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anti socs1  (Boster Bio)


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    Boster Bio anti socs1
    Anti Socs1, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+socs1/Anti-SOCS1+Antibody+Picoband/pmc12896625-44-0-6
    Average 93 stars, based on 10 article reviews
    anti socs1 - by Bioz Stars, 2026-10
    93/100 stars

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    other:

    Article Title: Echinacea Purpurea Polysaccharides Alleviate DSS-Induced Colitis in Rats by Regulating Gut Microbiota and Short-Chain Fatty Acid Metabolism
    Article Snippet: Anti-SOCS1 and Anti-GAPDH (HRP) was from BOSTER Biological Technology Co., Ltd. (Bejing, China).

    Article Title: NaAsO 2 regulates TLR4/MyD88/NF-κB signaling pathway through DNMT1/SOCS1 to cause apoptosis and inflammation in hepatic BRL-3A cells.
    Article Snippet: The exact molecular mechanism of arsenic-induced liver injury has not been fully elucidated.. The aim of the study was to investigate the potential mechanism of NaAsO2-induced cytotoxicity in BRL-3A cells and to provide a basis for the mechanism of arsenic poisoning.. BRL-3A cells were treated with different doses of NaAsO2, DNMT1 inhibitor (DC_517), TLR4 inhibitor (TAK-242), and transfection of SOCS1 plasmid.



