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Cell Signaling Technology Inc 1 ap
1 Ap, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 63 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sav1/SAV1+Rabbit+mAb/pm41926287-1020-159-176
Average 94 stars, based on 63 article reviews

1 ap - by Bioz Stars, 2026-09

94/100 stars

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Article Title: cis-Clerodane-type diterpenoids from Tinospora crispa and their anticancer potential.
Article Snippet: .. Membranes were blocked with 2% skim milk in TBST at 4 °C and then incubated overnight at 4 °C with the following primary antibodies: MST1 (1:1000, #14,946, Cell Signaling Technology), SAV1 (1:1000, #13301S, Cell Signaling Technology), MOB1 (1:1000, #13730S, Cell Signaling Technology), LATS1 (1:1000, #3477S, Cell Signaling Technology), phosphoYAP (p-YAP; 1:1000, #4911S, Cell Signaling Technology), YAP (1:1000, #14,074, Cell Signaling Technology), TAZ (1:1000, #83669S, Cell Signaling Technology), pan-TEAD (1:1000, #13295S, Cell Signaling Technology), phosphoAKT (p-AKT; 1:1000, #9275S, Cell Signaling Technology), AKT (1:1000, #9272S, Cell Signaling Technology), phospho-ERK1/2 (p-ERK1/2; 1:1000, #PAB16949, Abnova), total ERK1/2 (1:1000, #9102S, Cell Signaling Technology), STAT3 (1:1000, #9139S, Cell Signaling Technology), Cyclin D1 (1:1000, sc-8396, Santa Cruz Biotechnology), Waf1/Cip1/CDKN1A p21 (1:1000, sc-53870, Santa Cruz Biotechnology), Bax (1:1000, sc-23959, Santa Cruz Biotechnology), Bcl-2 (1:1000, sc-23960, Santa Cruz Biotechnology), Caspase-3 (1:1000, sc-56053, Santa Cruz Biotechnology), and E-cadherin (1:1000, #3195, Cell Signaling Technology). .. After washing, membranes were incubated with HRP-conjugated secondary antibodies: anti-mouse IgG (1:2000, #7076P2, Cell Signaling Technology) or antirabbit IgG (1:2000, #7074S, Cell Signaling Technology).

Article Title: cis -Clerodane-type diterpenoids from Tinospora crispa and their anticancer potential
Article Snippet: .. Membranes were blocked with 2% skim milk in TBST at 4 °C and then incubated overnight at 4 °C with the following primary antibodies: MST1 (1:1000, #14,946, Cell Signaling Technology), SAV1 (1:1000, #13301S, Cell Signaling Technology), MOB1 (1:1000, #13730S, Cell Signaling Technology), LATS1 (1:1000, #3477S, Cell Signaling Technology), phospho-YAP (p-YAP; 1:1000, #4911S, Cell Signaling Technology), YAP (1:1000, #14,074, Cell Signaling Technology), TAZ (1:1000, #83669S, Cell Signaling Technology), pan-TEAD (1:1000, #13295S, Cell Signaling Technology), phospho-AKT (p-AKT; 1:1000, #9275S, Cell Signaling Technology), AKT (1:1000, #9272S, Cell Signaling Technology), phospho-ERK1/2 (p-ERK1/2; 1:1000, # PAB16949 , Abnova), total ERK1/2 (1:1000, #9102S, Cell Signaling Technology), STAT3 (1:1000, #9139S, Cell Signaling Technology), Cyclin D1 (1:1000, sc-8396, Santa Cruz Biotechnology), Waf1/Cip1/CDKN1A p21 (1:1000, sc-53870, Santa Cruz Biotechnology), Bax (1:1000, sc-23959, Santa Cruz Biotechnology), Bcl-2 (1:1000, sc-23960, Santa Cruz Biotechnology), Caspase-3 (1:1000, sc-56053, Santa Cruz Biotechnology), and E-cadherin (1:1000, #3195, Cell Signaling Technology). .. After washing, membranes were incubated with HRP-conjugated secondary antibodies: anti-mouse IgG (1:2000, #7076P2, Cell Signaling Technology) or anti-rabbit IgG (1:2000, #7074S, Cell Signaling Technology).

other:

Article Title: The serotonin receptor 2b (5-HT 2B ) modulates heart remodeling following myocardial infarction via regulation of Hippo pathway
Article Snippet: Sav1 , Cell Signalling Technologies , Cat #13301; RRID:AB_2798176.

