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Cell Signaling Technology Inc anti cyr61
Anti Cyr61, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Effects of highly expressed proteins on EMT in OS.

Cyr61, 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
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Average 86 stars, based on 1 article reviews
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cyr61 - by Bioz Stars, 2023-03

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1) Product Images from "Regulation of the Epithelial to Mesenchymal Transition in Osteosarcoma"

Article Title: Regulation of the Epithelial to Mesenchymal Transition in Osteosarcoma

Journal: Biomolecules

doi: 10.3390/biom13020398

Figure Legend Snippet: Effects of highly expressed proteins on EMT in OS.

Techniques Used: Migration, In Vivo

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Primer sequences used in qRT-PCR assays

Anti Cyr61, 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
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1) Product Images from "WWP2 drives the progression of gastric cancer by facilitating the ubiquitination and degradation of LATS1 protein"

Article Title: WWP2 drives the progression of gastric cancer by facilitating the ubiquitination and degradation of LATS1 protein

Journal: Cell Communication and Signaling : CCS

doi: 10.1186/s12964-023-01050-2

Figure Legend Snippet: Primer sequences used in qRT-PCR assays

Techniques Used:

WWP2 orchestrates the Hippo-YAP1 pathway by ubiquitinating LATS1 protein. A, B Western blotting assays were performed to detect the protein expression of LATS1/2, YAP1, p-YAP and its downstream target genes CYR61 and CTGF in GC cells upon corresponding treatments as presented. C, D qRT‒PCR analysis of the mRNA expression of WWP2, LATS1, YAP1, CTGF, CYR61 and AREG in GC cells upon WWP2 upregulation or knockdown. E Western blotting analysis of LATS1 protein in modified SGC-7901 cells upon WWP2 silencing and treatment with CHX (25 μg/mL) for specific time points. F The abundance of LATS1 protein was quantified and is shown in line graphs. G, H Western blotting analysis of in vivo ubiquitination. G BGC-823 cells were co-transfected with WWP2 shRNA or scramble shRNA and treated with MG132 for 6 h before harvesting. H SGC-7901 cells were transfected with combinations of plasmids encoding HA-WWP2, Flag-LATS1 and His-Ub, and the cells were treated with MG132 for 6 h before being harvested for further study. Student’s t test: * p < 0.05, ** p < 0.01

Figure Legend Snippet: WWP2 orchestrates the Hippo-YAP1 pathway by ubiquitinating LATS1 protein. A, B Western blotting assays were performed to detect the protein expression of LATS1/2, YAP1, p-YAP and its downstream target genes CYR61 and CTGF in GC cells upon corresponding treatments as presented. C, D qRT‒PCR analysis of the mRNA expression of WWP2, LATS1, YAP1, CTGF, CYR61 and AREG in GC cells upon WWP2 upregulation or knockdown. E Western blotting analysis of LATS1 protein in modified SGC-7901 cells upon WWP2 silencing and treatment with CHX (25 μg/mL) for specific time points. F The abundance of LATS1 protein was quantified and is shown in line graphs. G, H Western blotting analysis of in vivo ubiquitination. G BGC-823 cells were co-transfected with WWP2 shRNA or scramble shRNA and treated with MG132 for 6 h before harvesting. H SGC-7901 cells were transfected with combinations of plasmids encoding HA-WWP2, Flag-LATS1 and His-Ub, and the cells were treated with MG132 for 6 h before being harvested for further study. Student’s t test: * p < 0.05, ** p < 0.01

Techniques Used: Western Blot, Expressing, Modification, In Vivo, Transfection, shRNA

LATS1 functions as a crucial mediator of WWP2 to promote GC cell proliferation and invasion. A, B The protein expression of WWP2, LATS1, YAP1, p -YAP and its downstream target genes, CTGF and CYR61, was detected by western blotting analysis in WWP2-silenced HGC-27 cells co-transfected with or without LATS1 siRNA. C, D Colony formation experiments were performed in WWP2-silenced HGC-27 cells co-transfected with or without LATS1 siRNA. E–H The invasive and migrative abilities were analyzed in WWP2-silenced HGC-27 cells co-transfected with or without LATS1 siRNA by transwell E, F or wound healing assays G, H , respectively. One-way ANOVA: * p < 0.05, ** p < 0.01

