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fgfr 3 antibody  (Novus Biologicals)
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Novus Biologicals fgfr 3 antibody
Fgfr 3 Antibody, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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fgfr3  (Novus Biologicals)
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Novus Biologicals fgfr3
Loss of <t>FGFR3</t> promotes the generation of weakly pathogenic CD117 + MLL-AF9-driven leukemia cells. (A) Representative flow cytometric analysis of MA-WT and MA-KO cells with CD117 and CD11b staining (B) In vitro colony-forming assay of MA-WT and MA-KO cells (n = 3). (C) Growth curve at indicated time from MA-WT and MA-KO cells (n = 5). (D,E) Effects of FGFR3 deletion in MLL-AF9-mediated in vivo leukemogenesis. Kaplan-Meier curves are shown for two groups of transplanted mice including MA-WT (n = 9), and MA-KO (n = 10) in a primary BMT assay (D) , and for two groups of transplanted mice including MA-WT (n = 11), and MA-KO (n = 12) in the secondary BMT assay (E) .* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
Fgfr3, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/fgfr3/product/Novus Biologicals
Average 93 stars, based on 1 article reviews
fgfr3 - by Bioz Stars, 2025-05
93/100 stars
  Buy from Supplier

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Loss of FGFR3 promotes the generation of weakly pathogenic CD117 + MLL-AF9-driven leukemia cells. (A) Representative flow cytometric analysis of MA-WT and MA-KO cells with CD117 and CD11b staining (B) In vitro colony-forming assay of MA-WT and MA-KO cells (n = 3). (C) Growth curve at indicated time from MA-WT and MA-KO cells (n = 5). (D,E) Effects of FGFR3 deletion in MLL-AF9-mediated in vivo leukemogenesis. Kaplan-Meier curves are shown for two groups of transplanted mice including MA-WT (n = 9), and MA-KO (n = 10) in a primary BMT assay (D) , and for two groups of transplanted mice including MA-WT (n = 11), and MA-KO (n = 12) in the secondary BMT assay (E) .* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Frontiers in Pharmacology

Article Title: Loss of FGFR3 Delays Acute Myeloid Leukemogenesis by Programming Weakly Pathogenic CD117-Positive Leukemia Stem-Like Cells

doi: 10.3389/fphar.2020.632809

Figure Lengend Snippet: Loss of FGFR3 promotes the generation of weakly pathogenic CD117 + MLL-AF9-driven leukemia cells. (A) Representative flow cytometric analysis of MA-WT and MA-KO cells with CD117 and CD11b staining (B) In vitro colony-forming assay of MA-WT and MA-KO cells (n = 3). (C) Growth curve at indicated time from MA-WT and MA-KO cells (n = 5). (D,E) Effects of FGFR3 deletion in MLL-AF9-mediated in vivo leukemogenesis. Kaplan-Meier curves are shown for two groups of transplanted mice including MA-WT (n = 9), and MA-KO (n = 10) in a primary BMT assay (D) , and for two groups of transplanted mice including MA-WT (n = 11), and MA-KO (n = 12) in the secondary BMT assay (E) .* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: For Western blotting and ChIP assays, the following antibodies were used: p-ERK (CST; #4370S; 1:1,000), ERK (Bioworld; BS1112; 1:1,000), AKT (CST; #9272S; 1:1,000), p-AKT (CST; 4060S; 1:1,000), FGFR1 (CST; 9740S; 1:1,000), p-FGFR1 (Affinity; AF3157; 1:1,000), ACTIN (CMCTAG; AT0001; 1:1,000), Goat Anti-Rabbit IgG (Bioworld; BS13278; 1:10,000), FGFR3 (NOVUS Biologicals; JM110–33; 1:1,000), ERG (abcam; ab92513; 1:1,000), HA Tag (Life Science; AB10004; 1:1,000).

Techniques: Staining, In Vitro, In Vivo

FGFR3 deletion significantly inhibits in vivo engraftment of leukemic mice. (A–C) The engraftment ability of GFP + MA-WT and MA-KO cells from BM and SP at day 7 (A) , day 14 (B) , and day 30 (C) after transplantation. (D) Representative image of hematoxylin and eosin-stained sections at day 30 after transplantation of MA-WT and MA-KO cells. ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Frontiers in Pharmacology

Article Title: Loss of FGFR3 Delays Acute Myeloid Leukemogenesis by Programming Weakly Pathogenic CD117-Positive Leukemia Stem-Like Cells

doi: 10.3389/fphar.2020.632809

Figure Lengend Snippet: FGFR3 deletion significantly inhibits in vivo engraftment of leukemic mice. (A–C) The engraftment ability of GFP + MA-WT and MA-KO cells from BM and SP at day 7 (A) , day 14 (B) , and day 30 (C) after transplantation. (D) Representative image of hematoxylin and eosin-stained sections at day 30 after transplantation of MA-WT and MA-KO cells. ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: For Western blotting and ChIP assays, the following antibodies were used: p-ERK (CST; #4370S; 1:1,000), ERK (Bioworld; BS1112; 1:1,000), AKT (CST; #9272S; 1:1,000), p-AKT (CST; 4060S; 1:1,000), FGFR1 (CST; 9740S; 1:1,000), p-FGFR1 (Affinity; AF3157; 1:1,000), ACTIN (CMCTAG; AT0001; 1:1,000), Goat Anti-Rabbit IgG (Bioworld; BS13278; 1:10,000), FGFR3 (NOVUS Biologicals; JM110–33; 1:1,000), ERG (abcam; ab92513; 1:1,000), HA Tag (Life Science; AB10004; 1:1,000).

