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stat1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc stat1
    Modulation of intracellular signaling pathways in HD, RA, and SLE cells exposed to environmental contaminants. Heatmap showing the relative expression and phosphorylation levels of key signaling proteins involved in immune regulation, inflammation, and cell survival <t>(STAT1,</t> STAT3, p38, AKT, and NFκB) and their phosphorylated forms in HD, RA, and SLE after exposure to PM, silica, and TCDD. Data are represented as z-score normalized values. Asterisks indicate statistically significant differences compared with the unstimulated control within each group (p < 0.05). AKT: protein kinase B; HD: healthy donors; NFκB: nuclear factor kappa-light-chain-enhancer of activated B cells; P: phosphorylated form; p38: p38 mitogen-activated protein kinase; PM: particulate matter; RA: rheumatoid arthritis; SLE: systemic lupus erythematosus; STAT: signal transducer and activator of transcription; TCDD: 2,3,7,8-tetrachlorodibenzo-p-dioxin.
    Stat1, 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/product/stat1/pmc12765182-85-12-16
    Average 86 stars, based on 1 article reviews
    stat1 - by Bioz Stars, 2026-10
    86/100 stars

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    1) Product Images from "Exploring the immunomodulatory effects of environmental contaminants on autoimmune patients: An in vitro approach"

    Article Title: Exploring the immunomodulatory effects of environmental contaminants on autoimmune patients: An in vitro approach

    Journal: Journal of Translational Autoimmunity

    doi: 10.1016/j.jtauto.2025.100341

    Modulation of intracellular signaling pathways in HD, RA, and SLE cells exposed to environmental contaminants. Heatmap showing the relative expression and phosphorylation levels of key signaling proteins involved in immune regulation, inflammation, and cell survival (STAT1, STAT3, p38, AKT, and NFκB) and their phosphorylated forms in HD, RA, and SLE after exposure to PM, silica, and TCDD. Data are represented as z-score normalized values. Asterisks indicate statistically significant differences compared with the unstimulated control within each group (p < 0.05). AKT: protein kinase B; HD: healthy donors; NFκB: nuclear factor kappa-light-chain-enhancer of activated B cells; P: phosphorylated form; p38: p38 mitogen-activated protein kinase; PM: particulate matter; RA: rheumatoid arthritis; SLE: systemic lupus erythematosus; STAT: signal transducer and activator of transcription; TCDD: 2,3,7,8-tetrachlorodibenzo-p-dioxin.
    Figure Legend Snippet: Modulation of intracellular signaling pathways in HD, RA, and SLE cells exposed to environmental contaminants. Heatmap showing the relative expression and phosphorylation levels of key signaling proteins involved in immune regulation, inflammation, and cell survival (STAT1, STAT3, p38, AKT, and NFκB) and their phosphorylated forms in HD, RA, and SLE after exposure to PM, silica, and TCDD. Data are represented as z-score normalized values. Asterisks indicate statistically significant differences compared with the unstimulated control within each group (p < 0.05). AKT: protein kinase B; HD: healthy donors; NFκB: nuclear factor kappa-light-chain-enhancer of activated B cells; P: phosphorylated form; p38: p38 mitogen-activated protein kinase; PM: particulate matter; RA: rheumatoid arthritis; SLE: systemic lupus erythematosus; STAT: signal transducer and activator of transcription; TCDD: 2,3,7,8-tetrachlorodibenzo-p-dioxin.

    Techniques Used: Protein-Protein interactions, Expressing, Phospho-proteomics, Control

    Related Articles

    Blocking Assay:

    Article Title: STING–STAT3–SOX18 Axis Drives EndMT and Epigenetic Reprogramming in SAVI Lung Fibrosis
    Article Snippet: For each sample, 20 μg of total protein was analyzed by Western blot using a Bio-Rad 4–20% Mini-PROTEAN TGX Gel and subsequently transferred onto nitrocellulose membranes. .. After blocking with LI-COR blocking buffer, the membranes were incubated with primary antibodies for VE-cadherin (1:1000, CST, Cat#2500S), CD31(1:1000, DAKO, Cat#M0823), SMA (1:2000, Abcam, Cat#ab7817), SM22 (1:1000, Abcam, Cat#ab14106), SOX18 (1:100, Santa Cruz, Cat#sc-166025), SLUG (1:1000, CST, Cat#9585S), P-STAT3 Y705 (1:1000, CST, Cat#9145S), STAT3 (1:1000, CST, Cat#9139S), P-STAT1 Y701 (1:1000, CST, Cat9167S), STAT1(1:1000, CST, Cat#9172S), P-STING S366 (1:1000, CST, Cat#19781S), STING (1:1000, CST, Cat#13647S), P-TBK1 S172 (1:1000, CST, Cat#5483S), TBK1 (1:1000, CST, Cat#3504S), P-IRF3 S396 (1:1000, CST, Cat#4947S), and IRF3 (1:1000, CST, Cat#11904S) overnight at 4°C; these antibodies are listed in the Key Resource table. .. Western blot samples were lysed in CHAPS buffer containing protease and phosphatase inhibitor cocktails (Invitrogen).