Figure Legend Snippet: LATS1 functions as a crucial mediator of WWP2 to promote GC cell proliferation and invasion. A, B The protein expression of WWP2, LATS1, YAP1, p -YAP and its downstream target genes, CTGF and CYR61, was detected by western blotting analysis in WWP2-silenced HGC-27 cells co-transfected with or without LATS1 siRNA. C, D Colony formation experiments were performed in WWP2-silenced HGC-27 cells co-transfected with or without LATS1 siRNA. E–H The invasive and migrative abilities were analyzed in WWP2-silenced HGC-27 cells co-transfected with or without LATS1 siRNA by transwell E, F or wound healing assays G, H , respectively. One-way ANOVA: * p < 0.05, ** p < 0.01

Techniques Used: Expressing, Western Blot, Transfection

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( A ) p - YAP and t-YAP expression in WT and jck kidneys. ( B ) p - TAZ and t-TAZ expression by Western blotting in WT and jck kidneys. ( C ) YAP and ( D ) TAZ expression by IHC in WT and jck kidney sections. Scale bars: 50 μm. ( E ) Expression of YAP and TAZ target genes <t>Cyr61</t> and Ctgf in jck kidneys compared with WT by quantitative real-time PCR and ( F ) by IHC. Data represent the mean ± SEM. * P < 0.05 and ** P < 0.01, by unpaired Student’s t test.

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1) Product Images from "SCF-SKP2 E3 ubiquitin ligase links mTORC1/ER stress/ISR with YAP activation in murine renal cystogenesis"

Article Title: SCF-SKP2 E3 ubiquitin ligase links mTORC1/ER stress/ISR with YAP activation in murine renal cystogenesis

Journal: The Journal of Clinical Investigation

doi: 10.1172/JCI153943

Figure Legend Snippet: ( A ) p - YAP and t-YAP expression in WT and jck kidneys. ( B ) p - TAZ and t-TAZ expression by Western blotting in WT and jck kidneys. ( C ) YAP and ( D ) TAZ expression by IHC in WT and jck kidney sections. Scale bars: 50 μm. ( E ) Expression of YAP and TAZ target genes Cyr61 and Ctgf in jck kidneys compared with WT by quantitative real-time PCR and ( F ) by IHC. Data represent the mean ± SEM. * P < 0.05 and ** P < 0.01, by unpaired Student’s t test.

Techniques Used: Expressing, Western Blot, Real-time Polymerase Chain Reaction

( A ) Urine output (microliters of urine over 4 hours) by mice of the indicated genotypes. ( B ) Representative expression levels of p-mTOR and t-mTOR, ATF4, and CHOP in the kidneys of mice of the indicated genotypes ( n = 4 mice for each genotype). ( C ) CYR61 and ( D ) MYC protein levels in kidneys from mice of the corresponding genotypes, as indicators of YAP target gene transcriptional activity ( n = 2 and 4, mice respectively, for each of the indicated genotypes). mRNA expression of the YAP target genes ( E ) Cyr61 , ( F ) Myc , ( G ) Ctgf , ( H ) Ankrd1 , and ( I ) Nppb by quantitative real-time PCR relative to Actb in kidney extracts from mice of the indicated genotypes ( n = 4 mice for each genotype). Data are representative of 2 independent experiments. ( J ) Taz mRNA expression in kidneys from mice of the indicated genotypes. Data represent the mean ± SEM. * P < 0.05, ** P < 0.01, and *** P < 0.001, by 1-way ANOVA followed by a Tukey-Kramer multiple-comparison test.

Figure Legend Snippet: ( A ) Urine output (microliters of urine over 4 hours) by mice of the indicated genotypes. ( B ) Representative expression levels of p-mTOR and t-mTOR, ATF4, and CHOP in the kidneys of mice of the indicated genotypes ( n = 4 mice for each genotype). ( C ) CYR61 and ( D ) MYC protein levels in kidneys from mice of the corresponding genotypes, as indicators of YAP target gene transcriptional activity ( n = 2 and 4, mice respectively, for each of the indicated genotypes). mRNA expression of the YAP target genes ( E ) Cyr61 , ( F ) Myc , ( G ) Ctgf , ( H ) Ankrd1 , and ( I ) Nppb by quantitative real-time PCR relative to Actb in kidney extracts from mice of the indicated genotypes ( n = 4 mice for each genotype). Data are representative of 2 independent experiments. ( J ) Taz mRNA expression in kidneys from mice of the indicated genotypes. Data represent the mean ± SEM. * P < 0.05, ** P < 0.01, and *** P < 0.001, by 1-way ANOVA followed by a Tukey-Kramer multiple-comparison test.