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    ABclonal Biotechnology socs1
    Focal rTSMS significantly inhibits CCI-induced neuroinflammation and upregulates SOCS3 in the spinal cord in vivo . (A) Representative immunofluorescence images showing the inhibitory effects of focal rTSMS on CCI-induced activation of microglia and astrocytes in the dorsal horn ( n = 3). Dashed box indicates the region of interest in the dorsal horn of the spinal cord. Scale bars: 100 μm. (B) Representative image of western blotting. (C, D) Re-administration of rTSMS significantly inhibited the CCI-induced upregulation of Iba-1 and GFAP ( n = 5). (E–G) Focal rTSMS significantly inhibited CCI-induced upregulation of IL-1β, IL-6, and TNF-α in the spinal cord ( n = 5). (H, I) Focal rTSMS significantly inhibited the CCI-induced increase in the protein levels of p-p38 and p-STAT3 in the spinal cord ( n = 5). (J) Focal rTSMS significantly upregulated SOCS3 in the spinal cord ( n = 5). (K) Focal rTSMS could not upregulate <t>SOCS1</t> in the spinal cord ( n = 5). Data are expressed as mean ± SD. # P < 0.05, ### P < 0.001, #### P < 0.0001, vs. Sham group; * P < 0.05, ** P < 0.01, *** P < 0.001, vs . CCI group (one‐way analysis of variance followed by Tukey’s multiple comparisons tests). CCI: Chronic constrictive injury; GFAP: glial fibrillary acidic protein; Iba-1: ionized calcium binding adaptor molecule-1; IL: interleukin; rTSMS: repetitive trans-spinal magnetic stimulation; SOCS: suppressor of cytokine signaling; STAT3: transducer and activator of transcription 3; TNF-α: tumor necrosis factor-alpha.
    Socs1, supplied by ABclonal 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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    anti socs1  (Affinity Biosciences)
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    Affinity Biosciences anti socs1
    Focal rTSMS significantly inhibits CCI-induced neuroinflammation and upregulates SOCS3 in the spinal cord in vivo . (A) Representative immunofluorescence images showing the inhibitory effects of focal rTSMS on CCI-induced activation of microglia and astrocytes in the dorsal horn ( n = 3). Dashed box indicates the region of interest in the dorsal horn of the spinal cord. Scale bars: 100 μm. (B) Representative image of western blotting. (C, D) Re-administration of rTSMS significantly inhibited the CCI-induced upregulation of Iba-1 and GFAP ( n = 5). (E–G) Focal rTSMS significantly inhibited CCI-induced upregulation of IL-1β, IL-6, and TNF-α in the spinal cord ( n = 5). (H, I) Focal rTSMS significantly inhibited the CCI-induced increase in the protein levels of p-p38 and p-STAT3 in the spinal cord ( n = 5). (J) Focal rTSMS significantly upregulated SOCS3 in the spinal cord ( n = 5). (K) Focal rTSMS could not upregulate <t>SOCS1</t> in the spinal cord ( n = 5). Data are expressed as mean ± SD. # P < 0.05, ### P < 0.001, #### P < 0.0001, vs. Sham group; * P < 0.05, ** P < 0.01, *** P < 0.001, vs . CCI group (one‐way analysis of variance followed by Tukey’s multiple comparisons tests). CCI: Chronic constrictive injury; GFAP: glial fibrillary acidic protein; Iba-1: ionized calcium binding adaptor molecule-1; IL: interleukin; rTSMS: repetitive trans-spinal magnetic stimulation; SOCS: suppressor of cytokine signaling; STAT3: transducer and activator of transcription 3; TNF-α: tumor necrosis factor-alpha.
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    https://www.bioz.com/product/anti+socs1/anti+socs1/pm42313305-104-32-9
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    anti socs1  (Proteintech)
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    Focal rTSMS significantly inhibits CCI-induced neuroinflammation and upregulates SOCS3 in the spinal cord in vivo . (A) Representative immunofluorescence images showing the inhibitory effects of focal rTSMS on CCI-induced activation of microglia and astrocytes in the dorsal horn ( n = 3). Dashed box indicates the region of interest in the dorsal horn of the spinal cord. Scale bars: 100 μm. (B) Representative image of western blotting. (C, D) Re-administration of rTSMS significantly inhibited the CCI-induced upregulation of Iba-1 and GFAP ( n = 5). (E–G) Focal rTSMS significantly inhibited CCI-induced upregulation of IL-1β, IL-6, and TNF-α in the spinal cord ( n = 5). (H, I) Focal rTSMS significantly inhibited the CCI-induced increase in the protein levels of p-p38 and p-STAT3 in the spinal cord ( n = 5). (J) Focal rTSMS significantly upregulated SOCS3 in the spinal cord ( n = 5). (K) Focal rTSMS could not upregulate <t>SOCS1</t> in the spinal cord ( n = 5). Data are expressed as mean ± SD. # P < 0.05, ### P < 0.001, #### P < 0.0001, vs. Sham group; * P < 0.05, ** P < 0.01, *** P < 0.001, vs . CCI group (one‐way analysis of variance followed by Tukey’s multiple comparisons tests). CCI: Chronic constrictive injury; GFAP: glial fibrillary acidic protein; Iba-1: ionized calcium binding adaptor molecule-1; IL: interleukin; rTSMS: repetitive trans-spinal magnetic stimulation; SOCS: suppressor of cytokine signaling; STAT3: transducer and activator of transcription 3; TNF-α: tumor necrosis factor-alpha.
    Anti Socs1, supplied by Proteintech, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rabbit anti socs1  (Proteintech)
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    Focal rTSMS significantly inhibits CCI-induced neuroinflammation and upregulates SOCS3 in the spinal cord in vivo . (A) Representative immunofluorescence images showing the inhibitory effects of focal rTSMS on CCI-induced activation of microglia and astrocytes in the dorsal horn ( n = 3). Dashed box indicates the region of interest in the dorsal horn of the spinal cord. Scale bars: 100 μm. (B) Representative image of western blotting. (C, D) Re-administration of rTSMS significantly inhibited the CCI-induced upregulation of Iba-1 and GFAP ( n = 5). (E–G) Focal rTSMS significantly inhibited CCI-induced upregulation of IL-1β, IL-6, and TNF-α in the spinal cord ( n = 5). (H, I) Focal rTSMS significantly inhibited the CCI-induced increase in the protein levels of p-p38 and p-STAT3 in the spinal cord ( n = 5). (J) Focal rTSMS significantly upregulated SOCS3 in the spinal cord ( n = 5). (K) Focal rTSMS could not upregulate <t>SOCS1</t> in the spinal cord ( n = 5). Data are expressed as mean ± SD. # P < 0.05, ### P < 0.001, #### P < 0.0001, vs. Sham group; * P < 0.05, ** P < 0.01, *** P < 0.001, vs . CCI group (one‐way analysis of variance followed by Tukey’s multiple comparisons tests). CCI: Chronic constrictive injury; GFAP: glial fibrillary acidic protein; Iba-1: ionized calcium binding adaptor molecule-1; IL: interleukin; rTSMS: repetitive trans-spinal magnetic stimulation; SOCS: suppressor of cytokine signaling; STAT3: transducer and activator of transcription 3; TNF-α: tumor necrosis factor-alpha.
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    anti socs1 psh09 68  (Huabio Inc)
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    Engineered probiotic PG mitigated radiation-induced intestinal injury by regulating the <t>SOCS1/JAK2/STAT3</t> pathway. a Principal Component Analysis (PCA) revealed differences in gene expression levels among groups. b KEGG Enrichment BarPlot for IR vs. IR + PG displayed the number of differential genes in the pathway represented on the horizontal axis, pathway names on the vertical axis, and colors representing KEGG Level 1 classification. c KEGG-enriched bar graph displaying the top 20 KEGG pathways with the smallest P-values. d The results of the KEGG enrichment analysis werw presented as a scatter plot. (e) The heatmap illustrated the relative expression levels of JAK-STAT signaling pathway-related genes in the IR and IR + PG groups. f Western blot analysis demonstrated the protein expression levels of SOCS1, p-JAK2, JAK2, p-STAT3, and STAT3 across groups
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    socs1  (Cell Signaling Technology Inc)
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    Cell Signaling Technology Inc socs1
    Engineered probiotic PG mitigated radiation-induced intestinal injury by regulating the <t>SOCS1/JAK2/STAT3</t> pathway. a Principal Component Analysis (PCA) revealed differences in gene expression levels among groups. b KEGG Enrichment BarPlot for IR vs. IR + PG displayed the number of differential genes in the pathway represented on the horizontal axis, pathway names on the vertical axis, and colors representing KEGG Level 1 classification. c KEGG-enriched bar graph displaying the top 20 KEGG pathways with the smallest P-values. d The results of the KEGG enrichment analysis werw presented as a scatter plot. (e) The heatmap illustrated the relative expression levels of JAK-STAT signaling pathway-related genes in the IR and IR + PG groups. f Western blot analysis demonstrated the protein expression levels of SOCS1, p-JAK2, JAK2, p-STAT3, and STAT3 across groups
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    anti socs1  (ABclonal Biotechnology)
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    Engineered probiotic PG mitigated radiation-induced intestinal injury by regulating the <t>SOCS1/JAK2/STAT3</t> pathway. a Principal Component Analysis (PCA) revealed differences in gene expression levels among groups. b KEGG Enrichment BarPlot for IR vs. IR + PG displayed the number of differential genes in the pathway represented on the horizontal axis, pathway names on the vertical axis, and colors representing KEGG Level 1 classification. c KEGG-enriched bar graph displaying the top 20 KEGG pathways with the smallest P-values. d The results of the KEGG enrichment analysis werw presented as a scatter plot. (e) The heatmap illustrated the relative expression levels of JAK-STAT signaling pathway-related genes in the IR and IR + PG groups. f Western blot analysis demonstrated the protein expression levels of SOCS1, p-JAK2, JAK2, p-STAT3, and STAT3 across groups
    Anti Socs1, supplied by ABclonal 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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    anti socs1  (Boster Bio)
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    Boster Bio anti socs1
    Engineered probiotic PG mitigated radiation-induced intestinal injury by regulating the <t>SOCS1/JAK2/STAT3</t> pathway. a Principal Component Analysis (PCA) revealed differences in gene expression levels among groups. b KEGG Enrichment BarPlot for IR vs. IR + PG displayed the number of differential genes in the pathway represented on the horizontal axis, pathway names on the vertical axis, and colors representing KEGG Level 1 classification. c KEGG-enriched bar graph displaying the top 20 KEGG pathways with the smallest P-values. d The results of the KEGG enrichment analysis werw presented as a scatter plot. (e) The heatmap illustrated the relative expression levels of JAK-STAT signaling pathway-related genes in the IR and IR + PG groups. f Western blot analysis demonstrated the protein expression levels of SOCS1, p-JAK2, JAK2, p-STAT3, and STAT3 across groups
    Anti Socs1, supplied by Boster Bio, 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/product/anti+socs1/Anti-SOCS1+Antibody+Picoband/pmc12896625-44-0-6
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    anti slc38a1 12039 1 ap proteintech  (Proteintech)
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    Proteintech anti slc38a1 12039 1 ap proteintech
    Engineered probiotic PG mitigated radiation-induced intestinal injury by regulating the <t>SOCS1/JAK2/STAT3</t> pathway. a Principal Component Analysis (PCA) revealed differences in gene expression levels among groups. b KEGG Enrichment BarPlot for IR vs. IR + PG displayed the number of differential genes in the pathway represented on the horizontal axis, pathway names on the vertical axis, and colors representing KEGG Level 1 classification. c KEGG-enriched bar graph displaying the top 20 KEGG pathways with the smallest P-values. d The results of the KEGG enrichment analysis werw presented as a scatter plot. (e) The heatmap illustrated the relative expression levels of JAK-STAT signaling pathway-related genes in the IR and IR + PG groups. f Western blot analysis demonstrated the protein expression levels of SOCS1, p-JAK2, JAK2, p-STAT3, and STAT3 across groups
    Anti Slc38a1 12039 1 Ap Proteintech, supplied by Proteintech, 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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    Image Search Results


