experiments. B, C, D, E. Western blot analysis of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK expression in the FLT3-ITD-D835Y/D835V/Y842C/F691L cells treated with ningetinib for 6 h. Tubulin was used as a loading control

    Article Snippet: The following antibodies were used: anti-p-FLT3 (#3464, CST), anti-FLT3 (#3462, CST), anti-p-STAT5 (#9351, CST), anti-STAT5 (#9363, CST), anti-ERK (#4695, CST), anti-p-ERK (#4370, CST), anti-AKT (#9272, CST), anti-p-AKT (#4060, CST), anti-tubulin-HRP (#HRP-66,031, Proteintech), anti-PARP1 (#13371-1-AP, Proteintech) and anti-caspase8 (#13423-1-AP, Proteintech).

    Techniques: In Vitro, Concentration Assay, Control, Western Blot, Expressing

    Ningetinib exhibits therapeutic potential in primary cells derived from patients with FLT3-ITD mutations. A, B, C, D. Cell viability values for primary BM cells from AML patients with FLT-ITD or FLT3-WT after treatment with different concentrations of ningetinib. The data are representative of three experiments. E. Cell viability values for PBMCs from healthy donors after treatment with different concentrations of ningetinib. F, G. Primary cells from FLT3-ITD-positive AML patients were cultured with ningetinib for 12 h. Proteins were extracted, and the expression of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK was assessed by western blot analysis. Data are presented as the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Journal: Cell Communication and Signaling : CCS

    Article Title: Ningetinib, a novel FLT3 inhibitor, overcomes secondary drug resistance in acute myeloid leukemia

    doi: 10.1186/s12964-024-01729-0

    Figure Lengend Snippet: Ningetinib exhibits therapeutic potential in primary cells derived from patients with FLT3-ITD mutations. A, B, C, D. Cell viability values for primary BM cells from AML patients with FLT-ITD or FLT3-WT after treatment with different concentrations of ningetinib. The data are representative of three experiments. E. Cell viability values for PBMCs from healthy donors after treatment with different concentrations of ningetinib. F, G. Primary cells from FLT3-ITD-positive AML patients were cultured with ningetinib for 12 h. Proteins were extracted, and the expression of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK was assessed by western blot analysis. Data are presented as the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Article Snippet: The following antibodies were used: anti-p-FLT3 (#3464, CST), anti-FLT3 (#3462, CST), anti-p-STAT5 (#9351, CST), anti-STAT5 (#9363, CST), anti-ERK (#4695, CST), anti-p-ERK (#4370, CST), anti-AKT (#9272, CST), anti-p-AKT (#4060, CST), anti-tubulin-HRP (#HRP-66,031, Proteintech), anti-PARP1 (#13371-1-AP, Proteintech) and anti-caspase8 (#13423-1-AP, Proteintech).

    Techniques: Derivative Assay, Cell Culture, Expressing, Western Blot

    Ningetinib inhibits FLT3 phosphorylation and exhibits antitumor activity against FLT3-ITD mutation in vivo. A, B, C. Western blot analysis of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK in the MV4-11 and MOLM13 cells after treatment with ningetinib at the indicated doses for 2 h or 6 h. D. Schematic representation of the leukemic mouse model induced by Ba/F3-FLT3-ITD cells. E. Schematic representation of xenograft experiments using human MOLM13 cells. F. Proportion of GFP-positive cells in the BM and SP of mice, measured by flow cytometry on Day 12 ( n = 3 mice per group). G. The survival curves of BaF3-FLT3-ITD-diseased mice treated with the vehicle ( n = 7), ningetinib ( n = 7), gilteritinib ( n = 7) or quizartinib ( n = 7). H. The percentage of human CD45 positive cells in BM and SP of MOLM13-diseased NSG mice detected by flow cytometry on day 22 ( n = 3 mice per group). Error bars indicate mean ± standard error, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Journal: Cell Communication and Signaling : CCS

    Article Title: Ningetinib, a novel FLT3 inhibitor, overcomes secondary drug resistance in acute myeloid leukemia