Techniques Used: Expressing, Activity Assay, Real-time Polymerase Chain Reaction

( A ) YAP immunostaining in kidney sections from Cre – (control) and Cre + EO and LO Pkd1 cond Pax8 Tet-On – mice. Scale bars: 100 μm. ( B ) p-mTOR, t-mTOR, YAP, CYR61, and SKP2 expression in kidney tissue extracts from Cre – and Cre + EO mice. ( C ) Schematic representation of the mechanistic pathways proposed to contribute to YAP-mediated renal cystogenesis and its progression. Lines represent direct/indirect activation (arrowhead) or inactivation (blunt end). The various drugs used for this study are indicated in red. Additional details are found in the body of the manuscript.

Figure Legend Snippet: ( A ) YAP immunostaining in kidney sections from Cre – (control) and Cre + EO and LO Pkd1 cond Pax8 Tet-On – mice. Scale bars: 100 μm. ( B ) p-mTOR, t-mTOR, YAP, CYR61, and SKP2 expression in kidney tissue extracts from Cre – and Cre + EO mice. ( C ) Schematic representation of the mechanistic pathways proposed to contribute to YAP-mediated renal cystogenesis and its progression. Lines represent direct/indirect activation (arrowhead) or inactivation (blunt end). The various drugs used for this study are indicated in red. Additional details are found in the body of the manuscript.

Techniques Used: Immunostaining, Expressing, Activation Assay

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mRNA expression of HIPPO signalling effectors after CAP treatment: mRNA expression of YAP, CTGF, and <t>Cyr61</t> in HaCaTs (a) and GM Fbs (b) measured 3, 6, 18, and 24 hr after CAP treatment by qPCR and normalized to relative gene expression ( ΔΔ CT values on a log2 scale). The x -axis represents CAP treatment time and incubation time after plasma treatment. Data are represented as mean ± SD of either three (a) or four (b) independent experiments. Statistical analysis was performed using unpaired t -test with Welch's correction for multiple comparisons, along with normalization to the untreated control.

cyr61 - by Bioz Stars, 2023-03

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1) Product Images from "The HIPPO Transducer YAP and Its Targets CTGF and Cyr61 Drive a Paracrine Signalling in Cold Atmospheric Plasma-Mediated Wound Healing"

Article Title: The HIPPO Transducer YAP and Its Targets CTGF and Cyr61 Drive a Paracrine Signalling in Cold Atmospheric Plasma-Mediated Wound Healing

Journal: Oxidative Medicine and Cellular Longevity

doi: 10.1155/2020/4910280

mRNA expression of HIPPO signalling effectors after CAP treatment: mRNA expression of YAP, CTGF, and Cyr61 in HaCaTs (a) and GM Fbs (b) measured 3, 6, 18, and 24 hr after CAP treatment by qPCR and normalized to relative gene expression ( ΔΔ CT values on a log2 scale). The x -axis represents CAP treatment time and incubation time after plasma treatment. Data are represented as mean ± SD of either three (a) or four (b) independent experiments. Statistical analysis was performed using unpaired t -test with Welch's correction for multiple comparisons, along with normalization to the untreated control.

Figure Legend Snippet: mRNA expression of HIPPO signalling effectors after CAP treatment: mRNA expression of YAP, CTGF, and Cyr61 in HaCaTs (a) and GM Fbs (b) measured 3, 6, 18, and 24 hr after CAP treatment by qPCR and normalized to relative gene expression ( ΔΔ CT values on a log2 scale). The x -axis represents CAP treatment time and incubation time after plasma treatment. Data are represented as mean ± SD of either three (a) or four (b) independent experiments. Statistical analysis was performed using unpaired t -test with Welch's correction for multiple comparisons, along with normalization to the untreated control.

Techniques Used: Expressing, Incubation

Effect of CAP on the HIPPO signalling pathway: the relative phosphorylation level of YAP is shown in GM Fbs (a) and HaCaT cells (b). CTGF and Cyr61 protein expression was enhanced after 10 and 30 s of CAP treatment in GM Fbs (c, d). CTGF expression slightly increased after 10 and 30 s of CAP treatments in HaCaT cells after approximately 3 hours (e). Representative blots are shown. The x -axis represents CAP treatment time and incubation time after plasma treatment. Data are represented as mean ± SD of at least three independent experiments. Statistical analysis was performed using unpaired t -test with Welch's correction for multiple comparisons, along with normalization to the untreated control.