    Article Title: Discovery of synthetic G-quadruplex DNA as SARS-CoV-2 helicase inhibitor with antiviral, anti-inflammatory and antioxidative properties
    Article Snippet: .. The membranes were blocked in blocking buffer (TBS [pH 7.6], 0.1% Tween-20, 5% nonfat dry milk) for at least 3 h at 4 °C and then incubated with the following primary antibody: p-JAK1 (Tyr1022/1023, #3331S, 1:1000), JAK1 (#3344 1:1000), p-JAK2 (Tyr1008‚ #8082S, 1:1000), JAK2 (#3230, 1:1000), p-TYK2 (Tyr1054/1055, #68790, 1:1000), TYK2 (#14193, 1:1000), p-STAT1 (Tyr701, #9171, 1:1000), STAT1 (#14994, 1:1000), p-STAT2 (Tyr690‚ #88410, 1:1000), STAT2 (#72604, 1:1000), p-STAT3 (Tyr705, #9145S, 1:500), STAT3 (#9139, 1:1000) and beta-actin (#3700, 1:2000) (all from CST, Frankfurt, Germany). .. HBE ALI lysates were analyzed with primary antibodies against GAPDH (#2118, 1:4000, CST), ISG15 (#sc-166755,1:200, Santa Cruz Biotechnology), Mx1 (#37849, 1:1000, CST), SARS-CoV-2 Nucleocapsid (#40143-R019, 1:10 000, Sino Biological), STAT1 (#9172, 1:1000, CST), phospho-STAT1 Y701 (#9171, 1:1000, CST).

    Incubation:

    Article Title: STING–STAT3–SOX18 Axis Drives EndMT and Epigenetic Reprogramming in SAVI Lung Fibrosis
    Article Snippet: For each sample, 20 μg of total protein was analyzed by Western blot using a Bio-Rad 4–20% Mini-PROTEAN TGX Gel and subsequently transferred onto nitrocellulose membranes. .. After blocking with LI-COR blocking buffer, the membranes were incubated with primary antibodies for VE-cadherin (1:1000, CST, Cat#2500S), CD31(1:1000, DAKO, Cat#M0823), SMA (1:2000, Abcam, Cat#ab7817), SM22 (1:1000, Abcam, Cat#ab14106), SOX18 (1:100, Santa Cruz, Cat#sc-166025), SLUG (1:1000, CST, Cat#9585S), P-STAT3 Y705 (1:1000, CST, Cat#9145S), STAT3 (1:1000, CST, Cat#9139S), P-STAT1 Y701 (1:1000, CST, Cat9167S), STAT1(1:1000, CST, Cat#9172S), P-STING S366 (1:1000, CST, Cat#19781S), STING (1:1000, CST, Cat#13647S), P-TBK1 S172 (1:1000, CST, Cat#5483S), TBK1 (1:1000, CST, Cat#3504S), P-IRF3 S396 (1:1000, CST, Cat#4947S), and IRF3 (1:1000, CST, Cat#11904S) overnight at 4°C; these antibodies are listed in the Key Resource table. .. Western blot samples were lysed in CHAPS buffer containing protease and phosphatase inhibitor cocktails (Invitrogen).

    Article Title: Discovery of synthetic G-quadruplex DNA as SARS-CoV-2 helicase inhibitor with antiviral, anti-inflammatory and antioxidative properties
    Article Snippet: .. The membranes were blocked in blocking buffer (TBS [pH 7.6], 0.1% Tween-20, 5% nonfat dry milk) for at least 3 h at 4 °C and then incubated with the following primary antibody: p-JAK1 (Tyr1022/1023, #3331S, 1:1000), JAK1 (#3344 1:1000), p-JAK2 (Tyr1008‚ #8082S, 1:1000), JAK2 (#3230, 1:1000), p-TYK2 (Tyr1054/1055, #68790, 1:1000), TYK2 (#14193, 1:1000), p-STAT1 (Tyr701, #9171, 1:1000), STAT1 (#14994, 1:1000), p-STAT2 (Tyr690‚ #88410, 1:1000), STAT2 (#72604, 1:1000), p-STAT3 (Tyr705, #9145S, 1:500), STAT3 (#9139, 1:1000) and beta-actin (#3700, 1:2000) (all from CST, Frankfurt, Germany). .. HBE ALI lysates were analyzed with primary antibodies against GAPDH (#2118, 1:4000, CST), ISG15 (#sc-166755,1:200, Santa Cruz Biotechnology), Mx1 (#37849, 1:1000, CST), SARS-CoV-2 Nucleocapsid (#40143-R019, 1:10 000, Sino Biological), STAT1 (#9172, 1:1000, CST), phospho-STAT1 Y701 (#9171, 1:1000, CST).

    Article Title: An interferon-independent innate immune response to double stranded RNA in embryonic stem cells
    Article Snippet: .. Cells were permeabilized with digitonin and incubated with p53 (10442-1-AP, Proteintech), Stat1 (14994S, Cell Signaling Technology), or Dhx9 (17721-1-AP, Proteintech) primary antibody overnight at 4°C. .. After washing, cells were incubated with the secondary antibody (B900610, Proteintech) for 1 hour at room temperature, followed by incubation with pAG-Tn5 transposase for 1 hour.

    Control:

    Article Title: Exploring the immunomodulatory effects of environmental contaminants on autoimmune patients: An in vitro approach
    Article Snippet: Following washes, membranes were incubated with HRP-conjugated secondary antibodies, and signals were detected using PierceTM ECL substrate (Thermo Scientific, Waltham, MA, USA) on a ChemiDocTM MP imaging system (Bio-Rad, Hercules, CA, USA). .. Membranes were stripped and re-probed for total AKT, NFκB p65, p38 MAPK, STAT1, STAT3, and β-actin (Cell Signaling Technology, Danvers, MA, USA; Santa Cruz Biotechnology, Dallas, TX, USA) as a loading control. ..