    doi: 10.1186/s12964-024-01729-0

    Figure Lengend Snippet: Ningetinib inhibits FLT3 phosphorylation and exhibits antitumor activity against FLT3-ITD mutation in vivo. A, B, C. Western blot analysis of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK in the MV4-11 and MOLM13 cells after treatment with ningetinib at the indicated doses for 2 h or 6 h. D. Schematic representation of the leukemic mouse model induced by Ba/F3-FLT3-ITD cells. E. Schematic representation of xenograft experiments using human MOLM13 cells. F. Proportion of GFP-positive cells in the BM and SP of mice, measured by flow cytometry on Day 12 ( n = 3 mice per group). G. The survival curves of BaF3-FLT3-ITD-diseased mice treated with the vehicle ( n = 7), ningetinib ( n = 7), gilteritinib ( n = 7) or quizartinib ( n = 7). H. The percentage of human CD45 positive cells in BM and SP of MOLM13-diseased NSG mice detected by flow cytometry on day 22 ( n = 3 mice per group). Error bars indicate mean ± standard error, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Article Snippet: The following antibodies were used: anti-p-FLT3 (#3464, CST), anti-FLT3 (#3462, CST), anti-p-STAT5 (#9351, CST), anti-STAT5 (#9363, CST), anti-ERK (#4695, CST), anti-p-ERK (#4370, CST), anti-AKT (#9272, CST), anti-p-AKT (#4060, CST), anti-tubulin-HRP (#HRP-66,031, Proteintech), anti-PARP1 (#13371-1-AP, Proteintech) and anti-caspase8 (#13423-1-AP, Proteintech).

    Techniques: Activity Assay, Mutagenesis, In Vivo, Western Blot, Flow Cytometry

    Ningetinib inhibits secondary resistant TKD mutations in vitro. A. Dose‒response curve for cells with secondary mutations (FLT3-ITD-D835Y/D835V/Y842C/N676D/F691L) after treatment with ningetinib for 48 h. The mean viability of triplicate at concentration 0 was normalized as 100% as control. Error bars indicate the mean ± standard error, n = 3 independent experiments. B, C, D, E. Western blot analysis of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK expression in the FLT3-ITD-D835Y/D835V/Y842C/F691L cells treated with ningetinib for 6 h. Tubulin was used as a loading control

    Journal: Cell Communication and Signaling : CCS

    Article Title: Ningetinib, a novel FLT3 inhibitor, overcomes secondary drug resistance in acute myeloid leukemia

    doi: 10.1186/s12964-024-01729-0

    Figure Lengend Snippet: Ningetinib inhibits secondary resistant TKD mutations in vitro. A. Dose‒response curve for cells with secondary mutations (FLT3-ITD-D835Y/D835V/Y842C/N676D/F691L) after treatment with ningetinib for 48 h. The mean viability of triplicate at concentration 0 was normalized as 100% as control. Error bars indicate the mean ± standard error, n = 3 independent experiments. B, C, D, E. Western blot analysis of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK expression in the FLT3-ITD-D835Y/D835V/Y842C/F691L cells treated with ningetinib for 6 h. Tubulin was used as a loading control

    Article Snippet: The following antibodies were used: anti-p-FLT3 (#3464, CST), anti-FLT3 (#3462, CST), anti-p-STAT5 (#9351, CST), anti-STAT5 (#9363, CST), anti-ERK (#4695, CST), anti-p-ERK (#4370, CST), anti-AKT (#9272, CST), anti-p-AKT (#4060, CST), anti-tubulin-HRP (#HRP-66,031, Proteintech), anti-PARP1 (#13371-1-AP, Proteintech) and anti-caspase8 (#13423-1-AP, Proteintech).

    Techniques: In Vitro, Concentration Assay, Control, Western Blot, Expressing

    Ningetinib exhibits therapeutic potential in primary cells derived from patients with FLT3-ITD mutations. A, B, C, D. Cell viability values for primary BM cells from AML patients with FLT-ITD or FLT3-WT after treatment with different concentrations of ningetinib. The data are representative of three experiments. E. Cell viability values for PBMCs from healthy donors after treatment with different concentrations of ningetinib. F, G. Primary cells from FLT3-ITD-positive AML patients were cultured with ningetinib for 12 h. Proteins were extracted, and the expression of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK was assessed by western blot analysis. Data are presented as the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Journal: Cell Communication and Signaling : CCS

    Article Title: Ningetinib, a novel FLT3 inhibitor, overcomes secondary drug resistance in acute myeloid leukemia

    doi: 10.1186/s12964-024-01729-0

    Figure Lengend Snippet: Ningetinib exhibits therapeutic potential in primary cells derived from patients with FLT3-ITD mutations. A, B, C, D. Cell viability values for primary BM cells from AML patients with FLT-ITD or FLT3-WT after treatment with different concentrations of ningetinib. The data are representative of three experiments. E. Cell viability values for PBMCs from healthy donors after treatment with different concentrations of ningetinib. F, G. Primary cells from FLT3-ITD-positive AML patients were cultured with ningetinib for 12 h. Proteins were extracted, and the expression of p-FLT3, FLT3, p-STAT5, STAT5, p-AKT, AKT, p-ERK and ERK was assessed by western blot analysis. Data are presented as the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Article Snippet: The following antibodies were used: anti-p-FLT3 (#3464, CST), anti-FLT3 (#3462, CST), anti-p-STAT5 (#9351, CST), anti-STAT5 (#9363, CST), anti-ERK (#4695, CST), anti-p-ERK (#4370, CST), anti-AKT (#9272, CST), anti-p-AKT (#4060, CST), anti-tubulin-HRP (#HRP-66,031, Proteintech), anti-PARP1 (#13371-1-AP, Proteintech) and anti-caspase8 (#13423-1-AP, Proteintech).