Figure Legend Snippet: Effect of CAP on the HIPPO signalling pathway: the relative phosphorylation level of YAP is shown in GM Fbs (a) and HaCaT cells (b). CTGF and Cyr61 protein expression was enhanced after 10 and 30 s of CAP treatment in GM Fbs (c, d). CTGF expression slightly increased after 10 and 30 s of CAP treatments in HaCaT cells after approximately 3 hours (e). Representative blots are shown. The x -axis represents CAP treatment time and incubation time after plasma treatment. Data are represented as mean ± SD of at least three independent experiments. Statistical analysis was performed using unpaired t -test with Welch's correction for multiple comparisons, along with normalization to the untreated control.

Techniques Used: Expressing, Incubation

Effect of NAC on the YAP-CTGF-Cyr61 signalling cascade: mRNA expression of YAP, CTGF, and Cyr61 in HaCaTs (a) and GM Fbs (b) measured 18 hr after CAP treatment by qPCR and normalized to relative gene expression ( ΔΔ CT values on a log2 scale). Data are presented as mean ± SD from at least three independent experiments, and statistical analysis was performed using unpaired t -test with Welch's correction.

Figure Legend Snippet: Effect of NAC on the YAP-CTGF-Cyr61 signalling cascade: mRNA expression of YAP, CTGF, and Cyr61 in HaCaTs (a) and GM Fbs (b) measured 18 hr after CAP treatment by qPCR and normalized to relative gene expression ( ΔΔ CT values on a log2 scale). Data are presented as mean ± SD from at least three independent experiments, and statistical analysis was performed using unpaired t -test with Welch's correction.

Techniques Used: Expressing

Effect of CAP on paracrine signalling between keratinocytes and fibroblasts: HaCaT cells were incubated with conditioned media harvested from untreated or 10 and 30 s CAP-treated GM Fbs. Relative wound density of HaCaT cells was monitored after 6, 12, 18, and 24 hr (a). Secreted CTGF and Cyr61 (pg/ml) was analysed by ELISA (b). Relative wound density in HaCaT cells was monitored after treatment with 10 and 50 ng/ml CTGF and 100 ng/ml and 1 μ g/ml Cyr61 (c, d). Data are presented as mean ± SD from three (a, c, d) or two (b) independent experiments, and statistical analysis was performed using 1- (b) or 2-way ANOVA (a, c, d).

Figure Legend Snippet: Effect of CAP on paracrine signalling between keratinocytes and fibroblasts: HaCaT cells were incubated with conditioned media harvested from untreated or 10 and 30 s CAP-treated GM Fbs. Relative wound density of HaCaT cells was monitored after 6, 12, 18, and 24 hr (a). Secreted CTGF and Cyr61 (pg/ml) was analysed by ELISA (b). Relative wound density in HaCaT cells was monitored after treatment with 10 and 50 ng/ml CTGF and 100 ng/ml and 1 μ g/ml Cyr61 (c, d). Data are presented as mean ± SD from three (a, c, d) or two (b) independent experiments, and statistical analysis was performed using 1- (b) or 2-way ANOVA (a, c, d).

Techniques Used: Incubation, Enzyme-linked Immunosorbent Assay

Schematic of keratinocyte activation by CAP modulated fibroblasts: the primary event in this scheme is the generation of reactive species in response to CAP treatment. These reactive species function as secondary messengers and stimulate the production of HIPPO signalling effectors such as CTGF in HaCaT and CTGF and Cyr61 by dermal fibroblasts in the vicinity. These extracellular matrix proteins that are released from fibroblasts in turn activate keratinocytes, accelerate migration, and promote wound healing.

Figure Legend Snippet: Schematic of keratinocyte activation by CAP modulated fibroblasts: the primary event in this scheme is the generation of reactive species in response to CAP treatment. These reactive species function as secondary messengers and stimulate the production of HIPPO signalling effectors such as CTGF in HaCaT and CTGF and Cyr61 by dermal fibroblasts in the vicinity. These extracellular matrix proteins that are released from fibroblasts in turn activate keratinocytes, accelerate migration, and promote wound healing.

