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p erk  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc p erk
    P Erk, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 13438 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p+p44+42+mapk/Phospho-p44%2F42+MAPK+(Erk1%2F2)+(Thr202%2FTyr204)+XP+Rabbit+mAb/pmc13042271-96-58-63
    Average 99 stars, based on 13438 article reviews
    p erk - by Bioz Stars, 2026-10
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    Incubation:

    Article Title: Targeting PDK4 attenuates neointimal hyperplasia and regulates VSMC phenotypic switching, apoptosis, and autophagy.
    Article Snippet: Neointimal hyperplasia, a predominant cause of restenosis and atherosclerosis, is regulated by the phenotypic modulation, migration and proliferation, of vascular smooth muscle cells (VSMCs).. Pyruvate dehydrogenase kinase 4 (PDK4) has been identified as a key metabolic regulator linked to cancer cell proliferation.. However, the specific mechanistic role of PDK4 in VSMC function and neointimal formation remains ambiguous.

    Article Title: cGAS-IFN-I responses by extracting nuclear DNA from dying cells via nucleocytosis.
    Article Snippet: Proteins were resolved on the NuPAGE 4–12% Bis-Tris Gel (Thermo Fisher Scientific), and electrotransferred to nitrocellulose membranes included in the iBlot Transfer Stack using the iBlot Dry Blotting System (Thermo Fisher Scientific). .. The membranes were blocked in 5% bovine serum albumin (BSA) in PBS with 0.1% Tween 20 and then incubated with primary antibodies against GAPDH (14C10; Cell Signalling Technology [CST], Danvers, MA, USA), IRF-3 (D83B9; CST), phosphorylated IRF-3 (p-IRF-3, Ser396) (4D4G; CST), TBK1/NAK (CST), p-TBK1/NAK (Ser172) (D52C2; CST), p44/42 MAPK (ERK1/2) (137F5; CST), p-p44/42 MAPK (ERK1/2, Thr202/Tyr204) (197G2; CST), stress activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK) (CST), and p-SAPK/ JNK (Thr183/Tyr185) (G9; CST). .. After washing, the membranes were incubated with anti-rabbit horseradish peroxidase (HRP)-conjugated secondary antibody (CST) or anti-mouse IgG HRP-conjugated secondary antibody (CST), and detected by HRP chemiluminescence.

    Article Title: cGAS-IFN-I responses by extracting nuclear DNA from dying cells via nucleocytosis
    Article Snippet: Proteins were resolved on the NuPAGE 4–12% Bis-Tris Gel (Thermo Fisher Scientific), and electrotransferred to nitrocellulose membranes included in the iBlot Transfer Stack using the iBlot Dry Blotting System (Thermo Fisher Scientific). .. The membranes were blocked in 5% bovine serum albumin (BSA) in PBS with 0.1% Tween 20 and then incubated with primary antibodies against GAPDH (14C10; Cell Signalling Technology [CST], Danvers, MA, USA), IRF-3 (D83B9; CST), phosphorylated IRF-3 (p-IRF-3, Ser396) (4D4G; CST), TBK1/NAK (CST), p-TBK1/NAK (Ser172) (D52C2; CST), p44/42 MAPK (ERK1/2) (137F5; CST), p-p44/42 MAPK (ERK1/2, Thr202/Tyr204) (197G2; CST), stress activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK) (CST), and p-SAPK/JNK (Thr183/Tyr185) (G9; CST). .. After washing, the membranes were incubated with anti-rabbit horseradish peroxidase (HRP)-conjugated secondary antibody (CST) or anti-mouse IgG HRP-conjugated secondary antibody (CST), and detected by HRP chemiluminescence.

    Article Title: The Pathogenic Roles of Local Vitamin D Metabolism Defect in Valve Inflammation and Calcification
    Article Snippet: .. The membranes were then incubated overnight at 4 °C with primary antibodies (1:1000) against Actin (Sc‐47778, Santa Cruz Biotechnology); p‐NF‐κB (p65, RelA) (3033S, Cell Signaling Technology); NF‐κB (p65, RelA) (8242S, Cell Signaling Technology); p‐p44/42 MAPK (9101S, Cell Signaling Technology); p44/42 MAPK (9102, Cell Signaling Technology). ..

    Western Blot:

    Article Title: Sphingosine-1-phosphate receptor modulators resensitize FLT3-ITD acute myeloid leukemia cells with NRAS mutations to FLT3 inhibitors
    Article Snippet: .. Lysate ( , ) immunoblots were probed with antibodies to p-STAT5 (Y694) (9351), STAT5 (94205), p-p44/42 MAPK (Erk1/2; T202/Y204) (9101), p44/42 MAPK (Erk1/2) (9107), p-Akt (S473) (T308) (4060) (4056), Akt (9272), p-GSK-3α/β (S21/9) (8566), GSK-3β (9832), SPHK1 (12071), p-p70 S6K (T389) (9206), p70 S6K (9202), p-BAD (S136) (4366), BAD (9239) (Cell Signaling Technology, Danvers, MA), and vinculin (V9264) (Invitrogen, Waltham, MA) at 1:1000 dilution overnight at 4°C, then with horseradish peroxidase-conjugated secondary antibodies for one hour at room temperature. ..