Article Title: Hernandonine-mediated autophagic cell death in hepatocellular carcinoma: Interplay of p53 and YAP signaling pathways.
Article Snippet: Hepatocellular carcinoma (HCC), the primary form of liver cancer, is the third leading cause of cancer-related death globally.. Hernandonine is a natural alkaloid derived from Hernandia nymphaeifolia that has been shown to exert various biological functions.. In a previous study, hernandonine was shown to suppress the proliferation of several solid tumor cell lines without affecting normal human cell lines.

Western Blot:

Article Title: MECOM and the PRDM gene family in uterine endometrial cancer: bioinformatics and experimental insights into pathogenesis and therapeutic potentials
Article Snippet: Subsequently, the membrane was washed four times with 1 × TBST buffer (Catalog Number: 9997S, Cell Signaling Technology, USA) for 8 min each. .. For western blot analysis, specific antibodies were used to detect target proteins, including MST1 (Catalog Number: 3682S, Cell Signaling Technology, USA), LATS1 (Catalog Number: 3477S, Cell Signaling Technology, USA), YAP (Catalog Number: 14074S, Cell Signaling Technology, USA), SAV1 (Catalog Number: 13301S, Cell Signaling Technology, USA), and MOB1 (Catalog Number: 13730S, Cell Signaling Technology, USA). ..

Article Title: MECOM and the PRDM gene family in uterine endometrial cancer: bioinformatics and experimental insights into pathogenesis and therapeutic potentials.
Article Snippet: Subsequently, the membrane was washed four times with 1 × TBST buffer (Catalog Number: 9997S, Cell Signaling Technology, USA) for 8 min each. .. For western blot analysis, specific antibodies were used to detect target proteins, including MST1 (Catalog Number: 3682S, Cell Signaling Technology, USA), LATS1 (Catalog Number: 3477S, Cell Signaling Technology, USA), YAP (Catalog Number: 14074S, Cell Signaling Technology, USA), SAV1 (Catalog Number: 13301S, Cell Signaling Technology, USA), and MOB1 (Catalog Number: 13730S, Cell Signaling Technology, USA). ..

Article Title: Hippo pathway deficiency reverses systolic heart failure post-infarction
Article Snippet: Samples were homogenized with a Dounce tissue homogenizer, passed through a 22-gauge needle, and sonicated for ten cycles (30 s on, 30 s off) in a Diagenode Bioruptor Pico Plus NGS. .. For western blot analysis, we used antibodies against total YAP (Novus NB110-58358), pYAP (Cell Signaling 4911S), pLats1 (Cell Signaling 9157), Sav1 (Novus NBP2-13282), Park2 (Cell Signaling 2132S), and α-tubulin (Sigma T5168). ..

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Regulation of the Hippo pathway by 5-HT 2B in cardiomyocytes (A) Western blot confirmation that Ad-FLAG-5-HT 2B infection in NRCMs resulted in the expression of FLAG- 5-HT 2B that was absent in Ad-LacZ-infected controls (representative image of n = 3 independent experiments). (B) YAP transcriptional activity was enhanced in NRCMs following 5-HT 2B overexpression ( n = 5 independent experiments with five technical replications in each experiment). (C) Representative images of GFP-YAP nuclear translocation in NRCMs overexpressing 5-HT 2B or control LacZ (scale bars, 100 μm). (D) Quantification of NRCMs with nuclear GFP-YAP showed that cells overexpressing 5-HT 2B exhibited a higher proportion of nuclear YAP ( n = 5 independent experiments with three technical replicates in each prep). (E and F) (E) Western blots and (F) quantification of band density showing a reduction in YAP phosphorylation in NRCMs overexpressing 5-HT 2B ( n = 3 independent experiments). (G and H) (G) Western blots and (H) quantification of band density showing a significant reduction in LATS1 phosphorylation in NRCMs overexpressing 5-HT 2B ( n = 3 independent experiments). (I and J) (I) Western blots and (J) quantification of band density showing no significant change in MST1 phosphorylation in NRCMs overexpressing 5-HT 2B ( n = 3 independent experiments). (K–M) (K) Western blots and (L) quantification of band density showing a reduction in expression of the LATS1 adaptor protein MOB1 in NRCMs overexpressing 5-HT 2B ( n = 3 independent experiments). (K) Western blots and (M) quantification of band density showing no change in expression of the MST adaptor protein Sav1 in NRCMs overexpressing 5-HT 2B ( n = 3 independent experiments). (N and O) (N) Western blots and (O) quantification of MYPT1 phosphorylation in NRCMs overexpressing 5-HT 2B indicated a possible role for ROCK1 linking 5-HT 2B with the Hippo pathway ( n = 3 independent experiments). (P) Immunoprecipitation analysis in cardiomyocytes overexpressing Flag-5-HT 2B using anti-Flag antibody followed by western blot detection using anti-LATS1 indicated possible interaction between 5-HT 2B and LATS1. All data are presented as mean ± SEM. Statistical tests used: (B, D, F, H, J, L, M, and O) Student’s t test.