Techniques Used: Activation Assay, Migration

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YAP confers resistance to cisplatin in ovarian cancer cells. Notes: ( A ) Cells were treated with different concentrations (0–50 μmol/L) of cisplatin for 48 hours. Cell viability was assessed using the CCK-8 assay. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( B ) The 50% maximal inhibitory concentration (IC 50 ) values of cisplatin in the cisplatin-sensitive parent cell line OV2008 and its resistant clone C13K were calculated. Each value represents the mean ± standard deviation values from three independent experiments (** P <0.01). ( C ) The messenger RNA levels of YAP, <t>Cyr61,</t> CTGF, and CCND1 in the cells were examined using a real-time polymerase chain-reaction kit. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( D ) Cell lysates were collected for Western blot analyses of the protein levels of YAP, Cyr61, CTGF, and CCND1.

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1) Product Images from "YAP induces cisplatin resistance through activation of autophagy in human ovarian carcinoma cells"

Article Title: YAP induces cisplatin resistance through activation of autophagy in human ovarian carcinoma cells

Journal: OncoTargets and therapy

doi: 10.2147/OTT.S102837

Figure Legend Snippet: YAP confers resistance to cisplatin in ovarian cancer cells. Notes: ( A ) Cells were treated with different concentrations (0–50 μmol/L) of cisplatin for 48 hours. Cell viability was assessed using the CCK-8 assay. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( B ) The 50% maximal inhibitory concentration (IC 50 ) values of cisplatin in the cisplatin-sensitive parent cell line OV2008 and its resistant clone C13K were calculated. Each value represents the mean ± standard deviation values from three independent experiments (** P <0.01). ( C ) The messenger RNA levels of YAP, Cyr61, CTGF, and CCND1 in the cells were examined using a real-time polymerase chain-reaction kit. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( D ) Cell lysates were collected for Western blot analyses of the protein levels of YAP, Cyr61, CTGF, and CCND1.

Techniques Used: CCK-8 Assay, Standard Deviation, Concentration Assay, Real-time Polymerase Chain Reaction, Western Blot

Effects of YAP knockdown on cisplatin sensitivity in resistant C13K cells via impairment of autophagy. Notes: After C13K cells were transfected with YAP small interfering RNA (siRNA) and control siRNA (37.5 nM) for 48 hours, they were treated with 50 μmol/L cisplatin for 48 hours. ( A ) Cell lysates were collected for Western blot analysis of the protein expression of YAP, Cyr61, CTGF, and CCND1. ( B ) Cell viability was determined using a CCK-8 assay. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( C ) The fluorescence intensity of rhodamine 123 in the cells was measured by fluorescence-activated cell sorting. Data shown represent the mean ± standard error values from three independent experiments (** P <0.01 vs the control siRNA group). ( D ) Cells were subjected to annexin V–propidium iodide staining. The apoptosis ratio represents the ratio of the number of cells in early stage apoptosis to that in advanced-stage apoptosis. Quantification of apoptotic cells: mean ± standard deviation values represent those from three independent experiments (** P <0.01). ( E ) Western blot analysis of the expression of cleaved caspase 3 and PARP and the autophagy-related proteins Atg-3 and Atg-5 in the control siRNA and YAP siRNA C13K cells. ( F ) Electron transmission microscopy for the detection of autophagosomes in the control siRNA and YAP siRNA C13K cells; the black arrows indicate the autophagic vacuoles (magnification 10,000×). Scale bars 2 μm.

Figure Legend Snippet: Effects of YAP knockdown on cisplatin sensitivity in resistant C13K cells via impairment of autophagy. Notes: After C13K cells were transfected with YAP small interfering RNA (siRNA) and control siRNA (37.5 nM) for 48 hours, they were treated with 50 μmol/L cisplatin for 48 hours. ( A ) Cell lysates were collected for Western blot analysis of the protein expression of YAP, Cyr61, CTGF, and CCND1. ( B ) Cell viability was determined using a CCK-8 assay. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( C ) The fluorescence intensity of rhodamine 123 in the cells was measured by fluorescence-activated cell sorting. Data shown represent the mean ± standard error values from three independent experiments (** P <0.01 vs the control siRNA group). ( D ) Cells were subjected to annexin V–propidium iodide staining. The apoptosis ratio represents the ratio of the number of cells in early stage apoptosis to that in advanced-stage apoptosis. Quantification of apoptotic cells: mean ± standard deviation values represent those from three independent experiments (** P <0.01). ( E ) Western blot analysis of the expression of cleaved caspase 3 and PARP and the autophagy-related proteins Atg-3 and Atg-5 in the control siRNA and YAP siRNA C13K cells. ( F ) Electron transmission microscopy for the detection of autophagosomes in the control siRNA and YAP siRNA C13K cells; the black arrows indicate the autophagic vacuoles (magnification 10,000×). Scale bars 2 μm.