    Article Title: DMAP1 Deficiency Suppresses Lung Cancer Progression by Destabilizing Replication Fork and Activating IFN Signaling-Mediated Anti-tumor Immunity.
    Article Snippet: .. Western blot antibodies used in this study: DMAP1 (10411-1-AP), CDK4 (11026-1-AP), Cyclin E2 (85803-3-RR), PARP1 (13371-1-AP), GAPDH (60004-1-Ig), Vinculin (66305-1-Ig), β-Tubulin (66240-1- Ig), and β-Actin (66009-1-Ig) antibodies were from Proteintech; Phospho-Chk2 (Thr68) (HY-P80799), RPA32/RPA2 (HY-P80975), Chk1 (HY-P80082), and Chk2 (HY-P80083) antibodies were from MCE; Rad51 (F1110), CDK2 (F0022), CDK6 (F0372), Cyclin A2 (F1033), Cyclin B1 (F2522), Cyclin D1 (F2524), Phospho-CDK1 (Thr161) + CDK2/3 (Thr160) (F3185), Phospho-CDK1/2/3 (Thr14) (F2120), RPA-pS33 (F2375), MCM2 (F0581), and PCNA (F0018) antibodies were from Selleck; Phospho-Chk1 (Ser345) (2348), Phospho-ATM (Ser1981) (5883), Phospho-TBK1 (Ser172) (5483), TBK1 (38066), Phospho-STING (Ser365) (72971), STING (13647), Phospho-Stat1 (Tyr701) (9167), Stat1 (14994), Phospho-IRF-7 (Ser437/438) (24129), IRF-7 (72073), Phospho-IRF-3 (Ser396) (4947), IRF-3 (4302), HA-Tag (3724), MAR/PAR (89190), and Phospho-ATR (Ser428) (2853) antibodies were from CST; CDK1 (A11420) antibody and Rabbit control IgG (AC005) were from Abclonal; Phospho-CDK6 (Tyr24) (AF2440) and Phospho-CDK4 (Thr172) (AF8007) antibodies were from Affinity Biosciences; Goat Anti-Rabbit IgG-HRP (CW0103) and Goat Anti-Mouse IgG-HRP (CW0102) antibodies were from CWBIO. .. Reagents and chemicals used in this study inclu CldU (MCE, HY-112669), IdU (MCE, HY-B0307), Vadimezan (Selleck, S1537), Nelfinavir (TargetMol, T7779), AG99 (TargetMol, T5155), Nicardipine (TargetMol, T1215), Pantoprazole (TargetMol, T6928), Lidocaine (TargetMol, T1144), Fulvestrant (TargetMol, T2146), Dydrogesterone (TargetMol, T3036), Carbenoxolone (TargetMol, T0992), Metoprolol (TargetMol, T0487), Moxifloxacin (TargetMol, T0331L), Cilomilast (Selleck, S1455), Avasimibe (Selleck, S2187), and Dacinostat (TargetMol, T2454).

    Western Blot:

    Article Title: DMAP1 Deficiency Suppresses Lung Cancer Progression by Destabilizing Replication Fork and Activating IFN Signaling-Mediated Anti-tumor Immunity.
    Article Snippet: .. Western blot antibodies used in this study: DMAP1 (10411-1-AP), CDK4 (11026-1-AP), Cyclin E2 (85803-3-RR), PARP1 (13371-1-AP), GAPDH (60004-1-Ig), Vinculin (66305-1-Ig), β-Tubulin (66240-1- Ig), and β-Actin (66009-1-Ig) antibodies were from Proteintech; Phospho-Chk2 (Thr68) (HY-P80799), RPA32/RPA2 (HY-P80975), Chk1 (HY-P80082), and Chk2 (HY-P80083) antibodies were from MCE; Rad51 (F1110), CDK2 (F0022), CDK6 (F0372), Cyclin A2 (F1033), Cyclin B1 (F2522), Cyclin D1 (F2524), Phospho-CDK1 (Thr161) + CDK2/3 (Thr160) (F3185), Phospho-CDK1/2/3 (Thr14) (F2120), RPA-pS33 (F2375), MCM2 (F0581), and PCNA (F0018) antibodies were from Selleck; Phospho-Chk1 (Ser345) (2348), Phospho-ATM (Ser1981) (5883), Phospho-TBK1 (Ser172) (5483), TBK1 (38066), Phospho-STING (Ser365) (72971), STING (13647), Phospho-Stat1 (Tyr701) (9167), Stat1 (14994), Phospho-IRF-7 (Ser437/438) (24129), IRF-7 (72073), Phospho-IRF-3 (Ser396) (4947), IRF-3 (4302), HA-Tag (3724), MAR/PAR (89190), and Phospho-ATR (Ser428) (2853) antibodies were from CST; CDK1 (A11420) antibody and Rabbit control IgG (AC005) were from Abclonal; Phospho-CDK6 (Tyr24) (AF2440) and Phospho-CDK4 (Thr172) (AF8007) antibodies were from Affinity Biosciences; Goat Anti-Rabbit IgG-HRP (CW0103) and Goat Anti-Mouse IgG-HRP (CW0102) antibodies were from CWBIO. .. Reagents and chemicals used in this study inclu CldU (MCE, HY-112669), IdU (MCE, HY-B0307), Vadimezan (Selleck, S1537), Nelfinavir (TargetMol, T7779), AG99 (TargetMol, T5155), Nicardipine (TargetMol, T1215), Pantoprazole (TargetMol, T6928), Lidocaine (TargetMol, T1144), Fulvestrant (TargetMol, T2146), Dydrogesterone (TargetMol, T3036), Carbenoxolone (TargetMol, T0992), Metoprolol (TargetMol, T0487), Moxifloxacin (TargetMol, T0331L), Cilomilast (Selleck, S1455), Avasimibe (Selleck, S2187), and Dacinostat (TargetMol, T2454).

