pegfp caveolin Search Results


pegfr y1173  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc pegfr y1173
(A) Heatmap of genes regulated by mevastatin in human primary keratinocytes. (B) Gene ontology analysis of biological processes enriched in mevastatin-treated keratinocytes. Diagram of RNA-Seq data showing mevastatin modulation of EGF signaling pathway by inhibiting cell proliferation while inducing cell migration in human keratinocytes (HEKs). Genes in red indicate mevastatin-induced genes involved in migration and genes in green indicate mevastatin-inhibited genes involved in proliferation. (C) Western blot and quantification of pEGFR <t>(Y1173)</t> and total EGFR and downstream effector pERK and total ERK in HEKs treated with 5 μM mevastatin for 48 hours (n = 6). Mevastatin significantly induced p-EGFR and its downstream effector p-ERK. Data are represented as mean ± SD and were analyzed by Student’s t test; *P < 0.05. (D) Confirmation of RNA-Seq data by qPCR of proliferation and migration genes known to be regulated by EGF signaling in HEKs treated with mevastatin (n = 6). Mevastatin inhibited genes involved in cell proliferation and induced genes involved in migration. Data are represented as mean ± SD and were analyzed by Student’s t test; *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001. (E) Western blot and quantification of mevastatin-induced migratory genes (ArhGEF1, Rac2) and proliferation genes (Cyclin B1) suppressed by mevastatin. (F) HEK scratch assay and cell proliferation assay treated in the presence or absence of 25 ng/mL EGF for 24 hours. 50 nM of PD 0332991, a CDK4 inhibitor, served as a control for cell proliferation assay. Mevastatin stimulated keratinocyte migration while inhibiting cell proliferation even in the presence of EGF. Data are represented as mean ± SD and were analyzed by a 1-way ANOVA followed by Holm-Sidak’s post hoc test, **P < 0.01, ***P < 0.001, ****P < 0.0001.
Pegfr Y1173, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/pegfr y1173/product/Cell Signaling Technology Inc
Average 96 stars, based on 1 article reviews
pegfr y1173 - by Bioz Stars, 2026-05
96/100 stars
  Buy from Supplier
pegfp caveolin  (Addgene inc)
93
Addgene inc pegfp caveolin
(A) Heatmap of genes regulated by mevastatin in human primary keratinocytes. (B) Gene ontology analysis of biological processes enriched in mevastatin-treated keratinocytes. Diagram of RNA-Seq data showing mevastatin modulation of EGF signaling pathway by inhibiting cell proliferation while inducing cell migration in human keratinocytes (HEKs). Genes in red indicate mevastatin-induced genes involved in migration and genes in green indicate mevastatin-inhibited genes involved in proliferation. (C) Western blot and quantification of pEGFR <t>(Y1173)</t> and total EGFR and downstream effector pERK and total ERK in HEKs treated with 5 μM mevastatin for 48 hours (n = 6). Mevastatin significantly induced p-EGFR and its downstream effector p-ERK. Data are represented as mean ± SD and were analyzed by Student’s t test; *P < 0.05. (D) Confirmation of RNA-Seq data by qPCR of proliferation and migration genes known to be regulated by EGF signaling in HEKs treated with mevastatin (n = 6). Mevastatin inhibited genes involved in cell proliferation and induced genes involved in migration. Data are represented as mean ± SD and were analyzed by Student’s t test; *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001. (E) Western blot and quantification of mevastatin-induced migratory genes (ArhGEF1, Rac2) and proliferation genes (Cyclin B1) suppressed by mevastatin. (F) HEK scratch assay and cell proliferation assay treated in the presence or absence of 25 ng/mL EGF for 24 hours. 50 nM of PD 0332991, a CDK4 inhibitor, served as a control for cell proliferation assay. Mevastatin stimulated keratinocyte migration while inhibiting cell proliferation even in the presence of EGF. Data are represented as mean ± SD and were analyzed by a 1-way ANOVA followed by Holm-Sidak’s post hoc test, **P < 0.01, ***P < 0.001, ****P < 0.0001.
Pegfp Caveolin, supplied by Addgene inc, 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/pegfp caveolin/product/Addgene inc
Average 93 stars, based on 1 article reviews
pegfp caveolin - by Bioz Stars, 2026-05
93/100 stars
  Buy from Supplier

Image Search Results


(A) Heatmap of genes regulated by mevastatin in human primary keratinocytes. (B) Gene ontology analysis of biological processes enriched in mevastatin-treated keratinocytes. Diagram of RNA-Seq data showing mevastatin modulation of EGF signaling pathway by inhibiting cell proliferation while inducing cell migration in human keratinocytes (HEKs). Genes in red indicate mevastatin-induced genes involved in migration and genes in green indicate mevastatin-inhibited genes involved in proliferation. (C) Western blot and quantification of pEGFR (Y1173) and total EGFR and downstream effector pERK and total ERK in HEKs treated with 5 μM mevastatin for 48 hours (n = 6). Mevastatin significantly induced p-EGFR and its downstream effector p-ERK. Data are represented as mean ± SD and were analyzed by Student’s t test; *P < 0.05. (D) Confirmation of RNA-Seq data by qPCR of proliferation and migration genes known to be regulated by EGF signaling in HEKs treated with mevastatin (n = 6). Mevastatin inhibited genes involved in cell proliferation and induced genes involved in migration. Data are represented as mean ± SD and were analyzed by Student’s t test; *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001. (E) Western blot and quantification of mevastatin-induced migratory genes (ArhGEF1, Rac2) and proliferation genes (Cyclin B1) suppressed by mevastatin. (F) HEK scratch assay and cell proliferation assay treated in the presence or absence of 25 ng/mL EGF for 24 hours. 50 nM of PD 0332991, a CDK4 inhibitor, served as a control for cell proliferation assay. Mevastatin stimulated keratinocyte migration while inhibiting cell proliferation even in the presence of EGF. Data are represented as mean ± SD and were analyzed by a 1-way ANOVA followed by Holm-Sidak’s post hoc test, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Journal: JCI Insight

