socs3 protein antibody  (Cell Signaling Technology Inc)

Journal: Scientific Reports

Article Title: Cancer-Associated fibroblasts regulate the development of cholangiocarcinoma through IL-6/STAT3/AKR1C3 signaling axis

doi: 10.1038/s41598-026-37583-y

Figure Lengend Snippet: The molecular mechanism of STAT3 signaling pathway regulated by AKR1C3 in CCA. (A) After treatment with IL-6, the expression levels of proliferation, invasion, drug resistance, glycolysis, and STAT3 signaling-associated proteins were detected by Western blot in QBC939 cells. IL-6, 30 ng/ml. (B) The mRNA expression levels of the SOCSs family in QBC939 cells after AKR1C3 knockdown were detected by Q-PCR. * P < 0.05 (C) The protein expression levels of SOCS1 and SOCS3 in CCA cells after AKR1C3 knockdown and overexpression were measured by Western blot. (D) Western blot was performed to assess the ubiquitination degradation of SOCS1 in shAKR1C3- or shCtrl-transfected QBC939 cells treated with 50 µM cyclohexane (CHX) at different times. (E) Co-IP assay was conducted to investigate the protein interaction between AKR1C3 and SOCS1 in QBC939 cells.

Article Snippet: Antibodies against SOCS3 (68631 S) and PFK-1 (55028-1-AP) were obtained from Proteintech. (Hubei, China).

Techniques: Expressing, Western Blot, Knockdown, Over Expression, Ubiquitin Proteomics, Transfection, Co-Immunoprecipitation Assay

Journal: Frontiers in immunology

Article Title: Ozone promotes macrophage efferocytosis and alleviates neuropathic pain by activating the AMPK/Gas6-MerTK/SOCS3 signaling pathway.

doi: 10.3389/fimmu.2024.1455771

Figure Lengend Snippet: FIGURE 4 Ozone suppresses neuroinflammatory responses by upregulating SOCS3 expression. (A, B) The SOCS3 and SOCS1 expression in BMDM were examined (n=3). (C-E) qPCR was performed to detect the transcription levels of inflammatory cytokines in BMDMs (n=3). Significant differences were revealed following one-way ANOVA (A–E) (*p < 0.05, **p < 0.01, and ***p < 0.001).

Article Snippet: The following reagents and antibodies were used in the study: bactin antibody from ABclonal (China), p-AMPK antibody from Cell Signaling Technology (USA), SOCS3 antibody and Protein S antibody from Santa Cruz Biotechnology (USA), Gas6 antibody from Abcam (USA), p-MerTK antibody from Thermo Fisher Scientific(USA), AICAR from Selleckchem (USA), Compound C from MedChemExpress (USA), UNC2541 from Topscience (China), BCECF from APExBIO (USA), Secondary antibodies for Western blot from Sigma (USA).

Techniques: Expressing

Journal: Frontiers in immunology

Article Title: Ozone promotes macrophage efferocytosis and alleviates neuropathic pain by activating the AMPK/Gas6-MerTK/SOCS3 signaling pathway.

doi: 10.3389/fimmu.2024.1455771

Figure Lengend Snippet: FIGURE 5 Ozone alleviates neuropathic pain by activating the AMPK/Gas6-MerTK/SOCS3 signaling pathway. (A) After establishing the mouse CCI model for 14 days, ozone (30mg, i.p.) was administered for 7 days. The sciatic nerves of mice were collected to measure the p-AMPK expression level. (B) Mice received AICAR (0.25mg/kg) and CC (100mg) pretreatment around the sciatic nerve half an hour in advance. Ozone (30mg, i.p.) was administered for 7 days, and the sciatic nerves were collected to investigate p-AMPK levels (n=6). (C, D) Western blot was used to examine the Gas6 expression of sciatic nerves and plasma in CCI mice (n=6). (E, F) After establishing the mouse CCI model for 14 days, mice received CC (100mg) pretreatment around the sciatic nerve half an hour in advance. Ozone (30mg, i.p.) was administered for 7 days, and the expression levels of Gas6 in the sciatic nerves and plasma were detected (n=6). (G, H) Western blot was used to measure the expression levels of Protein S (n=6). (I, J) p-ADAM17 and p- MerTK expression in the sciatic nerves were detected by western blot (n=6). (K, L) The expression levels of SOCS3 and SOCS1 in the sciatic nerves were examined (n=6). Significant differences were determined by one-way ANOVA (A-L). (*p < 0.05, **p < 0.01, and ***p < 0.001).

Article Snippet: The following reagents and antibodies were used in the study: bactin antibody from ABclonal (China), p-AMPK antibody from Cell Signaling Technology (USA), SOCS3 antibody and Protein S antibody from Santa Cruz Biotechnology (USA), Gas6 antibody from Abcam (USA), p-MerTK antibody from Thermo Fisher Scientific(USA), AICAR from Selleckchem (USA), Compound C from MedChemExpress (USA), UNC2541 from Topscience (China), BCECF from APExBIO (USA), Secondary antibodies for Western blot from Sigma (USA).

Techniques: Expressing, Western Blot, Clinical Proteomics

Journal: Frontiers in immunology

Article Title: Ozone promotes macrophage efferocytosis and alleviates neuropathic pain by activating the AMPK/Gas6-MerTK/SOCS3 signaling pathway.

doi: 10.3389/fimmu.2024.1455771

Figure Lengend Snippet: FIGURE 7 Schematic model indicates that ozone promotes macrophage efferocytosis and alleviates neuropathic pain. Ozone activities AMPK/GAS6/MerTK signaling pathway to promote macrophage efferocytosis and clear the apoptotic cells, inducing SOCS3- mediated neuroinflammation tolerance to attenuate neuropathic pain.