    Recombinase Polymerase Amplification:

    Article Title: DMAP1 Deficiency Suppresses Lung Cancer Progression by Destabilizing Replication Fork and Activating IFN Signaling-Mediated Anti-tumor Immunity.
    Article Snippet: .. Western blot antibodies used in this study: DMAP1 (10411-1-AP), CDK4 (11026-1-AP), Cyclin E2 (85803-3-RR), PARP1 (13371-1-AP), GAPDH (60004-1-Ig), Vinculin (66305-1-Ig), β-Tubulin (66240-1- Ig), and β-Actin (66009-1-Ig) antibodies were from Proteintech; Phospho-Chk2 (Thr68) (HY-P80799), RPA32/RPA2 (HY-P80975), Chk1 (HY-P80082), and Chk2 (HY-P80083) antibodies were from MCE; Rad51 (F1110), CDK2 (F0022), CDK6 (F0372), Cyclin A2 (F1033), Cyclin B1 (F2522), Cyclin D1 (F2524), Phospho-CDK1 (Thr161) + CDK2/3 (Thr160) (F3185), Phospho-CDK1/2/3 (Thr14) (F2120), RPA-pS33 (F2375), MCM2 (F0581), and PCNA (F0018) antibodies were from Selleck; Phospho-Chk1 (Ser345) (2348), Phospho-ATM (Ser1981) (5883), Phospho-TBK1 (Ser172) (5483), TBK1 (38066), Phospho-STING (Ser365) (72971), STING (13647), Phospho-Stat1 (Tyr701) (9167), Stat1 (14994), Phospho-IRF-7 (Ser437/438) (24129), IRF-7 (72073), Phospho-IRF-3 (Ser396) (4947), IRF-3 (4302), HA-Tag (3724), MAR/PAR (89190), and Phospho-ATR (Ser428) (2853) antibodies were from CST; CDK1 (A11420) antibody and Rabbit control IgG (AC005) were from Abclonal; Phospho-CDK6 (Tyr24) (AF2440) and Phospho-CDK4 (Thr172) (AF8007) antibodies were from Affinity Biosciences; Goat Anti-Rabbit IgG-HRP (CW0103) and Goat Anti-Mouse IgG-HRP (CW0102) antibodies were from CWBIO. .. Reagents and chemicals used in this study inclu CldU (MCE, HY-112669), IdU (MCE, HY-B0307), Vadimezan (Selleck, S1537), Nelfinavir (TargetMol, T7779), AG99 (TargetMol, T5155), Nicardipine (TargetMol, T1215), Pantoprazole (TargetMol, T6928), Lidocaine (TargetMol, T1144), Fulvestrant (TargetMol, T2146), Dydrogesterone (TargetMol, T3036), Carbenoxolone (TargetMol, T0992), Metoprolol (TargetMol, T0487), Moxifloxacin (TargetMol, T0331L), Cilomilast (Selleck, S1455), Avasimibe (Selleck, S2187), and Dacinostat (TargetMol, T2454).

    Sequencing:

    Article Title: Sheng Jiangsan alleviated influenza-induced acute lung injury by regulating Lactobacillus murinus.
    Article Snippet: Please cite this article as: Lu, S., Shengle, Q., Shiqing, L., Huihuang, D., Qiaolian, C., Ruifeng, C., Pei, F., Xiao, W., Conglin, L., Xiaoqian, S., Zhonghao, F., Xin, Z., Qian, G., Xiangying, A., Weiqi, P., Yutao, W., Luping, L., Zifeng, Y., Sheng Jiangsan alleviated influenza-induced acute lung injury by regulating Lactobacillus murinus, Journal of Ethnopharmacology, https://doi.org/10.1016/j.jep.2026.121524.

    other:

    Article Title: Extracellular matrix rigidity controls breast cancer metastasis via TYK2-mediated mechanotransduction.
    Article Snippet: Antibodies were conjugated to protein G beads (LYN) or protein A beads (TYK2) (Invitrogen), crosslinked using disuccinimidyl suberate (Pierce) as per manufacturer’s protocol, incubated with lysates overnight at 4°C, washed eight times with IP lysis buffer supplemented with 200 mM NaCl, and eluted by incubation in LDS sample buffer with 50 mM DTT at 70°C for 10 minutes.

    Extraction:

    Article Title: An interferon-independent innate immune response to double stranded RNA in embryonic stem cells
    Article Snippet: .. Following 10-fold dilution of the lysate with extraction buffer C (EBC)-bovine serum albumin (BSA) (50 mM Tris-HCl [pH 6.8], 180 mM NaCl, 0.5% NP-40, and 0.5% BSA) plus protease inhibitors (11697498001, Roche), the cell lysates were immunoprecipitated with anti-p53 (10442-1-AP, Proteintech) or Stat1 (14994S, Cell Signaling Technology) antibody. .. The bound proteins were eluted with 2× SDS loading buffer at 95°C for 5 min. Western blot analysis was performed using an anti-Ubiquitin (sc-8017, Santa Cruz Biotechnology) antibody.

    Immunoprecipitation:

    Article Title: An interferon-independent innate immune response to double stranded RNA in embryonic stem cells
    Article Snippet: .. Following 10-fold dilution of the lysate with extraction buffer C (EBC)-bovine serum albumin (BSA) (50 mM Tris-HCl [pH 6.8], 180 mM NaCl, 0.5% NP-40, and 0.5% BSA) plus protease inhibitors (11697498001, Roche), the cell lysates were immunoprecipitated with anti-p53 (10442-1-AP, Proteintech) or Stat1 (14994S, Cell Signaling Technology) antibody. .. The bound proteins were eluted with 2× SDS loading buffer at 95°C for 5 min. Western blot analysis was performed using an anti-Ubiquitin (sc-8017, Santa Cruz Biotechnology) antibody.