Techniques Used: Transfection, Small Interfering RNA, Western Blot, Expressing, CCK-8 Assay, Standard Deviation, Fluorescence, FACS, Staining, Transmission Assay, Microscopy

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Target validation in vitro and in vivo. (A) Validation of mRNA levels of a subset of PDGF-regulated genes (HMOX1, PDGFRB, <t>CYR61,</t> CXCL12, GDF15 and DIAPH3) in pBSMC. (B, C) PDGF-induced changes in expression of the CXCL12, CYR61 and HMOX1 genes were evaluated in the context of MYC (B) and JNK/JUN (C) inhibition, using real time RT-PCR analysis. (D) Protein level changes in PDGFRβ, CYR61 and GDF15 in response to PDGF treatment for different times were verified by immunoblot analysis. Data are representative of three independent trials. (E) Sensitivity of PDGF-induced changes in PDGFRβ and CYR61 and to inhibition of JNK and MYC was assessed by immunoblot analysis. The long exposure is included to appreciate differences in sensitivity of PDGFRβ to JNK and MYC inhibition. (F) Immunoblot analysis of whole bladder tissue (WB, n = 2, pooled) or bladder smooth muscle (BSM, n = 5, pooled) from mice subjected to sham surgery (Sh) or outlet obstruction (Obs) were blotted with the indicated antibodies; serum-depleted pBSMC treated without (-) or with 1 nM PDGF-BB for 2 h (+) were included as negative and positive controls respectively. (G) Bladder smooth muscle tissues from sham-operated (Sham, n = 3) or obstructed mice (Obs, n = 3) were subjected to real-time RT-PCR analysis for the indicated transcripts.

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1) Product Images from "Integration of proteomic and transcriptomic profiles identifies a novel PDGF-MYC network in human smooth muscle cells"

Article Title: Integration of proteomic and transcriptomic profiles identifies a novel PDGF-MYC network in human smooth muscle cells

Journal: Cell Communication and Signaling : CCS

doi: 10.1186/s12964-014-0044-z

Target validation in vitro and in vivo. (A) Validation of mRNA levels of a subset of PDGF-regulated genes (HMOX1, PDGFRB, CYR61, CXCL12, GDF15 and DIAPH3) in pBSMC. (B, C) PDGF-induced changes in expression of the CXCL12, CYR61 and HMOX1 genes were evaluated in the context of MYC (B) and JNK/JUN (C) inhibition, using real time RT-PCR analysis. (D) Protein level changes in PDGFRβ, CYR61 and GDF15 in response to PDGF treatment for different times were verified by immunoblot analysis. Data are representative of three independent trials. (E) Sensitivity of PDGF-induced changes in PDGFRβ and CYR61 and to inhibition of JNK and MYC was assessed by immunoblot analysis. The long exposure is included to appreciate differences in sensitivity of PDGFRβ to JNK and MYC inhibition. (F) Immunoblot analysis of whole bladder tissue (WB, n = 2, pooled) or bladder smooth muscle (BSM, n = 5, pooled) from mice subjected to sham surgery (Sh) or outlet obstruction (Obs) were blotted with the indicated antibodies; serum-depleted pBSMC treated without (-) or with 1 nM PDGF-BB for 2 h (+) were included as negative and positive controls respectively. (G) Bladder smooth muscle tissues from sham-operated (Sham, n = 3) or obstructed mice (Obs, n = 3) were subjected to real-time RT-PCR analysis for the indicated transcripts.

Figure Legend Snippet: Target validation in vitro and in vivo. (A) Validation of mRNA levels of a subset of PDGF-regulated genes (HMOX1, PDGFRB, CYR61, CXCL12, GDF15 and DIAPH3) in pBSMC. (B, C) PDGF-induced changes in expression of the CXCL12, CYR61 and HMOX1 genes were evaluated in the context of MYC (B) and JNK/JUN (C) inhibition, using real time RT-PCR analysis. (D) Protein level changes in PDGFRβ, CYR61 and GDF15 in response to PDGF treatment for different times were verified by immunoblot analysis. Data are representative of three independent trials. (E) Sensitivity of PDGF-induced changes in PDGFRβ and CYR61 and to inhibition of JNK and MYC was assessed by immunoblot analysis. The long exposure is included to appreciate differences in sensitivity of PDGFRβ to JNK and MYC inhibition. (F) Immunoblot analysis of whole bladder tissue (WB, n = 2, pooled) or bladder smooth muscle (BSM, n = 5, pooled) from mice subjected to sham surgery (Sh) or outlet obstruction (Obs) were blotted with the indicated antibodies; serum-depleted pBSMC treated without (-) or with 1 nM PDGF-BB for 2 h (+) were included as negative and positive controls respectively. (G) Bladder smooth muscle tissues from sham-operated (Sham, n = 3) or obstructed mice (Obs, n = 3) were subjected to real-time RT-PCR analysis for the indicated transcripts.