    Focal rTSMS significantly inhibits CCI-induced neuroinflammation and upregulates SOCS3 in the spinal cord in vivo . (A) Representative immunofluorescence images showing the inhibitory effects of focal rTSMS on CCI-induced activation of microglia and astrocytes in the dorsal horn ( n = 3). Dashed box indicates the region of interest in the dorsal horn of the spinal cord. Scale bars: 100 μm. (B) Representative image of western blotting. (C, D) Re-administration of rTSMS significantly inhibited the CCI-induced upregulation of Iba-1 and GFAP ( n = 5). (E–G) Focal rTSMS significantly inhibited CCI-induced upregulation of IL-1β, IL-6, and TNF-α in the spinal cord ( n = 5). (H, I) Focal rTSMS significantly inhibited the CCI-induced increase in the protein levels of p-p38 and p-STAT3 in the spinal cord ( n = 5). (J) Focal rTSMS significantly upregulated SOCS3 in the spinal cord ( n = 5). (K) Focal rTSMS could not upregulate SOCS1 in the spinal cord ( n = 5). Data are expressed as mean ± SD. # P < 0.05, ### P < 0.001, #### P < 0.0001, vs. Sham group; * P < 0.05, ** P < 0.01, *** P < 0.001, vs . CCI group (one‐way analysis of variance followed by Tukey’s multiple comparisons tests). CCI: Chronic constrictive injury; GFAP: glial fibrillary acidic protein; Iba-1: ionized calcium binding adaptor molecule-1; IL: interleukin; rTSMS: repetitive trans-spinal magnetic stimulation; SOCS: suppressor of cytokine signaling; STAT3: transducer and activator of transcription 3; TNF-α: tumor necrosis factor-alpha.