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    Wuhan Sanying Biotechnology p stat1 rabbit polyclonal antibody
    Modulation of intracellular signaling pathways in HD, RA, and SLE cells exposed to environmental contaminants. Heatmap showing the relative expression and phosphorylation levels of key signaling proteins involved in immune regulation, inflammation, and cell survival <t>(STAT1,</t> STAT3, p38, AKT, and NFκB) and their phosphorylated forms in HD, RA, and SLE after exposure to PM, silica, and TCDD. Data are represented as z-score normalized values. Asterisks indicate statistically significant differences compared with the unstimulated control within each group (p < 0.05). AKT: protein kinase B; HD: healthy donors; NFκB: nuclear factor kappa-light-chain-enhancer of activated B cells; P: phosphorylated form; p38: p38 mitogen-activated protein kinase; PM: particulate matter; RA: rheumatoid arthritis; SLE: systemic lupus erythematosus; STAT: signal transducer and activator of transcription; TCDD: 2,3,7,8-tetrachlorodibenzo-p-dioxin.
    P Stat1 Rabbit Polyclonal Antibody, supplied by Wuhan Sanying Biotechnology, 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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    stat1 ko b6 129 s cg stat1 tm1dlv j  (Jackson Laboratory)
    86
    Jackson Laboratory stat1 ko b6 129 s cg stat1 tm1dlv j
    IFN-γ suppresses type 3 inflammation through <t>STAT1.</t> (A) Schematic of experimental model used. (B) Total cell number, (C) Neutrophil, (D) TRAMs (E) Ly6C+ Monocytes, and (F) MoAMs in BALs of female and male WT and STAT1 KO mice 8 hours post treatment as enumerated using flow cytometry. Fold changes in aggregated data were calculated relative to the -IFN-γ treatment group within each sex. Unpaired t test. (G) Principal component analysis (PCA) plot of compiled BAL cellularity data from C57BL/6J WT and STAT1 KO mice based on total cell numbers and 11 distinct cell types identified by flow cytometry. (H) PCA loadings indicating the magnitude and direction of each variable’s contribution to a principal component. p value: *≤ 0.05, **≤ 0.01, ***≤ 0.001, ****≤ 0.0001. All data have n≥3 mice, 2 experiments, mean ± SEM.
    Stat1 Ko B6 129 S Cg Stat1 Tm1dlv J, supplied by Jackson Laboratory, 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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    p stat1 antibody py701 4a  (Santa Cruz Biotechnology)
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    Santa Cruz Biotechnology p stat1 antibody py701 4a
    IFN-γ suppresses type 3 inflammation through <t>STAT1.</t> (A) Schematic of experimental model used. (B) Total cell number, (C) Neutrophil, (D) TRAMs (E) Ly6C+ Monocytes, and (F) MoAMs in BALs of female and male WT and STAT1 KO mice 8 hours post treatment as enumerated using flow cytometry. Fold changes in aggregated data were calculated relative to the -IFN-γ treatment group within each sex. Unpaired t test. (G) Principal component analysis (PCA) plot of compiled BAL cellularity data from C57BL/6J WT and STAT1 KO mice based on total cell numbers and 11 distinct cell types identified by flow cytometry. (H) PCA loadings indicating the magnitude and direction of each variable’s contribution to a principal component. p value: *≤ 0.05, **≤ 0.01, ***≤ 0.001, ****≤ 0.0001. All data have n≥3 mice, 2 experiments, mean ± SEM.
    P Stat1 Antibody Py701 4a, supplied by Santa Cruz Biotechnology, 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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    stat1 antibody c 136  (Santa Cruz Biotechnology)
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    Santa Cruz Biotechnology stat1 antibody c 136
    HDCA-treated ameliorate inflammation and modulate lipid metabolism in vivo. (A) Acetyl-CoA levels decreased over time in HDCA-treated Tregs. (B – E) Quantitative real-time PCR analysis of the mRNA expression of key lipogenic genes, including (B) fatty acid synthase (FASN), (C) acetyl-CoA carboxylase (ACC), (D) SCD1, and (E) SREBP-1c, in Tregs with or without HDCA treatment. (F) Functional metabolic flux assay using 13 C-glucose tracing shows decreased enrichment of labeled β-hydroxypalmitate in the HDCA-treated group. (G) Immunoblot analysis of phosphorylated <t>STAT1</t> in Tregs following HDCA exposure, and quantification statistical analysis results are presented in the bar graphs. (H) Representative IHC images show reduced IL-21 expression in atherosclerotic lesions of mice following HDCA treatment (magnification, 5 × ; scale bar, 50 μm). (I) Plasma cholesterol levels were measured by enzymatic colorimetry assay in FXR-sufficient controls and FXR KO mice ± HDCA. (J) Plasma triglyceride levels in the Vector and FXR KO groups were quantified at 0, 6, 12, and 18 h by a colorimetric assay. (K) Hemodynamic profiling assessed heart rate, systolic blood pressure (SBP), and diastolic blood pressure (DBP) for each group. (L – M) Ratios of monounsaturated to saturated fatty acids (MUFA/SFA) and polyunsaturated to saturated fatty acids (PUFA/SFA) in serum cholesterol esters (CE) and triglycerides (TG) were quantified by lipidomics in FXR-sufficient control and FXR KO mice ± HDCA. Data are presented as the mean ± SD (n = 3-5 biological replicates). ∗ P < 0.05, ∗∗ P < 0.01.
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    Image Search Results