Article Title: Mevastatin promotes healing by targeting caveolin-1 to restore EGFR signaling

doi: 10.1172/jci.insight.129320

Figure Lengend Snippet: (A) Heatmap of genes regulated by mevastatin in human primary keratinocytes. (B) Gene ontology analysis of biological processes enriched in mevastatin-treated keratinocytes. Diagram of RNA-Seq data showing mevastatin modulation of EGF signaling pathway by inhibiting cell proliferation while inducing cell migration in human keratinocytes (HEKs). Genes in red indicate mevastatin-induced genes involved in migration and genes in green indicate mevastatin-inhibited genes involved in proliferation. (C) Western blot and quantification of pEGFR (Y1173) and total EGFR and downstream effector pERK and total ERK in HEKs treated with 5 μM mevastatin for 48 hours (n = 6). Mevastatin significantly induced p-EGFR and its downstream effector p-ERK. Data are represented as mean ± SD and were analyzed by Student’s t test; *P < 0.05. (D) Confirmation of RNA-Seq data by qPCR of proliferation and migration genes known to be regulated by EGF signaling in HEKs treated with mevastatin (n = 6). Mevastatin inhibited genes involved in cell proliferation and induced genes involved in migration. Data are represented as mean ± SD and were analyzed by Student’s t test; *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001. (E) Western blot and quantification of mevastatin-induced migratory genes (ArhGEF1, Rac2) and proliferation genes (Cyclin B1) suppressed by mevastatin. (F) HEK scratch assay and cell proliferation assay treated in the presence or absence of 25 ng/mL EGF for 24 hours. 50 nM of PD 0332991, a CDK4 inhibitor, served as a control for cell proliferation assay. Mevastatin stimulated keratinocyte migration while inhibiting cell proliferation even in the presence of EGF. Data are represented as mean ± SD and were analyzed by a 1-way ANOVA followed by Holm-Sidak’s post hoc test, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Article Snippet: For immunofluorescence staining, tissue sections of discarded DFUs were treated with mevastatin as described above and used for staining with anti–phospho-EGFR (Y1173) (53A5) (rabbit, 1:100; Cell Signaling Technology; 4407) or anti-Cav1 (D46G3) (rabbit, 1:200; Cell Signaling Technology; 3267). pEGFR (Y1173) and Cav1 staining was visualized with Alexa Fluor 488–conjugated goat anti–rabbit antibody (1:500; Invitrogen; A11008) and mounted with Prolong DAPI Gold antifade reagent (Invitrogen) to visualize cell nuclei.

Techniques: RNA Sequencing Assay, Migration, Western Blot, Wound Healing Assay, Proliferation Assay

(A and B) Western blot and quantification of pEGFR (Y1173) and total EGFR in acute healthy wounds (AWs) (n = 5) and diabetic foot ulcers (DFUs) (n = 6). pEGFR is downregulated in DFUs compared with AWs. Data are represented as mean ± SEM and were analyzed by Student’s t test; *P < 0.05. (C and D) Western blot and quantification of p-EGFR and total EGFR from samples obtained from the nonhealing edge of patients with DFUs treated with 5 μM mevastatin for 48 hours (n = 5). Mevastatin significantly induced pEGFR in samples obtained from the nonhealing edge of DFUs compared with vehicle-treated control. Data are represented as mean ± SEM and were analyzed by a ratio-paired t test; **P < 0.01. (E) Immunofluorescence staining of pEGFR in mevastatin-treated DFUs. Mevastatin strongly induced p-EGFR compared with vehicle-treated control. Scale bar: 100 μm.

Journal: JCI Insight

Article Title: Mevastatin promotes healing by targeting caveolin-1 to restore EGFR signaling

doi: 10.1172/jci.insight.129320

Figure Lengend Snippet: (A and B) Western blot and quantification of pEGFR (Y1173) and total EGFR in acute healthy wounds (AWs) (n = 5) and diabetic foot ulcers (DFUs) (n = 6). pEGFR is downregulated in DFUs compared with AWs. Data are represented as mean ± SEM and were analyzed by Student’s t test; *P < 0.05. (C and D) Western blot and quantification of p-EGFR and total EGFR from samples obtained from the nonhealing edge of patients with DFUs treated with 5 μM mevastatin for 48 hours (n = 5). Mevastatin significantly induced pEGFR in samples obtained from the nonhealing edge of DFUs compared with vehicle-treated control. Data are represented as mean ± SEM and were analyzed by a ratio-paired t test; **P < 0.01. (E) Immunofluorescence staining of pEGFR in mevastatin-treated DFUs. Mevastatin strongly induced p-EGFR compared with vehicle-treated control. Scale bar: 100 μm.

Article Snippet: For immunofluorescence staining, tissue sections of discarded DFUs were treated with mevastatin as described above and used for staining with anti–phospho-EGFR (Y1173) (53A5) (rabbit, 1:100; Cell Signaling Technology; 4407) or anti-Cav1 (D46G3) (rabbit, 1:200; Cell Signaling Technology; 3267). pEGFR (Y1173) and Cav1 staining was visualized with Alexa Fluor 488–conjugated goat anti–rabbit antibody (1:500; Invitrogen; A11008) and mounted with Prolong DAPI Gold antifade reagent (Invitrogen) to visualize cell nuclei.

Techniques: Western Blot, Immunofluorescence, Staining