Techniques: In Vivo, Transplantation Assay, Staining

FGFR3 deletion programs CD117 + leukemia cells by activating the FGFR1-ERG-CD117 signaling pathway. (A) Representative flow cytometric analysis of CD117 + CD11b +/low in MA-WT and MA-KO cells with FGFR inhibitor (PD173074, 4 μM), AKT inhibitor (LY294002, 50 μM), and MEK inhibitor (PD98059, 50 μM). (B) Western blot analysis of ERG expression in 293T cells expressing CA-FGFR1. (C,D) Flow cytometric analysis of CD117 + CD11b +/low in WT-ERG cells (C) and KO-shERG cells. (D,E) ChIP-qPCR assay of potential binding of ERG at the promoter region of CD117 (n = 4) (F) luciferase report assay of transcriptional regulation function of ERG (n = 4). (G) Western blot analysis of ERG expression in 293T cells expressing CA-FGFR1 in the presence of signaling inhibitor. (H) The expression of p -FGFR1, p -ERK1/2, p -AKT, and ERG in MA-WT and MA-KO cells treated with PD173074 (5 μM), LY294002 (50 μM), and PD98059 (50 μM) for 16 h ** p < 0.01, **** p < 0.0001.

Journal: Frontiers in Pharmacology

Article Title: Loss of FGFR3 Delays Acute Myeloid Leukemogenesis by Programming Weakly Pathogenic CD117-Positive Leukemia Stem-Like Cells

doi: 10.3389/fphar.2020.632809

Figure Lengend Snippet: FGFR3 deletion programs CD117 + leukemia cells by activating the FGFR1-ERG-CD117 signaling pathway. (A) Representative flow cytometric analysis of CD117 + CD11b +/low in MA-WT and MA-KO cells with FGFR inhibitor (PD173074, 4 μM), AKT inhibitor (LY294002, 50 μM), and MEK inhibitor (PD98059, 50 μM). (B) Western blot analysis of ERG expression in 293T cells expressing CA-FGFR1. (C,D) Flow cytometric analysis of CD117 + CD11b +/low in WT-ERG cells (C) and KO-shERG cells. (D,E) ChIP-qPCR assay of potential binding of ERG at the promoter region of CD117 (n = 4) (F) luciferase report assay of transcriptional regulation function of ERG (n = 4). (G) Western blot analysis of ERG expression in 293T cells expressing CA-FGFR1 in the presence of signaling inhibitor. (H) The expression of p -FGFR1, p -ERK1/2, p -AKT, and ERG in MA-WT and MA-KO cells treated with PD173074 (5 μM), LY294002 (50 μM), and PD98059 (50 μM) for 16 h ** p < 0.01, **** p < 0.0001.

Article Snippet: For Western blotting and ChIP assays, the following antibodies were used: p-ERK (CST; #4370S; 1:1,000), ERK (Bioworld; BS1112; 1:1,000), AKT (CST; #9272S; 1:1,000), p-AKT (CST; 4060S; 1:1,000), FGFR1 (CST; 9740S; 1:1,000), p-FGFR1 (Affinity; AF3157; 1:1,000), ACTIN (CMCTAG; AT0001; 1:1,000), Goat Anti-Rabbit IgG (Bioworld; BS13278; 1:10,000), FGFR3 (NOVUS Biologicals; JM110–33; 1:1,000), ERG (abcam; ab92513; 1:1,000), HA Tag (Life Science; AB10004; 1:1,000).

Techniques: Western Blot, Expressing, Binding Assay, Luciferase

FGFR3 deletion decreases the expression of the inflammation factors and the extended survival time of MA-KO cell-transplanted mice could be neutralized by overexpression of CCL3. (A) Gene list rank about inflammatory response genes from RNA-seq data. (B) Heat map on the expression level of inflammatory response genes in MA-WT samples (W1, W2, and W3) and MA-KO samples (F1, F2, and F3). (C) Differential expression genes from (B) by qRT-PCR analysis (n = 4). (D,E) The concentration of CCL3 (D) and CCL4 (E) in BM supernatant of leukemic mice at day 30 after transplantation by ELISA (n = 4). (F) Overexpression of CCL3 in MA-WT and MA-KO cells (n = 4). (G) Number of cell migration from 100,000MA-WT-CCL3 or MA-KO-CCL3 cells compared with respective control cells (n = 3). (H,I) Kaplan-Meier curves are shown for in vivo leukemogenesis in two groups of mice transplanted with leukemia cells, including MA-WT-puro cells (n = 6), and MA-WT-CCL3 cells (n = 5) (H) as well as MA-KO-puro cells (n = 6), and MA-KO-CCL3 cells (n = 5) (I) . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Frontiers in Pharmacology