    a Schematic of m 6 Am-seq in naïve CD4 + T cells. b Metagene profiles of m 6 Am peak distribution along normalized transcripts. c KEGG pathway enrichment analysis of m 6 Am-modified genes in naïve CD4 + T cells. d Schematic of RiboTag-seq in naïve CD4 + T cells. e Volcano plots of differential translation efficiency (TE) between cKO and WT naïve CD4 + T cells based on RiboTag-seq data. TE was calculated as the ratio of Fragments Per Kilobase of exon model per Million mapped fragments (FPKM) in RiboTag-seq to FPKM in input RNA-seq. f Venn diagram of TE-upregulated genes and m 6 Am-modified genes in naïve CD4 + T cells. g RiboTag-qPCR analysis of Stat1 mRNA association with ribosomes in naïve CD4 + T cells ( n = 4). h–j Representative immunoblot ( h ) and corresponding quantitative data ( i ) ( n = 8), along with representative histograms (left) and quantitative analysis (right) in ( j ) ( n = 6) reveal STAT1 expression in naïve CD4 + T cells from WT or cKO mice. k Schematic (left) and the quantification (right) of the dual-luciferase reporter assay used to characterize the effect of A-to-T substitution at the first nucleotide after the m 7 G cap in the 5’-UTR of Stat1 ( n = 12). l Quantification of IFN-γ expression in Th1-differentiated CD4 + T cells treated with a STAT1 inhibitor (WT or cKO Group n = 6, other Group n = 5). Each n represents biologically independent samples ( k ) or independent samples from individual mouse ( a , e , g – j , l ). Error bars represent means ± SEM; two-tailed, unpaired t -test ( g , i–k ); one-way ANOVA ( l ). p -values are shown on the graphs, and p -values < 0.0001 are reported as such.

    Journal: Nature Communications

    Article Title: Blocking the m 6 Am methyltransferase PCIF1 releases STAT1-mediated Th1 immunity to potentiate cancer immunotherapy

    doi: 10.1038/s41467-026-75269-1

    Figure Lengend Snippet: a Schematic of m 6 Am-seq in naïve CD4 + T cells. b Metagene profiles of m 6 Am peak distribution along normalized transcripts. c KEGG pathway enrichment analysis of m 6 Am-modified genes in naïve CD4 + T cells. d Schematic of RiboTag-seq in naïve CD4 + T cells. e Volcano plots of differential translation efficiency (TE) between cKO and WT naïve CD4 + T cells based on RiboTag-seq data. TE was calculated as the ratio of Fragments Per Kilobase of exon model per Million mapped fragments (FPKM) in RiboTag-seq to FPKM in input RNA-seq. f Venn diagram of TE-upregulated genes and m 6 Am-modified genes in naïve CD4 + T cells. g RiboTag-qPCR analysis of Stat1 mRNA association with ribosomes in naïve CD4 + T cells ( n = 4). h–j Representative immunoblot ( h ) and corresponding quantitative data ( i ) ( n = 8), along with representative histograms (left) and quantitative analysis (right) in ( j ) ( n = 6) reveal STAT1 expression in naïve CD4 + T cells from WT or cKO mice. k Schematic (left) and the quantification (right) of the dual-luciferase reporter assay used to characterize the effect of A-to-T substitution at the first nucleotide after the m 7 G cap in the 5’-UTR of Stat1 ( n = 12). l Quantification of IFN-γ expression in Th1-differentiated CD4 + T cells treated with a STAT1 inhibitor (WT or cKO Group n = 6, other Group n = 5). Each n represents biologically independent samples ( k ) or independent samples from individual mouse ( a , e , g – j , l ). Error bars represent means ± SEM; two-tailed, unpaired t -test ( g , i–k ); one-way ANOVA ( l ). p -values are shown on the graphs, and p -values < 0.0001 are reported as such.

    Article Snippet: During the first 24 h of Th1 differentiation from naïve CD4 + T cells, the STAT1 inhibitor Fludarabine (2.5 μM; MedChemExpress, 21679-14-1) was added.

    Techniques: Modification, RNA Sequencing, Western Blot, Expressing, Luciferase, Reporter Assay, Two Tailed Test

    Modulation of intracellular signaling pathways in HD, RA, and SLE cells exposed to environmental contaminants. Heatmap showing the relative expression and phosphorylation levels of key signaling proteins involved in immune regulation, inflammation, and cell survival (STAT1, STAT3, p38, AKT, and NFκB) and their phosphorylated forms in HD, RA, and SLE after exposure to PM, silica, and TCDD. Data are represented as z-score normalized values. Asterisks indicate statistically significant differences compared with the unstimulated control within each group (p < 0.05). AKT: protein kinase B; HD: healthy donors; NFκB: nuclear factor kappa-light-chain-enhancer of activated B cells; P: phosphorylated form; p38: p38 mitogen-activated protein kinase; PM: particulate matter; RA: rheumatoid arthritis; SLE: systemic lupus erythematosus; STAT: signal transducer and activator of transcription; TCDD: 2,3,7,8-tetrachlorodibenzo-p-dioxin.

    Journal: Journal of Translational Autoimmunity

    Article Title: Exploring the immunomodulatory effects of environmental contaminants on autoimmune patients: An in vitro approach

    doi: 10.1016/j.jtauto.2025.100341

    Figure Lengend Snippet: Modulation of intracellular signaling pathways in HD, RA, and SLE cells exposed to environmental contaminants. Heatmap showing the relative expression and phosphorylation levels of key signaling proteins involved in immune regulation, inflammation, and cell survival (STAT1, STAT3, p38, AKT, and NFκB) and their phosphorylated forms in HD, RA, and SLE after exposure to PM, silica, and TCDD. Data are represented as z-score normalized values. Asterisks indicate statistically significant differences compared with the unstimulated control within each group (p < 0.05). AKT: protein kinase B; HD: healthy donors; NFκB: nuclear factor kappa-light-chain-enhancer of activated B cells; P: phosphorylated form; p38: p38 mitogen-activated protein kinase; PM: particulate matter; RA: rheumatoid arthritis; SLE: systemic lupus erythematosus; STAT: signal transducer and activator of transcription; TCDD: 2,3,7,8-tetrachlorodibenzo-p-dioxin.