Article Snippet: The following reagents and antibodies were used in the study: bactin antibody from ABclonal (China), p-AMPK antibody from Cell Signaling Technology (USA), SOCS3 antibody and Protein S antibody from Santa Cruz Biotechnology (USA), Gas6 antibody from Abcam (USA), p-MerTK antibody from Thermo Fisher Scientific(USA), AICAR from Selleckchem (USA), Compound C from MedChemExpress (USA), UNC2541 from Topscience (China), BCECF from APExBIO (USA), Secondary antibodies for Western blot from Sigma (USA).

Techniques:

Journal: Aging (Albany NY)

Article Title: SPTBN1 suppresses the progression of epithelial ovarian cancer via SOCS3-mediated blockade of the JAK/STAT3 signaling pathway

doi: 10.18632/aging.103303

Figure Lengend Snippet: Loss of SPTBN1 activates the JAK/STAT3 signaling pathway through downregulation of SOCS3. ( A ) Assessments of JAK/STAT signaling pathway-associated proteins by western blot after SPTBN1 knockdown cooperated with SOCS3 overexpression in HO8910 cells (left), and SPTBN1 overexpression cooperated with SOCS3 knockdown (right). ( B ) DNA gel electrophoresis after PCR. Mouse embryonic fibroblasts (MEFs) were cultured from SPTBN1 -/- embryos (n=2), SPTBN1 +/- embryos (n=3) and wild-type embryos (n=2). The genotypes of MEFs were identified by PCR and DNA gel electrophoresis. Lanes 1 and 2: SPTBN1 -/- MEFs; lanes 3, 4, and 5: SPTBN1 +/- MEFs; lanes 6 and 7: SPTBN1 -/- MEFs. ( C ) Assessments of EMT and JAK/STAT3 signaling pathway-associated proteins by western blot in SPTBN1 -/- , SPTBN1 +/- , and SPTBN1 +/+ MEFs. Lanes 1 and 2: SPTBN1 -/- MEFs; lanes 3, 4, and 5: SPTBN1 +/- MEFs; lanes 6 and 7: SPTBN1 -/- MEFs. Loss of SPTBN1 can promote EMT, inhibit SOCS3 and activate the JAK/STAT signaling pathway.

Article Snippet: The primary antibody against SPTBN1 was from GenScript Corporation (Nanjing, China), and other primary antibodies against SOCS3, JAK2, p-JAK2 (Tyr1007/1008), STAT3, p-STAT3 (Tyr705) and EMT-related proteins were from Cell Signaling Technology (Danvers, MA, USA). β-Actin (Cell Signaling Technology, Danvers, MA, USA) as a loading control was also detected.

Techniques: Western Blot, Knockdown, Over Expression, DNA Gel Electrophoresis, Cell Culture

Journal: Aging (Albany NY)

Article Title: SPTBN1 suppresses the progression of epithelial ovarian cancer via SOCS3-mediated blockade of the JAK/STAT3 signaling pathway

doi: 10.18632/aging.103303

Figure Lengend Snippet: SOCS3 overexpression or the JAK2 inhibitor reverses the inhibitory effects of SPTBN1 on cell viability and migration. ( A , B ) In vitro cell migration assay. * P < 0.05 vs LV-RFP+LV-GFP, # P < 0.05 vs LV-SPTBN1sh+LV-GFP, n=3. ( C , D ) Comparison of protein ( C ) and mRNA ( D ) levels of the EMT-related proteins E-cadherin (E-cad) and Vimentin (Vim). The expression of SOCS3 and E-cadherin was decreased and Vimentin was increased by the loss of SPTBN1, while SOCS3 overexpression reversed the effects of the loss of SPTBN1. * P <0.05 ** P <0.01 vs LV-RFP+LV-GFP, ## P <0.01 vs LV-SPTBN1sh+LV-GFP, n=3. ( E – H ) Cell viability was determined by CCK8 assay. SOCS3 overexpression reversed the enhanced cell viability due to the loss of SPTBN1 in A2780 ( E ) and HO8910 cells ( F ). # P <0.05, ## P <0.01 vs LV-RFP+LV-GFP, * P <0.05 vs LV-SPTBN1sh+LV-GFP, n=3. The JAK2 inhibitor Ag490 or tofacitinib (Tofa) inhibited cell viability and reversed the promoting effect of the loss of SPTBN1 in A2780 ( G ) and HO8910 cells ( H ). * P <0.05, ** P <0.01 vs LV-RFP, # P <0.05 vs LV-SPTBN1sh, n = 3.

Article Snippet: The primary antibody against SPTBN1 was from GenScript Corporation (Nanjing, China), and other primary antibodies against SOCS3, JAK2, p-JAK2 (Tyr1007/1008), STAT3, p-STAT3 (Tyr705) and EMT-related proteins were from Cell Signaling Technology (Danvers, MA, USA). β-Actin (Cell Signaling Technology, Danvers, MA, USA) as a loading control was also detected.

Techniques: Over Expression, Migration, In Vitro, Cell Migration Assay, Comparison, Expressing, CCK-8 Assay