Techniques Used: In Vitro, In Vivo, Expressing, Inhibition, Quantitative RT-PCR, Western Blot

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MiR-129-5p mimics repressed YAP and its target gene expression in PC-3 cells. Notes: ( A ) MiR-129-5p overexpression decreased YAP mRNA level in PC-3 cells. ( B ) Western blot showed that YAP protein level was reduced toward miR-129-5p overexpression. ( C ) Quantitative analysis of YAP protein level in ( B ). ( D ) MiR-129-5p overexpression decreased CTGF and <t>CYR61</t> mRNA levels in PC-3 cells. ( E ) Western blot showed that CTGF and <t>CYR61</t> <t>protein</t> levels were reduced toward miR-129-5p overexpression. ( F ) Quantitative analysis of CTGF and CYR61 protein levels in ( E ). ** P <0.01, *** P <0.001.

Cyr61, supplied by Cell Signaling Technology Inc, 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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1) Product Images from "miR-129-5p inhibits prostate cancer proliferation via targeting ETV1"

Article Title: miR-129-5p inhibits prostate cancer proliferation via targeting ETV1

Journal: OncoTargets and therapy

doi: 10.2147/OTT.S183435

Figure Legend Snippet: MiR-129-5p mimics repressed YAP and its target gene expression in PC-3 cells. Notes: ( A ) MiR-129-5p overexpression decreased YAP mRNA level in PC-3 cells. ( B ) Western blot showed that YAP protein level was reduced toward miR-129-5p overexpression. ( C ) Quantitative analysis of YAP protein level in ( B ). ( D ) MiR-129-5p overexpression decreased CTGF and CYR61 mRNA levels in PC-3 cells. ( E ) Western blot showed that CTGF and CYR61 protein levels were reduced toward miR-129-5p overexpression. ( F ) Quantitative analysis of CTGF and CYR61 protein levels in ( E ). ** P <0.01, *** P <0.001.

Techniques Used: Expressing, Over Expression, Western Blot

MiR-129-5p downregulation elevated YAP and its target gene expression in RWPE-1 cells. Notes: ( A ) MiR-129-5p downregulation increased YAP mRNA level in RWPE-1 cells. ( B ) Western blot showed that YAP protein level was elevated toward miR-129-5p downregulation. ( C ) Quantitative analysis of YAP protein level in ( B ). ( D ) MiR-129-5p downregulation increased CTGF and CYR61 mRNA levels in RWPE-1 cells. ( E ) Western blot showed that CTGF and CYR61 protein levels were elevated toward miR-129-5p downregulation. ( F ) Quantitative analysis of CTGF and CYR61 protein levels in ( E ). * P <0.05, ** P <0.01, *** P <0.001.

Figure Legend Snippet: MiR-129-5p downregulation elevated YAP and its target gene expression in RWPE-1 cells. Notes: ( A ) MiR-129-5p downregulation increased YAP mRNA level in RWPE-1 cells. ( B ) Western blot showed that YAP protein level was elevated toward miR-129-5p downregulation. ( C ) Quantitative analysis of YAP protein level in ( B ). ( D ) MiR-129-5p downregulation increased CTGF and CYR61 mRNA levels in RWPE-1 cells. ( E ) Western blot showed that CTGF and CYR61 protein levels were elevated toward miR-129-5p downregulation. ( F ) Quantitative analysis of CTGF and CYR61 protein levels in ( E ). * P <0.05, ** P <0.01, *** P <0.001.

Techniques Used: Expressing, Western Blot

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Cell Signaling Technology Inc cyr61
7,8-DHF upregulated protein level of <t>Cyr61</t> in HK-2 cells damaged by hypoxia. Data were presented as the mean ± SD ( n = 5 per group). ∗∗∗ P < 0.001 versus control group. && P < 0.01 versus hypoxia alone (DMSO) group.