    Article Snippet: Membranes were stripped and re-probed for total AKT, NFκB p65, p38 MAPK, STAT1, STAT3, and β-actin (Cell Signaling Technology, Danvers, MA, USA; Santa Cruz Biotechnology, Dallas, TX, USA) as a loading control.

    Techniques: Protein-Protein interactions, Expressing, Phospho-proteomics, Control

    Modulation of intracellular signaling pathways in HD, RA, and SLE cells exposed to environmental contaminants. Heatmap showing the relative expression and phosphorylation levels of key signaling proteins involved in immune regulation, inflammation, and cell survival (STAT1, STAT3, p38, AKT, and NFκB) and their phosphorylated forms in HD, RA, and SLE after exposure to PM, silica, and TCDD. Data are represented as z-score normalized values. Asterisks indicate statistically significant differences compared with the unstimulated control within each group (p < 0.05). AKT: protein kinase B; HD: healthy donors; NFκB: nuclear factor kappa-light-chain-enhancer of activated B cells; P: phosphorylated form; p38: p38 mitogen-activated protein kinase; PM: particulate matter; RA: rheumatoid arthritis; SLE: systemic lupus erythematosus; STAT: signal transducer and activator of transcription; TCDD: 2,3,7,8-tetrachlorodibenzo-p-dioxin.

    Journal: Journal of Translational Autoimmunity

    Article Title: Exploring the immunomodulatory effects of environmental contaminants on autoimmune patients: An in vitro approach

    doi: 10.1016/j.jtauto.2025.100341

    Figure Lengend Snippet: Modulation of intracellular signaling pathways in HD, RA, and SLE cells exposed to environmental contaminants. Heatmap showing the relative expression and phosphorylation levels of key signaling proteins involved in immune regulation, inflammation, and cell survival (STAT1, STAT3, p38, AKT, and NFκB) and their phosphorylated forms in HD, RA, and SLE after exposure to PM, silica, and TCDD. Data are represented as z-score normalized values. Asterisks indicate statistically significant differences compared with the unstimulated control within each group (p < 0.05). AKT: protein kinase B; HD: healthy donors; NFκB: nuclear factor kappa-light-chain-enhancer of activated B cells; P: phosphorylated form; p38: p38 mitogen-activated protein kinase; PM: particulate matter; RA: rheumatoid arthritis; SLE: systemic lupus erythematosus; STAT: signal transducer and activator of transcription; TCDD: 2,3,7,8-tetrachlorodibenzo-p-dioxin.

    Article Snippet: Membranes were blocked with 5 % non-fat milk in TBS-T and incubated overnight at 4 °C with primary antibodies against phospho-AKT (Thr308), phospho-NFκB p65 (Ser536), phospho-p38 MAPK (Thr180/Tyr182), phospho-STAT1 (Tyr701), and phospho-STAT3 (Tyr705) (Cell Signaling Technology, Danvers, MA, USA; Santa Cruz Biotechnology, Dallas, TX, USA).

    Techniques: Protein-Protein interactions, Expressing, Phospho-proteomics, Control

    IFN-γ suppresses type 3 inflammation through STAT1. (A) Schematic of experimental model used. (B) Total cell number, (C) Neutrophil, (D) TRAMs (E) Ly6C+ Monocytes, and (F) MoAMs in BALs of female and male WT and STAT1 KO mice 8 hours post treatment as enumerated using flow cytometry. Fold changes in aggregated data were calculated relative to the -IFN-γ treatment group within each sex. Unpaired t test. (G) Principal component analysis (PCA) plot of compiled BAL cellularity data from C57BL/6J WT and STAT1 KO mice based on total cell numbers and 11 distinct cell types identified by flow cytometry. (H) PCA loadings indicating the magnitude and direction of each variable’s contribution to a principal component. p value: *≤ 0.05, **≤ 0.01, ***≤ 0.001, ****≤ 0.0001. All data have n≥3 mice, 2 experiments, mean ± SEM.

    Journal: Frontiers in Immunology

    Article Title: Second-order regulation: IFN-γ suppresses IL-17A-mediated type 3 inflammation

    doi: 10.3389/fimmu.2026.1744476

    Figure Lengend Snippet: IFN-γ suppresses type 3 inflammation through STAT1. (A) Schematic of experimental model used. (B) Total cell number, (C) Neutrophil, (D) TRAMs (E) Ly6C+ Monocytes, and (F) MoAMs in BALs of female and male WT and STAT1 KO mice 8 hours post treatment as enumerated using flow cytometry. Fold changes in aggregated data were calculated relative to the -IFN-γ treatment group within each sex. Unpaired t test. (G) Principal component analysis (PCA) plot of compiled BAL cellularity data from C57BL/6J WT and STAT1 KO mice based on total cell numbers and 11 distinct cell types identified by flow cytometry. (H) PCA loadings indicating the magnitude and direction of each variable’s contribution to a principal component. p value: *≤ 0.05, **≤ 0.01, ***≤ 0.001, ****≤ 0.0001. All data have n≥3 mice, 2 experiments, mean ± SEM.

    Article Snippet: 6-week-old C57BL/6J (stock# 000664), IFN-γ KO (B6.129S7-Ifng tm1Ts /J, Stock# 002287), and STAT1 KO (B6.129S(Cg)-Stat1 tm1Dlv /J, Stock# 012606) mice were obtained from Jackson labs (USA) and subsequently bred in-house to ensure acclimation to local conditions.