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    <t>STAT1-TGM2-VEGFR2</t> axis drives inflammatory angiogenesis in IBD. (A) The mRNA transcription of TGM2 was significantly upregulated upon stimulation with inflammatory cytokines IL-9, IL-23, and IFN-γ in HIMECs (n = 3 in each group). (B, C) The results of WB demonstrated that stimulation with IL-9, IL-23, and IFN-γ upregulated the protein expression of TGM2 in HIMEC. (D) Stimulation with inflammatory cytokines IL-9, IL-23, and IFN-γ significantly augmented the in vitro angiogenic capacity of HIMECs, while knockdown of TGM2 effectively reversed this effect. (E, F) IL-9, IL-23 and IFN-γ stimulation significantly enhanced the phosphorylation of VEGFR2 at Tyr1059, Tyr1214 and activated the downstream pathways such as FAK, PLC-γ and MAPK pathways in HIMEC, which were reversed by TGM2 knockdown. (G) IF results showed VEGFR2 co-localizes with TGM2 in HIMEC, mainly on the cell membrane. (H) Co-IP results substantiated the interaction between TGM2 and VEGFR2. (I) The CHIP assay confirmed the binding of STAT1 to the upstream promoter region of TGM2, thereby facilitating transcription following IFN-γ stimulation. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).
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    Image Search Results


    STAT1-TGM2-VEGFR2 axis drives inflammatory angiogenesis in IBD. (A) The mRNA transcription of TGM2 was significantly upregulated upon stimulation with inflammatory cytokines IL-9, IL-23, and IFN-γ in HIMECs (n = 3 in each group). (B, C) The results of WB demonstrated that stimulation with IL-9, IL-23, and IFN-γ upregulated the protein expression of TGM2 in HIMEC. (D) Stimulation with inflammatory cytokines IL-9, IL-23, and IFN-γ significantly augmented the in vitro angiogenic capacity of HIMECs, while knockdown of TGM2 effectively reversed this effect. (E, F) IL-9, IL-23 and IFN-γ stimulation significantly enhanced the phosphorylation of VEGFR2 at Tyr1059, Tyr1214 and activated the downstream pathways such as FAK, PLC-γ and MAPK pathways in HIMEC, which were reversed by TGM2 knockdown. (G) IF results showed VEGFR2 co-localizes with TGM2 in HIMEC, mainly on the cell membrane. (H) Co-IP results substantiated the interaction between TGM2 and VEGFR2. (I) The CHIP assay confirmed the binding of STAT1 to the upstream promoter region of TGM2, thereby facilitating transcription following IFN-γ stimulation. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

    Journal: Journal of Advanced Research

    Article Title: Transglutaminase 2 modulates inflammatory angiogenesis via vascular endothelial growth factor receptor 2 pathway in inflammatory bowel disease

    doi: 10.1016/j.jare.2025.07.002

    Figure Lengend Snippet: STAT1-TGM2-VEGFR2 axis drives inflammatory angiogenesis in IBD. (A) The mRNA transcription of TGM2 was significantly upregulated upon stimulation with inflammatory cytokines IL-9, IL-23, and IFN-γ in HIMECs (n = 3 in each group). (B, C) The results of WB demonstrated that stimulation with IL-9, IL-23, and IFN-γ upregulated the protein expression of TGM2 in HIMEC. (D) Stimulation with inflammatory cytokines IL-9, IL-23, and IFN-γ significantly augmented the in vitro angiogenic capacity of HIMECs, while knockdown of TGM2 effectively reversed this effect. (E, F) IL-9, IL-23 and IFN-γ stimulation significantly enhanced the phosphorylation of VEGFR2 at Tyr1059, Tyr1214 and activated the downstream pathways such as FAK, PLC-γ and MAPK pathways in HIMEC, which were reversed by TGM2 knockdown. (G) IF results showed VEGFR2 co-localizes with TGM2 in HIMEC, mainly on the cell membrane. (H) Co-IP results substantiated the interaction between TGM2 and VEGFR2. (I) The CHIP assay confirmed the binding of STAT1 to the upstream promoter region of TGM2, thereby facilitating transcription following IFN-γ stimulation. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

    Article Snippet: The antibody-protein complexes were immunoprecipitated using an anti-p-STAT1 antibody (9107, CST, USA) and control IgG.

    Techniques: Expressing, In Vitro, Knockdown, Phospho-proteomics, Membrane, Co-Immunoprecipitation Assay, Binding Assay