7,8-DHF upregulated protein level of <t>Cyr61</t> in HK-2 cells damaged by hypoxia. Data were presented as the mean ± SD ( n = 5 per group). ∗∗∗ P < 0.001 versus control group. && P < 0.01 versus hypoxia alone (DMSO) group.

cyr61 - by Bioz Stars, 2023-03

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1) Product Images from "7,8-DHF Treatment Induces Cyr61 Expression to Suppress Hypoxia Induced ER Stress in HK-2 Cells"

Article Title: 7,8-DHF Treatment Induces Cyr61 Expression to Suppress Hypoxia Induced ER Stress in HK-2 Cells

Journal: BioMed Research International

doi: 10.1155/2016/5029797

7,8-DHF upregulated protein level of Cyr61 in HK-2 cells damaged by hypoxia. Data were presented as the mean ± SD ( n = 5 per group). ∗∗∗ P < 0.001 versus control group. && P < 0.01 versus hypoxia alone (DMSO) group.

Figure Legend Snippet: 7,8-DHF upregulated protein level of Cyr61 in HK-2 cells damaged by hypoxia. Data were presented as the mean ± SD ( n = 5 per group). ∗∗∗ P < 0.001 versus control group. && P < 0.01 versus hypoxia alone (DMSO) group.

Techniques Used:

Protective effect of Cyr61 in hypoxia induced HK-2 apoptosis. (a) The changes of Cyr61 protein level after transfection. (b) Quantitative assessment of apoptotic cells by annexin V FITC/PI staining. (c) The changes of cleaved Caspase-3 protein level. Data were presented as the mean ± SD ( n = 5 per group). ∗∗ P < 0.01 and ∗∗∗ P < 0.001 versus control group. & P < 0.05 and &&& P < 0.001 versus hypoxia alone (empty plasmid) group.

Figure Legend Snippet: Protective effect of Cyr61 in hypoxia induced HK-2 apoptosis. (a) The changes of Cyr61 protein level after transfection. (b) Quantitative assessment of apoptotic cells by annexin V FITC/PI staining. (c) The changes of cleaved Caspase-3 protein level. Data were presented as the mean ± SD ( n = 5 per group). ∗∗ P < 0.01 and ∗∗∗ P < 0.001 versus control group. & P < 0.05 and &&& P < 0.001 versus hypoxia alone (empty plasmid) group.

Techniques Used: Transfection, Staining, Plasmid Preparation

7,8-DHF suppressed expression of CHOP. (a), (b), (c), and (d) mRNA expression of ER stress biomarkers after 7,8-DHF treatment in hypoxia induced HK-2 cells. (e) The changes of Cyr61 protein level after 7,8-DHF treatment. Data were presented as the mean ± SD ( n = 4 per group). ∗ P < 0.05 versus hypoxia alone (DMSO) group.

Figure Legend Snippet: 7,8-DHF suppressed expression of CHOP. (a), (b), (c), and (d) mRNA expression of ER stress biomarkers after 7,8-DHF treatment in hypoxia induced HK-2 cells. (e) The changes of Cyr61 protein level after 7,8-DHF treatment. Data were presented as the mean ± SD ( n = 4 per group). ∗ P < 0.05 versus hypoxia alone (DMSO) group.

Techniques Used: Expressing

Overexpression of Cyr61 downregulated CHOP protein level. (a) mRNA expression level of GRP78 and CHOP upon Cyr61 overexpression in hypoxia cultured HK-2 cells. (b) The changes of CHOP protein level with overexpression of Cyr61. Data were presented as the mean ± SD ( n = 4 per group). ∗∗ P < 0.01 versus hypoxia alone (empty plasmid) group.

Figure Legend Snippet: Overexpression of Cyr61 downregulated CHOP protein level. (a) mRNA expression level of GRP78 and CHOP upon Cyr61 overexpression in hypoxia cultured HK-2 cells. (b) The changes of CHOP protein level with overexpression of Cyr61. Data were presented as the mean ± SD ( n = 4 per group). ∗∗ P < 0.01 versus hypoxia alone (empty plasmid) group.

Techniques Used: Over Expression, Expressing, Cell Culture, Plasmid Preparation

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Cell Signaling Technology Inc cyr61
Cyr61, 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/cyr61/product/Cell Signaling Technology Inc
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cyr61 - by Bioz Stars, 2023-03

86/100 stars

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1) Product Images from "The HIPPO Transducer YAP and Its Targets CTGF and Cyr61 Drive a Paracrine Signalling in Cold Atmospheric Plasma-Mediated Wound Healing"

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