    Techniques: Flow Cytometry

    HDCA-treated ameliorate inflammation and modulate lipid metabolism in vivo. (A) Acetyl-CoA levels decreased over time in HDCA-treated Tregs. (B – E) Quantitative real-time PCR analysis of the mRNA expression of key lipogenic genes, including (B) fatty acid synthase (FASN), (C) acetyl-CoA carboxylase (ACC), (D) SCD1, and (E) SREBP-1c, in Tregs with or without HDCA treatment. (F) Functional metabolic flux assay using 13 C-glucose tracing shows decreased enrichment of labeled β-hydroxypalmitate in the HDCA-treated group. (G) Immunoblot analysis of phosphorylated STAT1 in Tregs following HDCA exposure, and quantification statistical analysis results are presented in the bar graphs. (H) Representative IHC images show reduced IL-21 expression in atherosclerotic lesions of mice following HDCA treatment (magnification, 5 × ; scale bar, 50 μm). (I) Plasma cholesterol levels were measured by enzymatic colorimetry assay in FXR-sufficient controls and FXR KO mice ± HDCA. (J) Plasma triglyceride levels in the Vector and FXR KO groups were quantified at 0, 6, 12, and 18 h by a colorimetric assay. (K) Hemodynamic profiling assessed heart rate, systolic blood pressure (SBP), and diastolic blood pressure (DBP) for each group. (L – M) Ratios of monounsaturated to saturated fatty acids (MUFA/SFA) and polyunsaturated to saturated fatty acids (PUFA/SFA) in serum cholesterol esters (CE) and triglycerides (TG) were quantified by lipidomics in FXR-sufficient control and FXR KO mice ± HDCA. Data are presented as the mean ± SD (n = 3-5 biological replicates). ∗ P < 0.05, ∗∗ P < 0.01.

    Journal: Redox Biology

    Article Title: Hyodeoxycholic acid attenuates atherosclerosis by antagonizing FXR and modulating the PD-1/mTORC1 signaling axis

    doi: 10.1016/j.redox.2026.104096

    Figure Lengend Snippet: HDCA-treated ameliorate inflammation and modulate lipid metabolism in vivo. (A) Acetyl-CoA levels decreased over time in HDCA-treated Tregs. (B – E) Quantitative real-time PCR analysis of the mRNA expression of key lipogenic genes, including (B) fatty acid synthase (FASN), (C) acetyl-CoA carboxylase (ACC), (D) SCD1, and (E) SREBP-1c, in Tregs with or without HDCA treatment. (F) Functional metabolic flux assay using 13 C-glucose tracing shows decreased enrichment of labeled β-hydroxypalmitate in the HDCA-treated group. (G) Immunoblot analysis of phosphorylated STAT1 in Tregs following HDCA exposure, and quantification statistical analysis results are presented in the bar graphs. (H) Representative IHC images show reduced IL-21 expression in atherosclerotic lesions of mice following HDCA treatment (magnification, 5 × ; scale bar, 50 μm). (I) Plasma cholesterol levels were measured by enzymatic colorimetry assay in FXR-sufficient controls and FXR KO mice ± HDCA. (J) Plasma triglyceride levels in the Vector and FXR KO groups were quantified at 0, 6, 12, and 18 h by a colorimetric assay. (K) Hemodynamic profiling assessed heart rate, systolic blood pressure (SBP), and diastolic blood pressure (DBP) for each group. (L – M) Ratios of monounsaturated to saturated fatty acids (MUFA/SFA) and polyunsaturated to saturated fatty acids (PUFA/SFA) in serum cholesterol esters (CE) and triglycerides (TG) were quantified by lipidomics in FXR-sufficient control and FXR KO mice ± HDCA. Data are presented as the mean ± SD (n = 3-5 biological replicates). ∗ P < 0.05, ∗∗ P < 0.01.

    Article Snippet: Proteins were detected using the following antibodies: anti-CPT1a antibody (ab234111, abcam), anti-beta actin antibody (ab8226, abcam), anti-PERK antibody (ab229912, abcam), anti-ERK1+ERK2 antibody (ab184699, abcam), anti-S6K1 antibody (ab14708, abcam), anti-S6K1 (phospho T229) antibody (ab5231, abcam), Rac1/2/3 antibody (G-2) (sc-514583, Santa Cruz), anti-Calpain 1 antibody (ab108400, abcam), anti-MMP2 antibody (ab92536, abcam), anti-IL-10 antibody (ab310329, abcam), anti-ZNF671 antibody (HPA046099, Sigma-Aldrich), anti-MAPK6/ERK3 antibody (ab53277, abcam), SIAH1 recombinant rabbit monoclonal antibody (PSH01-80) (MA5-51926, Thermo Fisher), p-Stat1 antibody (pY701.4A) (sc-136229, Santa Cruz), Stat1 antibody (C-136) (sc-464, Santa Cruz), anti-FXR1 antibody (ab155124, abcam), phospho-Raptor (Ser792) polyclonal antibody (PA5-118730, Thermo Fisher), anti-PD1 antibody (ab214421, abcam), SHP-2 antibody (3752S, Cell Signaling Technology), IL-10R antibody (3F9) (sc-53654, Santa Cruz), GAPDH antibody (6C5) (sc-32233, Santa Cruz), rabbit anti-mouse IgG H&L (HRP) (ab6728, abcam), goat anti-rabbit IgG (H + L) highly cross-adsorbed secondary antibody, Alexa FluorTM Plus 488 (A32731, Thermo Fisher).

    Techniques: In Vivo, Real-time Polymerase Chain Reaction, Expressing, Functional Assay, Flux Assay, Labeling, Western Blot, Clinical Proteomics, Colorimetric Assay, Plasmid Preparation, Control