    Journal: Neural Regeneration Research

    Article Title: Trans-spinal magnetic stimulation upregulates microglial SOCS3 to attenuate neuroinflammation in chronic constriction injury–induced neuropathic pain

    doi: 10.4103/NRR.NRR-D-24-00912

    Figure Lengend Snippet: Focal rTSMS significantly inhibits CCI-induced neuroinflammation and upregulates SOCS3 in the spinal cord in vivo . (A) Representative immunofluorescence images showing the inhibitory effects of focal rTSMS on CCI-induced activation of microglia and astrocytes in the dorsal horn ( n = 3). Dashed box indicates the region of interest in the dorsal horn of the spinal cord. Scale bars: 100 μm. (B) Representative image of western blotting. (C, D) Re-administration of rTSMS significantly inhibited the CCI-induced upregulation of Iba-1 and GFAP ( n = 5). (E–G) Focal rTSMS significantly inhibited CCI-induced upregulation of IL-1β, IL-6, and TNF-α in the spinal cord ( n = 5). (H, I) Focal rTSMS significantly inhibited the CCI-induced increase in the protein levels of p-p38 and p-STAT3 in the spinal cord ( n = 5). (J) Focal rTSMS significantly upregulated SOCS3 in the spinal cord ( n = 5). (K) Focal rTSMS could not upregulate SOCS1 in the spinal cord ( n = 5). Data are expressed as mean ± SD. # P < 0.05, ### P < 0.001, #### P < 0.0001, vs. Sham group; * P < 0.05, ** P < 0.01, *** P < 0.001, vs . CCI group (one‐way analysis of variance followed by Tukey’s multiple comparisons tests). CCI: Chronic constrictive injury; GFAP: glial fibrillary acidic protein; Iba-1: ionized calcium binding adaptor molecule-1; IL: interleukin; rTSMS: repetitive trans-spinal magnetic stimulation; SOCS: suppressor of cytokine signaling; STAT3: transducer and activator of transcription 3; TNF-α: tumor necrosis factor-alpha.