    Techniques: Derivative Assay, Cell Culture, Expressing, Western Blot

    A , B Flow cytometry analysis (left) and MFI intensity (right) demonstrate the expression levels of p-STAT5, p-S6, p-AKT473 and p-Erk in NK cells from Mst1/2 fl/fl and Mst1/2 fl/fl CD122 Cre mice upon stimulation with or without IL-15 (50 ng/mL) for 30 min ( n ≥ 4). C Gene-set enrichment analysis of RNA-seq data shows the enrichment of hallmark-IL6-JAK-STAT3-signaling related genes in Mst1/2-deficient NK cells compared to WT NK cells. D Flow cytometry analysis (left) and MFI intensity (right) reveals the expression level of p-STAT3 (Ser727) in NK cells from Mst1/2 fl/fl and Mst1/2 fl/fl CD122 Cre mice upon stimulation with or without IL-15 (50 ng/mL) for 30 min ( n = 4). E ChIP-qPCR analysis demonstrated binding of p-STAT3 conserved motifs in the Tcf7 5′ regulatory region (−17.5 kb), while no binding was observed in a region without p-STAT3-binding motifs (+0.2 kb), serving as a negative control. The experiments were using sorted NK cells from WT mice with anti-p-STAT3 antibody or isotype-matched IgG. F – I WT splenocytes were treated with DMSO, Mst1 inhibitor XMU-MP-1 (1 mM, MedChemExpress) or p-STAT3 inhibitor Stattic (1 mM, MedChemExpress) for 24 h, followed by flow cytometry analysis. The representative plots (left) and summary data (right) show the expression level of p-STAT3 (F), TCF1 ( G ), total cellular ROS ( H ) and the percentage of 7AAD + NK cells ( I ) ( n = 4). J Schematic illustration of Mst1/2 regulate NK cell survival and function via controlling metabolic state and transcriptional activity. Data A , B and D – I are representative of three independent experiments with similar results.

    Journal: Cell Death & Disease

    Article Title: Hippo kinases Mst1 and Mst2 maintain NK cell homeostasis by orchestrating metabolic state and transcriptional activity

    doi: 10.1038/s41419-024-06828-x

    Figure Lengend Snippet: A , B Flow cytometry analysis (left) and MFI intensity (right) demonstrate the expression levels of p-STAT5, p-S6, p-AKT473 and p-Erk in NK cells from Mst1/2 fl/fl and Mst1/2 fl/fl CD122 Cre mice upon stimulation with or without IL-15 (50 ng/mL) for 30 min ( n ≥ 4). C Gene-set enrichment analysis of RNA-seq data shows the enrichment of hallmark-IL6-JAK-STAT3-signaling related genes in Mst1/2-deficient NK cells compared to WT NK cells. D Flow cytometry analysis (left) and MFI intensity (right) reveals the expression level of p-STAT3 (Ser727) in NK cells from Mst1/2 fl/fl and Mst1/2 fl/fl CD122 Cre mice upon stimulation with or without IL-15 (50 ng/mL) for 30 min ( n = 4). E ChIP-qPCR analysis demonstrated binding of p-STAT3 conserved motifs in the Tcf7 5′ regulatory region (−17.5 kb), while no binding was observed in a region without p-STAT3-binding motifs (+0.2 kb), serving as a negative control. The experiments were using sorted NK cells from WT mice with anti-p-STAT3 antibody or isotype-matched IgG. F – I WT splenocytes were treated with DMSO, Mst1 inhibitor XMU-MP-1 (1 mM, MedChemExpress) or p-STAT3 inhibitor Stattic (1 mM, MedChemExpress) for 24 h, followed by flow cytometry analysis. The representative plots (left) and summary data (right) show the expression level of p-STAT3 (F), TCF1 ( G ), total cellular ROS ( H ) and the percentage of 7AAD + NK cells ( I ) ( n = 4). J Schematic illustration of Mst1/2 regulate NK cell survival and function via controlling metabolic state and transcriptional activity. Data A , B and D – I are representative of three independent experiments with similar results.

    Article Snippet: Monoclonal antibodies against mouse TCF1 (Cat#9066S), phospho-Mob1 (Thr35) (Cat#8699), Bim (C34C5) Rabbit mAb (Cat#12186), Phospho-Stat5 (Tyr694) (Cat#9359), phospho-p44/42 MAPK (Erk1/2) (Thr202/Tyr204) (Cat#4370S) and polyclonal antibodies against mouse Mst1 (Cat#3682) were obtained from Cell Signaling Technology (Beverly, MA).

    Techniques: Flow Cytometry, Expressing, RNA Sequencing Assay, Binding Assay, Negative Control, Activity Assay