Article Title: Loss of FGFR3 Delays Acute Myeloid Leukemogenesis by Programming Weakly Pathogenic CD117-Positive Leukemia Stem-Like Cells

doi: 10.3389/fphar.2020.632809

Figure Lengend Snippet: FGFR3 deletion decreases the expression of the inflammation factors and the extended survival time of MA-KO cell-transplanted mice could be neutralized by overexpression of CCL3. (A) Gene list rank about inflammatory response genes from RNA-seq data. (B) Heat map on the expression level of inflammatory response genes in MA-WT samples (W1, W2, and W3) and MA-KO samples (F1, F2, and F3). (C) Differential expression genes from (B) by qRT-PCR analysis (n = 4). (D,E) The concentration of CCL3 (D) and CCL4 (E) in BM supernatant of leukemic mice at day 30 after transplantation by ELISA (n = 4). (F) Overexpression of CCL3 in MA-WT and MA-KO cells (n = 4). (G) Number of cell migration from 100,000MA-WT-CCL3 or MA-KO-CCL3 cells compared with respective control cells (n = 3). (H,I) Kaplan-Meier curves are shown for in vivo leukemogenesis in two groups of mice transplanted with leukemia cells, including MA-WT-puro cells (n = 6), and MA-WT-CCL3 cells (n = 5) (H) as well as MA-KO-puro cells (n = 6), and MA-KO-CCL3 cells (n = 5) (I) . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: For Western blotting and ChIP assays, the following antibodies were used: p-ERK (CST; #4370S; 1:1,000), ERK (Bioworld; BS1112; 1:1,000), AKT (CST; #9272S; 1:1,000), p-AKT (CST; 4060S; 1:1,000), FGFR1 (CST; 9740S; 1:1,000), p-FGFR1 (Affinity; AF3157; 1:1,000), ACTIN (CMCTAG; AT0001; 1:1,000), Goat Anti-Rabbit IgG (Bioworld; BS13278; 1:10,000), FGFR3 (NOVUS Biologicals; JM110–33; 1:1,000), ERG (abcam; ab92513; 1:1,000), HA Tag (Life Science; AB10004; 1:1,000).

Techniques: Expressing, Over Expression, RNA Sequencing Assay, Quantitative RT-PCR, Concentration Assay, Transplantation Assay, Enzyme-linked Immunosorbent Assay, Migration, In Vivo

Schematic model of FGFR3 signaling in AML. Schematic model showed that FGFR3 might upregulate CCL expression by activating MEK-ERK1/2 to maintain leukemogenesis. In addition, FGFR3 deletion programs weakly pathogenic CD117 + leukemia stem-like cells by activating FGFR1-AKT-ERG-CD117 signaling. Furthermore, ERG does not only promote the stemness of LSCs by upregulating the expression of CD117, but also suppresses in vivo leukemogenesis by inhibiting the expression of chemokines genes.

Journal: Frontiers in Pharmacology

Article Title: Loss of FGFR3 Delays Acute Myeloid Leukemogenesis by Programming Weakly Pathogenic CD117-Positive Leukemia Stem-Like Cells

doi: 10.3389/fphar.2020.632809

Figure Lengend Snippet: Schematic model of FGFR3 signaling in AML. Schematic model showed that FGFR3 might upregulate CCL expression by activating MEK-ERK1/2 to maintain leukemogenesis. In addition, FGFR3 deletion programs weakly pathogenic CD117 + leukemia stem-like cells by activating FGFR1-AKT-ERG-CD117 signaling. Furthermore, ERG does not only promote the stemness of LSCs by upregulating the expression of CD117, but also suppresses in vivo leukemogenesis by inhibiting the expression of chemokines genes.

Article Snippet: For Western blotting and ChIP assays, the following antibodies were used: p-ERK (CST; #4370S; 1:1,000), ERK (Bioworld; BS1112; 1:1,000), AKT (CST; #9272S; 1:1,000), p-AKT (CST; 4060S; 1:1,000), FGFR1 (CST; 9740S; 1:1,000), p-FGFR1 (Affinity; AF3157; 1:1,000), ACTIN (CMCTAG; AT0001; 1:1,000), Goat Anti-Rabbit IgG (Bioworld; BS13278; 1:10,000), FGFR3 (NOVUS Biologicals; JM110–33; 1:1,000), ERG (abcam; ab92513; 1:1,000), HA Tag (Life Science; AB10004; 1:1,000).

Techniques: Expressing, In Vivo