    Article Snippet: The primary antibodies used included β-actin (rabbit, 1:5000; Abclonal, Wuhan, China, Cat# AC026, RRID: AB_2768234), SOCS3 (rabbit, 1:1000; Abclonal, Cat# A0694, RRID: AB_2757345), SOCS1 (rabbit, 1:1000; Abclonal, Cat# A7754, RRID: AB_2772339), CaMKKβ (rabbit; Cell Signaling Technology, Danvers, MA, USA, Cat# 16810, RRID: AB_2798771), phospho-CaMKKβ(Ser511) (rabbit, 1:500; Cell Signaling Technology, Cat# 12818, RRID: AB_2798034), phosphorylated AMPK (Thr172) (p-AMPK; rabbit, 1:1000; Cell Signaling Technology, Cat# 2535S, RRID: AB_331250), AMPK (rabbit, 1:2000; Abcam, Cambridge, UK, Cat# ab32047, RRID: AB_722764), glial fibrillary acidic protein (GFAP; rabbit, 1:1000; Cell Signaling Technology, Cat# 12389S, RRID:AB_2631098), ionized calcium binding adaptor molecule-1 (Iba-1; goat, 1:1000; Abcam, Cat# ab48004, RRID: AB_870576), matrix metalloproteinase 9 (MMP-9; rabbit,1:1000; Proteintech, Rosemont, IL, USA, Cat# 10375-2-AP, RRID: AB_2919732), phospho-signal transducer and activator of transcription 3 (rabbit, 1:1000; Abclonal, Cat# AP0070, RRID: AB_2771569), signal transducer and activator of transcription 3 (STAT3; rabbit, 1:1000; Abclonal, Cat# A1192, RRID: AB_2861642), phospho-p38 mitogen-activated protein kinase (p-p38; rabbit, 1:1000; Cell Signaling Technology; Cat# 4511, RRID: AB_2139682), p38 mitogen-activated protein kinase (p38; rabbit, 1:1000; Cell Signaling Technology, Cat# 4511, RRID: AB_11178801), TNF-α (1:1000; Abclonal, Cat# A20851), IL-1β (1:1000; Abclonal, Cat# A16288), and IL-6 (rabbit, 1:1000; Abcam, Cat# ab6672, RRID: AB_2127460).

    Techniques: In Vivo, Immunofluorescence, Activation Assay, Western Blot, Binding Assay

    Engineered probiotic PG mitigated radiation-induced intestinal injury by regulating the SOCS1/JAK2/STAT3 pathway. a Principal Component Analysis (PCA) revealed differences in gene expression levels among groups. b KEGG Enrichment BarPlot for IR vs. IR + PG displayed the number of differential genes in the pathway represented on the horizontal axis, pathway names on the vertical axis, and colors representing KEGG Level 1 classification. c KEGG-enriched bar graph displaying the top 20 KEGG pathways with the smallest P-values. d The results of the KEGG enrichment analysis werw presented as a scatter plot. (e) The heatmap illustrated the relative expression levels of JAK-STAT signaling pathway-related genes in the IR and IR + PG groups. f Western blot analysis demonstrated the protein expression levels of SOCS1, p-JAK2, JAK2, p-STAT3, and STAT3 across groups

    Journal: Bioresources and Bioprocessing

    Article Title: Propionate-engineered probiotics reduce radiation-induced intestinal damage

    doi: 10.1186/s40643-026-01020-9

    Figure Lengend Snippet: Engineered probiotic PG mitigated radiation-induced intestinal injury by regulating the SOCS1/JAK2/STAT3 pathway. a Principal Component Analysis (PCA) revealed differences in gene expression levels among groups. b KEGG Enrichment BarPlot for IR vs. IR + PG displayed the number of differential genes in the pathway represented on the horizontal axis, pathway names on the vertical axis, and colors representing KEGG Level 1 classification. c KEGG-enriched bar graph displaying the top 20 KEGG pathways with the smallest P-values. d The results of the KEGG enrichment analysis werw presented as a scatter plot. (e) The heatmap illustrated the relative expression levels of JAK-STAT signaling pathway-related genes in the IR and IR + PG groups. f Western blot analysis demonstrated the protein expression levels of SOCS1, p-JAK2, JAK2, p-STAT3, and STAT3 across groups

    Article Snippet: The primary antibodies included anti-SOCS1 (PSH09-68), JAK2 (SY0245), p-JAK2 (SY24-03), STAT3 (SY24-08), p-STAT3 (SZ43-01), and GAPDH (SA30-01), all purchased from HuaBio-Antibodies Co., Ltd (Hangzhou, China).

    Techniques: Gene Expression, Expressing, Western Blot