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Proteintech anti idi1
Anti Idi1, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+idi1/IDI1+Antibody/pmc12905572-61-14-21
Average 93 stars, based on 9 article reviews

anti idi1 - by Bioz Stars, 2026-09

93/100 stars

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Article Title: The SOX10-ACAT2-Cholesterol Synthesis Axis Is Required for Melanoma Proliferation
Article Snippet: The following primary antibodies were used: anti-HMGCR, anti-SOAT1 (Abcam), anti-Flag M2 (Sigma-Aldrich), anti-ACAT2, anti-HMGCS1, anti-IDI1, anti-FDPS, anti-ACAT1, anti-SOX10, anti-TAF15, and anti-β-actin (Proteintech).

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(A) Chemical structure of MgIG. (B) Flowchart illustrating the modeling process for the NIAAA model. (C) Representative results of H&E and Oil Red O staining from the livers of mice in Ctrl, A-Ctrl and MgIG groups (n = 5). (D) Alterations in NAS (NAFLD activity score) and Oil Red O quantification (a.v.: arbitrary value) (n = 5). (E) Ratios of liver weight to body weight (LW/BW) in mice (n = 5). (F) Alterations in serum biochemical parameters (ALT, AST and TG) in mice in three groups (n = 5). (G) Alterations in mRNA expression of lipid metabolism genes ( Srebp-1c , Srebp2 , Acc1 , and Scd1 ), systemic inflammation markers ( Tnf-α , Il-6, Il-6, and Il-16 ), and apoptosis-related genes ( Bax and Bcl2 ) in the mice liver. The data are presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Scale bar: 50 μm.

Journal: bioRxiv

Article Title: Magnesium isoglycyrrhizinate alleviates alcohol-associated liver disease through targeting HSD11B1

doi: 10.1101/2025.10.02.679991

Figure Lengend Snippet: (A) Chemical structure of MgIG. (B) Flowchart illustrating the modeling process for the NIAAA model. (C) Representative results of H&E and Oil Red O staining from the livers of mice in Ctrl, A-Ctrl and MgIG groups (n = 5). (D) Alterations in NAS (NAFLD activity score) and Oil Red O quantification (a.v.: arbitrary value) (n = 5). (E) Ratios of liver weight to body weight (LW/BW) in mice (n = 5). (F) Alterations in serum biochemical parameters (ALT, AST and TG) in mice in three groups (n = 5). (G) Alterations in mRNA expression of lipid metabolism genes ( Srebp-1c , Srebp2 , Acc1 , and Scd1 ), systemic inflammation markers ( Tnf-α , Il-6, Il-6, and Il-16 ), and apoptosis-related genes ( Bax and Bcl2 ) in the mice liver. The data are presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Scale bar: 50 μm.

Article Snippet: Antibodies against IDI1 (#11166-2-AP) and SREBP2 (#28212-1-AP) were obtained from Proteintech (Wuhan, China).

Techniques: Staining, Activity Assay, Expressing

(A, B) Co-IP was used to verify the direct binding between HSD11B1 and SREBP2 with or without MgIG treatment. (C, D) Alterations in protein levels of HSD11B1, p-SREBP2, n-SREBP2, and IDI1 in AML-12 cells induced by EtOH/PA, following knockdown or overexpression of Hsd11b1 , with and without MgIG treatment (n = 3). (E) Immunofluorescent staining was conducted to visualize the distribution and expression of SREBP2 (red) in EtoH/PA-induced AML-12 cells, with or without MgIG, following Hsd11b1 knockdown or overexpression. (F) Co-IP was used to verify the direct binding between HSD11B1 and IDI1. (G) Effects of Srebp2 on Idi1 transcriptional regulation were measured by luciferase assays in AML-12 and 293T cell lines. Idi1-wild-type (WT) or Idi1-mutant (Mut), plasmids with WT promoter cDNA clone of Idi1 or with mutant promoter cDNA clone plasmid; pRL-TK, an internal control reporter plasmid. (H, I) The expression levels of Hsd11b1 , Srebp2 , and Idi1 in normal liver were measured following the knockdown of Hsd11b1 , Srebp2 , and Idi1 , or the overexpression of Hsd11b1 and Idi1 , respectively (n = 4). (J, K) The expression levels of Hsd11b1 , Srebp2 , and Idi1 in ALD liver were measured following the knockdown of Hsd11b1 , Srebp2 , and Idi1 , or the overexpression of Hsd11b1 and Idi1 , respectively (n = 5). Data are expressed as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001. **** P < 0.0001. Scale bar: 10 μm.

Journal: bioRxiv

Article Title: Magnesium isoglycyrrhizinate alleviates alcohol-associated liver disease through targeting HSD11B1

doi: 10.1101/2025.10.02.679991

Figure Lengend Snippet: (A, B) Co-IP was used to verify the direct binding between HSD11B1 and SREBP2 with or without MgIG treatment. (C, D) Alterations in protein levels of HSD11B1, p-SREBP2, n-SREBP2, and IDI1 in AML-12 cells induced by EtOH/PA, following knockdown or overexpression of Hsd11b1 , with and without MgIG treatment (n = 3). (E) Immunofluorescent staining was conducted to visualize the distribution and expression of SREBP2 (red) in EtoH/PA-induced AML-12 cells, with or without MgIG, following Hsd11b1 knockdown or overexpression. (F) Co-IP was used to verify the direct binding between HSD11B1 and IDI1. (G) Effects of Srebp2 on Idi1 transcriptional regulation were measured by luciferase assays in AML-12 and 293T cell lines. Idi1-wild-type (WT) or Idi1-mutant (Mut), plasmids with WT promoter cDNA clone of Idi1 or with mutant promoter cDNA clone plasmid; pRL-TK, an internal control reporter plasmid. (H, I) The expression levels of Hsd11b1 , Srebp2 , and Idi1 in normal liver were measured following the knockdown of Hsd11b1 , Srebp2 , and Idi1 , or the overexpression of Hsd11b1 and Idi1 , respectively (n = 4). (J, K) The expression levels of Hsd11b1 , Srebp2 , and Idi1 in ALD liver were measured following the knockdown of Hsd11b1 , Srebp2 , and Idi1 , or the overexpression of Hsd11b1 and Idi1 , respectively (n = 5). Data are expressed as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001. **** P < 0.0001. Scale bar: 10 μm.

Article Snippet: Antibodies against IDI1 (#11166-2-AP) and SREBP2 (#28212-1-AP) were obtained from Proteintech (Wuhan, China).

Techniques: Co-Immunoprecipitation Assay, Binding Assay, Knockdown, Over Expression, Staining, Expressing, Luciferase, Mutagenesis, Plasmid Preparation, Control

(A-D) Representative liver H&E and Oil Red O staining results from ALD mice with Hsd11b1 , Srebp2 , or Idi1 knockdown or overexpression, with and/or without MgIG co-treatment. Changes in quantitative NAS (NAFLD activity score) and Oil Red staining (area %) were calculated and analyzed (n = 5). (E-F) Changes of serum ALT and TNF-α from ALD mice with Hsd11b1 , Srebp2 , or Idi1 knockdown or overexpression, with and/or without MgIG co-treatment (n = 5). (G) Alterations in protein levels of HSD11B1, p-SREBP2, n-SREBP 2, and Idi1 in ALD mice, following knockdown or overexpression of Hsd11b1 , with and without MgIG co-treatment (n = 3). Data are expressed as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Scale bar: 50 μm.

Journal: bioRxiv

Article Title: Magnesium isoglycyrrhizinate alleviates alcohol-associated liver disease through targeting HSD11B1

doi: 10.1101/2025.10.02.679991

Figure Lengend Snippet: (A-D) Representative liver H&E and Oil Red O staining results from ALD mice with Hsd11b1 , Srebp2 , or Idi1 knockdown or overexpression, with and/or without MgIG co-treatment. Changes in quantitative NAS (NAFLD activity score) and Oil Red staining (area %) were calculated and analyzed (n = 5). (E-F) Changes of serum ALT and TNF-α from ALD mice with Hsd11b1 , Srebp2 , or Idi1 knockdown or overexpression, with and/or without MgIG co-treatment (n = 5). (G) Alterations in protein levels of HSD11B1, p-SREBP2, n-SREBP 2, and Idi1 in ALD mice, following knockdown or overexpression of Hsd11b1 , with and without MgIG co-treatment (n = 3). Data are expressed as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Scale bar: 50 μm.

Article Snippet: Antibodies against IDI1 (#11166-2-AP) and SREBP2 (#28212-1-AP) were obtained from Proteintech (Wuhan, China).

Techniques: Staining, Knockdown, Over Expression, Activity Assay

(A) Quantitative PCR validation of RNA-seq results revealed changes in Idi1 gene expression in AML-12 cells treated with ethanol/PA, with or without 0.25 mg/ml MgIG co-treatment (n = 4). (B) Quantitative PCR results confirmed the knockdown efficiency of Idi1 genes by siRNA in AML-12 cells. The changes in AML-12 cell viability following Idi1 siRNA transfection (24 h) were also assessed (n = 4). (C) Quantitative PCR results confirmed the overexpression efficiency of Idi1 genes via plasmid transfection in AML-12 cells. Changes in AML-12 cell viability following Idi1 plasmid transfection (24 h) were also evaluated (n = 4). (D) Changes in cell viability and apoptosis ratios were assessed in ethanol/PA-treated AML-12 cells, with or without 0.25 mg/ml MgIG, following Idi1 knockdown/overexpression (n = 4). (E, F) Western blot results for TNF-α, IL-6, Bax, and Bcl-2 and cell supernatant results for TNF-α and IL-6 in AML-12 cells treated with ethanol/PA and ethanol/PA + MgIG, with or without Idi1 knockdown/overexpression (n = 3). (G, H) Nile Red staining area (%) with corresponding representative cell staining images. Data are expressed as mean ± SD. For Western blot quantification: * P < 0.05, ** P < 0.01, *** P < 0.001. Scale bar: 20 μm.

Journal: bioRxiv

Article Title: Magnesium isoglycyrrhizinate alleviates alcohol-associated liver disease through targeting HSD11B1

doi: 10.1101/2025.10.02.679991

Figure Lengend Snippet: (A) Quantitative PCR validation of RNA-seq results revealed changes in Idi1 gene expression in AML-12 cells treated with ethanol/PA, with or without 0.25 mg/ml MgIG co-treatment (n = 4). (B) