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anti collagen 1α1  (Novus Biologicals)


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    Structured Review

    Novus Biologicals anti collagen 1α1
    Anti Collagen 1α1, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 88 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti collagen 1α1/product/Novus Biologicals
    Average 94 stars, based on 88 article reviews
    anti collagen 1α1 - by Bioz Stars, 2026-02
    94/100 stars

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    Santa Cruz Biotechnology collagen type 1α1 chain
    Figure 2. A KD in combination with gemcitabine has no effect on liver lipid accumulation. (A) Hematoxylin and eosin and (B) Mason trichome staining images for liver isolated from female and male KPC mice treated with a CD or a KD. All images were digitally scanned at x20 original magnification. (C) Immunoblotting for fibronectin and <t>Col1A1</t> from liver homogenates from CG‑ and KG‑treated female and male KPC mice following 2 months of treatment, with β‑actin as the loading control. Representative images are shown. Each band represents an independent liver homogenate sample obtained from either female or male KPC mice treated with the CD or the KD. Bands were quantified and results are expressed as a proportion of the control. Values are presented as mean ± SEM. n=4‑5 animals/group/sex. KPC, LSL‑KrasLSL‑G12D/+Trp53R172H/+Pdx‑1‑Cre; Col1A1, collagen type <t>1α1</t> chain; CG, control plus gemcitabine group; ketogenic plus gemcitabine group; CD, control diet; KD, ketogenic diet.
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    Fig. 4. Inhibition of cGAS-STING signaling pathway alleviates TGF-β1-induced profibrotic gene expression in HSCs. Expression levels of cGAS and STING were measured using WB after transfection with si-NC, cGAS-siRNA or STING-siRNA in LX-2 cells (A–D). LX-2 cells were subjected to CCK-8 assays after treatment with various concentrations of TGF-β1 for 24 h (E). LX-2 cells were transfected with cGAS-siRNA and STING-siRNA, then treated with TGF-β1 (20 ng/mL) for 24 h. The levels of α-SMA mRNA expression and Col-1α1 protein expression were detected (F and G). mRNA expression levels of cGAS, STING, IRF3, TBK1, and in flammatory factors (e.g., IL-1β, IL-6, CXCL-1, and IFN-β) were measured in the control group (untreated LX-2 cells), the model group (activated LX-2 cells), the si- cGAS group, and the si-STING group (I and J). *: P < 0.05; **: P < 0.01; ***: P < 0.001 vs. control group.

    Journal: International immunopharmacology

    Article Title: Activation of cGAS-STING signaling pathway promotes liver fibrosis and hepatic sinusoidal microthrombosis.

    doi: 10.1016/j.intimp.2023.111132

    Figure Lengend Snippet: Fig. 4. Inhibition of cGAS-STING signaling pathway alleviates TGF-β1-induced profibrotic gene expression in HSCs. Expression levels of cGAS and STING were measured using WB after transfection with si-NC, cGAS-siRNA or STING-siRNA in LX-2 cells (A–D). LX-2 cells were subjected to CCK-8 assays after treatment with various concentrations of TGF-β1 for 24 h (E). LX-2 cells were transfected with cGAS-siRNA and STING-siRNA, then treated with TGF-β1 (20 ng/mL) for 24 h. The levels of α-SMA mRNA expression and Col-1α1 protein expression were detected (F and G). mRNA expression levels of cGAS, STING, IRF3, TBK1, and in flammatory factors (e.g., IL-1β, IL-6, CXCL-1, and IFN-β) were measured in the control group (untreated LX-2 cells), the model group (activated LX-2 cells), the si- cGAS group, and the si-STING group (I and J). *: P < 0.05; **: P < 0.01; ***: P < 0.001 vs. control group.

    Article Snippet: The primary antibodies were as follows: cGAS (1:1000, CST, USA), STING (1:1000, Abcam, USA), Phospho-STING (1:1000, Abcam, USA), Col-1α1 (1:1000, Proteintech, USA), β-actin (1:5000, Proteintech, USA) and GAPDH (1:5000, Proteintech, USA).

    Techniques: Inhibition, Gene Expression, Expressing, Transfection, CCK-8 Assay, Control

    Fig. 5. Overexpression of cGAS-STING signaling pathway exacerbates TGF-β1-mediated activation of HSCs. Expression levels of cGAS and STING were detected by WB after transfection with empty-vector , cGAS-overexpression plasmid or STING-overexpression plasmid (A-D). Transfected LX-2 cells were treated with TGF-β1 (20 ng/mL) for 24 h, then subjected to analysis of Col-1α1 and α-SMA expression levels via RT-qPCR and WB (E and F). mRNA expression levels of cGAS, STING, IRF3, TBK1, and inflammatory factors (IL-1β, IL-6, CXCL-1, and IFN-β) in the control group (untreated LX-2 cells), the model group (activated LX-2 cells), the si-cGAS and si-STING group, the cGAS-OE and STING-OE group (G and H). LX-2 cells were transfected with si-cGAS, si-STING, cGAS-OE or STING-OE, and then treated with TGF-β1. The protein expression of Phospho-STING was determined by Western blotting (I and J). *: P < 0.05; **: P < 0.01; ***: P < 0.001 vs. con trol group.