Journal: iScience

Article Title: The serotonin receptor 2b (5-HT 2B ) modulates heart remodeling following myocardial infarction via regulation of Hippo pathway

doi: 10.1016/j.isci.2026.114825

Figure Lengend Snippet: Regulation of the Hippo pathway by 5-HT 2B in cardiomyocytes (A) Western blot confirmation that Ad-FLAG-5-HT 2B infection in NRCMs resulted in the expression of FLAG- 5-HT 2B that was absent in Ad-LacZ-infected controls (representative image of n = 3 independent experiments). (B) YAP transcriptional activity was enhanced in NRCMs following 5-HT 2B overexpression ( n = 5 independent experiments with five technical replications in each experiment). (C) Representative images of GFP-YAP nuclear translocation in NRCMs overexpressing 5-HT 2B or control LacZ (scale bars, 100 μm). (D) Quantification of NRCMs with nuclear GFP-YAP showed that cells overexpressing 5-HT 2B exhibited a higher proportion of nuclear YAP ( n = 5 independent experiments with three technical replicates in each prep). (E and F) (E) Western blots and (F) quantification of band density showing a reduction in YAP phosphorylation in NRCMs overexpressing 5-HT 2B ( n = 3 independent experiments). (G and H) (G) Western blots and (H) quantification of band density showing a significant reduction in LATS1 phosphorylation in NRCMs overexpressing 5-HT 2B ( n = 3 independent experiments). (I and J) (I) Western blots and (J) quantification of band density showing no significant change in MST1 phosphorylation in NRCMs overexpressing 5-HT 2B ( n = 3 independent experiments). (K–M) (K) Western blots and (L) quantification of band density showing a reduction in expression of the LATS1 adaptor protein MOB1 in NRCMs overexpressing 5-HT 2B ( n = 3 independent experiments). (K) Western blots and (M) quantification of band density showing no change in expression of the MST adaptor protein Sav1 in NRCMs overexpressing 5-HT 2B ( n = 3 independent experiments). (N and O) (N) Western blots and (O) quantification of MYPT1 phosphorylation in NRCMs overexpressing 5-HT 2B indicated a possible role for ROCK1 linking 5-HT 2B with the Hippo pathway ( n = 3 independent experiments). (P) Immunoprecipitation analysis in cardiomyocytes overexpressing Flag-5-HT 2B using anti-Flag antibody followed by western blot detection using anti-LATS1 indicated possible interaction between 5-HT 2B and LATS1. All data are presented as mean ± SEM. Statistical tests used: (B, D, F, H, J, L, M, and O) Student’s t test.

Article Snippet: Sav1 , Cell Signalling Technologies , Cat #13301; RRID:AB_2798176.

Techniques: Western Blot, Infection, Expressing, Activity Assay, Over Expression, Translocation Assay, Control, Phospho-proteomics, Immunoprecipitation

EGFR interacts with SAV1 and promotes YAP activation. A : Lysates from MIO-M1 Müller cells were co-immunoprecipitated with control immunoglobulin G (IgG) or anti-EGFR antibody, followed by immunoblotting with an anti-SAV1 antibody. n = 3 biological replicates. B : MIO-M1 Müller cells were transfected with flag-EGFR expression plasmid. The co-immunoprecipitation assay was performed using lysates from MIO-M1 Müller cells by an anti-flag antibody, followed by immunoblotting with an anti-SAV1 antibody. n = 3 biological replicates. C : Lysates from MIO-M1 Müller cells were co-immunoprecipitated with control IgG or anti-SAV1 antibody, followed by immunoblotting with an anti-EGFR antibody. n = 3 biological replicates. D : Representative SAV1 and EGFR double staining in the MIO-M1 Müller cells was examined by immunofluorescence (IF) staining. Scale bar = 20 µm. E : Western blot assay for EGFR, SAV1 and YAP expression in the MIO-M1 Müller cells through gain or loss of function of EGFR. n = 3 biological replicates. F : Expression of YAP in the nucleus of MIO-M1 Müller cells with gain or loss of function of EGFR was detected by Western blotting. n = 3 biological replicates. G : RT-PCR assay for mRNA levels of CTGF and CYR61 in MIO-M1 Müller cells through gain or loss of function of EGFR. n = 5 biological replicates. * p < 0.05; ** p < 0.01

Journal: Journal of Translational Medicine

Article Title: The epidermal growth factor receptor regulates YAP signalling and promotes diabetic retinal fibrosis by modulating the degradation of SAV1

doi: 10.1186/s12967-025-07357-7

Figure Lengend Snippet: EGFR interacts with SAV1 and promotes YAP activation. A : Lysates from MIO-M1 Müller cells were co-immunoprecipitated with control immunoglobulin G (IgG) or anti-EGFR antibody, followed by immunoblotting with an anti-SAV1 antibody. n = 3 biological replicates. B : MIO-M1 Müller cells were transfected with flag-EGFR expression plasmid. The co-immunoprecipitation assay was performed using lysates from MIO-M1 Müller cells by an anti-flag antibody, followed by immunoblotting with an anti-SAV1 antibody. n = 3 biological replicates. C : Lysates from MIO-M1 Müller cells were co-immunoprecipitated with control IgG or anti-SAV1 antibody, followed by immunoblotting with an anti-EGFR antibody. n = 3 biological replicates. D : Representative SAV1 and EGFR double staining in the MIO-M1 Müller cells was examined by immunofluorescence (IF) staining. Scale bar = 20 µm. E : Western blot assay for EGFR, SAV1 and YAP expression in the MIO-M1 Müller cells through gain or loss of function of EGFR. n = 3 biological replicates. F : Expression of YAP in the nucleus of MIO-M1 Müller cells with gain or loss of function of EGFR was detected by Western blotting. n = 3 biological replicates. G : RT-PCR assay for mRNA levels of CTGF and CYR61 in MIO-M1 Müller cells through gain or loss of function of EGFR. n = 5 biological replicates. * p < 0.05; ** p < 0.01

Article Snippet: Specific antibodies targeting EGFR, SAV1, YAP, Herc4, ɑ-SMA, CTGF, fibronectin, vimentin, E-cadherin, and collagen I were purchased from Santa Cruz Biotechnology (TX).

Techniques: Activation Assay, Immunoprecipitation, Control, Western Blot, Transfection, Expressing, Plasmid Preparation, Co-Immunoprecipitation Assay, Double Staining, Immunofluorescence, Staining, Reverse Transcription Polymerase Chain Reaction

EGFR mediates SAV1 proteasomal degradation. A : RT-PCR assay for mRNA level of SAV1 in MIO-M1 Müller cells through gain or loss of function of EGFR; n = 5 biological replicates. B : Western blot assay for endogenous protein level of SAV1 in MIO-M1 Müller cells transfected with increasing amount of EGFR expression plasmid. n = 3 biological replicates. C : Western blot assay for EGFR and SAV1 expression in the MIO-M1 Müller cells with transfection of flag-EGFR plasmid treated with or without a proteasome inhibitor MG132 (20 mM) for 6 h. n = 3 biological replicates. D : Western blot assay for the half-life of endogenous SAV1 protein in MIO-M1 Müller cells transfected with flag-EGFR and treated with cycloheximide(CHX) at 100 µg/ml for the different times. n = 3 biological replicates. E : Western blot assay for the half-life of endogenous SAV1 protein in MIO-M1 Müller cells transfected with EGFR-siRNA and treated with CHX at 100 µg/ml for the different times. n = 3 biological replicates. * p < 0.05; ** p < 0.01

Journal: Journal of Translational Medicine

Article Title: The epidermal growth factor receptor regulates YAP signalling and promotes diabetic retinal fibrosis by modulating the degradation of SAV1

doi: 10.1186/s12967-025-07357-7

Figure Lengend Snippet: EGFR mediates SAV1 proteasomal degradation. A : RT-PCR assay for mRNA level of SAV1 in MIO-M1 Müller cells through gain or loss of function of EGFR; n = 5 biological replicates. B : Western blot assay for endogenous protein level of SAV1 in MIO-M1 Müller cells transfected with increasing amount of EGFR expression plasmid. n = 3 biological replicates. C : Western blot assay for EGFR and SAV1 expression in the MIO-M1 Müller cells with transfection of flag-EGFR plasmid treated with or without a proteasome inhibitor MG132 (20 mM) for 6 h. n = 3 biological replicates. D : Western blot assay for the half-life of endogenous SAV1 protein in MIO-M1 Müller cells transfected with flag-EGFR and treated with cycloheximide(CHX) at 100 µg/ml for the different times. n = 3 biological replicates. E : Western blot assay for the half-life of endogenous SAV1 protein in MIO-M1 Müller cells transfected with EGFR-siRNA and treated with CHX at 100 µg/ml for the different times. n = 3 biological replicates. * p < 0.05; ** p < 0.01

Article Snippet: Specific antibodies targeting EGFR, SAV1, YAP, Herc4, ɑ-SMA, CTGF, fibronectin, vimentin, E-cadherin, and collagen I were purchased from Santa Cruz Biotechnology (TX).

Techniques: Reverse Transcription Polymerase Chain Reaction, Western Blot, Transfection, Expressing, Plasmid Preparation

EGFR mediates SAV1 degradation through promoting its binding to Herc4. A : Lysates from MIO-M1 Müller cells were co-immunoprecipitated with control IgG or anti-EGFR antibody, followed by immunoblotting with an anti-Herc4 antibody. n = 3 biological replicates. B : MIO-M1 Müller cells were transfected with flag-EGFR expression plasmid. The co-immunoprecipitation assay was performed using lysates from MIO-M1 Müller cells by an anti-flag antibody, followed by immunoblotting with an anti-Herc4 antibody. n = 3 biological replicates. C : Representative Herc4 and EGFR double staining in the MIO-M1 Müller cells was examined by immunohistochemical measurement. Scale bar = 20 µm. D : Total lysate was extracted from MIO-M1 Müller cells for two-step coIP. The first ip was performed with IgG or anti-EGFR antibody. The eluate from the first ip was then used for the second ip with anti-Herc4 antibody or IgG. n = 3 biological replicates. E : MIO-M1 Müller cells were transfected with flag-EGFR or flag plasmid. The co-immunoprecipitation assay was performed using lysates from MIO-M1 Müller cells by an anti-Herc4 antibody, followed by immunoblotting to detect SAV1 and Herc4. n = 3 biological replicates. F : MIO-M1 Müller cells were transfected with EGFR-siRNA or control-siRNA. The co-immunoprecipitation assay was performed using lysates from MIO-M1 Müller cells by an anti-Herc4 antibody, followed by immunoblotting to detect SAV1 and Herc4. G : Western blot assay for Herc4, YAP and SAV1 expression in the MIO-M1 Müller cells with transfection of flag-EGFR plasmid and co-transected with or without Herc4-siRNA. n = 3 biological replicates. * p < 0.05; ** p < 0.01

Journal: Journal of Translational Medicine

Article Title: The epidermal growth factor receptor regulates YAP signalling and promotes diabetic retinal fibrosis by modulating the degradation of SAV1

doi: 10.1186/s12967-025-07357-7

Figure Lengend Snippet: EGFR mediates SAV1 degradation through promoting its binding to Herc4. A : Lysates from MIO-M1 Müller cells were co-immunoprecipitated with control IgG or anti-EGFR antibody, followed by immunoblotting with an anti-Herc4 antibody. n = 3 biological replicates. B : MIO-M1 Müller cells were transfected with flag-EGFR expression plasmid. The co-immunoprecipitation assay was performed using lysates from MIO-M1 Müller cells by an anti-flag antibody, followed by immunoblotting with an anti-Herc4 antibody. n = 3 biological replicates. C : Representative Herc4 and EGFR double staining in the MIO-M1 Müller cells was examined by immunohistochemical measurement. Scale bar = 20 µm. D : Total lysate was extracted from MIO-M1 Müller cells for two-step coIP. The first ip was performed with IgG or anti-EGFR antibody. The eluate from the first ip was then used for the second ip with anti-Herc4 antibody or IgG. n = 3 biological replicates. E : MIO-M1 Müller cells were transfected with flag-EGFR or flag plasmid. The co-immunoprecipitation assay was performed using lysates from MIO-M1 Müller cells by an anti-Herc4 antibody, followed by immunoblotting to detect SAV1 and Herc4. n = 3 biological replicates. F : MIO-M1 Müller cells were transfected with EGFR-siRNA or control-siRNA. The co-immunoprecipitation assay was performed using lysates from MIO-M1 Müller cells by an anti-Herc4 antibody, followed by immunoblotting to detect SAV1 and Herc4. G : Western blot assay for Herc4, YAP and SAV1 expression in the MIO-M1 Müller cells with transfection of flag-EGFR plasmid and co-transected with or without Herc4-siRNA. n = 3 biological replicates. * p < 0.05; ** p < 0.01

Article Snippet: Specific antibodies targeting EGFR, SAV1, YAP, Herc4, ɑ-SMA, CTGF, fibronectin, vimentin, E-cadherin, and collagen I were purchased from Santa Cruz Biotechnology (TX).

Techniques: Binding Assay, Immunoprecipitation, Control, Western Blot, Transfection, Expressing, Plasmid Preparation, Co-Immunoprecipitation Assay, Double Staining, Immunohistochemical staining

Inhibition of EGFR suppresses YAP activation and alleviates diabetic retinal fibrosis. A : The diabetic mice models were randomized to treatment with erlotinib ( n = 10) or vehicle ( n = 10) beginning immediately after pvr induction. Control mice were also treatment with vehicle or Erlotinib( n = 10). B : Western blot assay for EGFR, SAV1, and YAP expression in the retinas of diabetic mice with or without erlotinib. n = 3 mice. C : Representative SAV1 and YAP staining in the retinas of diabetic mice with or without erlotinib was examined by immunohistochemical measurement. Scale bar = 50 µm. D : Western blot assay for ɑ-SMA, fibronectin, vimentin and E-cadherin expression in the retinas of diabetic mice with or without erlotinib. n = 3 mice. E : Representative images of Masson’s staining in the retinas of diabetic mice with or without erlotinib (black arrow indicates the presence of epiretinal fibrotic membrane). F : Western blot assay for E-cadherin, fibronectin, collagen I and ɑ-SMA expression in the MIO-M1 Müller cells through gain or loss of function of EGFR. n = 3 biological replicates. G : Western blot assay for YAP, EGFR, collagen I, and ɑ-SMA expression in the MIO-M1 Müller cells with transfection of flag-YAP plasmid and co-transected with or without EGFR-siRNA. n = 3 biological replicates. * p < 0.05; ** p < 0.01

Journal: Journal of Translational Medicine

Article Title: The epidermal growth factor receptor regulates YAP signalling and promotes diabetic retinal fibrosis by modulating the degradation of SAV1

doi: 10.1186/s12967-025-07357-7

Figure Lengend Snippet: Inhibition of EGFR suppresses YAP activation and alleviates diabetic retinal fibrosis. A : The diabetic mice models were randomized to treatment with erlotinib ( n = 10) or vehicle ( n = 10) beginning immediately after pvr induction. Control mice were also treatment with vehicle or Erlotinib( n = 10). B : Western blot assay for EGFR, SAV1, and YAP expression in the retinas of diabetic mice with or without erlotinib. n = 3 mice. C : Representative SAV1 and YAP staining in the retinas of diabetic mice with or without erlotinib was examined by immunohistochemical measurement. Scale bar = 50 µm. D : Western blot assay for ɑ-SMA, fibronectin, vimentin and E-cadherin expression in the retinas of diabetic mice with or without erlotinib. n = 3 mice. E : Representative images of Masson’s staining in the retinas of diabetic mice with or without erlotinib (black arrow indicates the presence of epiretinal fibrotic membrane). F : Western blot assay for E-cadherin, fibronectin, collagen I and ɑ-SMA expression in the MIO-M1 Müller cells through gain or loss of function of EGFR. n = 3 biological replicates. G : Western blot assay for YAP, EGFR, collagen I, and ɑ-SMA expression in the MIO-M1 Müller cells with transfection of flag-YAP plasmid and co-transected with or without EGFR-siRNA. n = 3 biological replicates. * p < 0.05; ** p < 0.01

Article Snippet: Specific antibodies targeting EGFR, SAV1, YAP, Herc4, ɑ-SMA, CTGF, fibronectin, vimentin, E-cadherin, and collagen I were purchased from Santa Cruz Biotechnology (TX).

Techniques: Inhibition, Activation Assay, Control, Western Blot, Expressing, Staining, Immunohistochemical staining, Membrane, Transfection, Plasmid Preparation

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