    Journal: International immunopharmacology

    Article Title: Activation of cGAS-STING signaling pathway promotes liver fibrosis and hepatic sinusoidal microthrombosis.

    doi: 10.1016/j.intimp.2023.111132

    Figure Lengend Snippet: Fig. 5. Overexpression of cGAS-STING signaling pathway exacerbates TGF-β1-mediated activation of HSCs. Expression levels of cGAS and STING were detected by WB after transfection with empty-vector , cGAS-overexpression plasmid or STING-overexpression plasmid (A-D). Transfected LX-2 cells were treated with TGF-β1 (20 ng/mL) for 24 h, then subjected to analysis of Col-1α1 and α-SMA expression levels via RT-qPCR and WB (E and F). mRNA expression levels of cGAS, STING, IRF3, TBK1, and inflammatory factors (IL-1β, IL-6, CXCL-1, and IFN-β) in the control group (untreated LX-2 cells), the model group (activated LX-2 cells), the si-cGAS and si-STING group, the cGAS-OE and STING-OE group (G and H). LX-2 cells were transfected with si-cGAS, si-STING, cGAS-OE or STING-OE, and then treated with TGF-β1. The protein expression of Phospho-STING was determined by Western blotting (I and J). *: P < 0.05; **: P < 0.01; ***: P < 0.001 vs. con trol group.

    Article Snippet: The primary antibodies were as follows: cGAS (1:1000, CST, USA), STING (1:1000, Abcam, USA), Phospho-STING (1:1000, Abcam, USA), Col-1α1 (1:1000, Proteintech, USA), β-actin (1:5000, Proteintech, USA) and GAPDH (1:5000, Proteintech, USA).

    Techniques: Over Expression, Activation Assay, Expressing, Transfection, Plasmid Preparation, Quantitative RT-PCR, Control, Western Blot

    Figure 2. A KD in combination with gemcitabine has no effect on liver lipid accumulation. (A) Hematoxylin and eosin and (B) Mason trichome staining images for liver isolated from female and male KPC mice treated with a CD or a KD. All images were digitally scanned at x20 original magnification. (C) Immunoblotting for fibronectin and Col1A1 from liver homogenates from CG‑ and KG‑treated female and male KPC mice following 2 months of treatment, with β‑actin as the loading control. Representative images are shown. Each band represents an independent liver homogenate sample obtained from either female or male KPC mice treated with the CD or the KD. Bands were quantified and results are expressed as a proportion of the control. Values are presented as mean ± SEM. n=4‑5 animals/group/sex. KPC, LSL‑KrasLSL‑G12D/+Trp53R172H/+Pdx‑1‑Cre; Col1A1, collagen type 1α1 chain; CG, control plus gemcitabine group; ketogenic plus gemcitabine group; CD, control diet; KD, ketogenic diet.

    Journal: Oncology letters

    Article Title: Hepatic safety profile of pancreatic cancer‑bearing mice fed a ketogenic diet in combination with gemcitabine.

    doi: 10.3892/ol.2023.14067

    Figure Lengend Snippet: Figure 2. A KD in combination with gemcitabine has no effect on liver lipid accumulation. (A) Hematoxylin and eosin and (B) Mason trichome staining images for liver isolated from female and male KPC mice treated with a CD or a KD. All images were digitally scanned at x20 original magnification. (C) Immunoblotting for fibronectin and Col1A1 from liver homogenates from CG‑ and KG‑treated female and male KPC mice following 2 months of treatment, with β‑actin as the loading control. Representative images are shown. Each band represents an independent liver homogenate sample obtained from either female or male KPC mice treated with the CD or the KD. Bands were quantified and results are expressed as a proportion of the control. Values are presented as mean ± SEM. n=4‑5 animals/group/sex. KPC, LSL‑KrasLSL‑G12D/+Trp53R172H/+Pdx‑1‑Cre; Col1A1, collagen type 1α1 chain; CG, control plus gemcitabine group; ketogenic plus gemcitabine group; CD, control diet; KD, ketogenic diet.

    Article Snippet: In addition, 3‐hydroxymethyl‐3‐methylglutaryl‐CoA synthase (HMGCS; cat. no. sc‐373681; RRID: AB_10947237), sterol regulatory element binding protein 1 (SREBP1; cat. no. sc‐13551; RRID: AB_628282), peroxisome prolifer‐ ator‐activated receptor α (PPARα; cat. no. sc‐398394; RRID: AB_2885073), fatty acid synthase (FAS; cat. no. sc‐74540; RRID: AB_1121387), phospho‐acetyl‐CoA carboxylase (p‐ACC; cat. no. sc‐271965; RRID: AB_10710517), fibronectin (cat. no. sc‐271098, RRID: AB_10608215), collagen type 1α1 chain (Col1A1; cat. no. sc‐59772; RRID: AB_1121787) and toll‐like receptor 4 (TLR4; cat. no. sc‐293072; RRID: AB_10611320) primary antibodies were purchased from Santa Cruz Biotechnology, Inc.

    Techniques: Staining, Isolation, Western Blot, Control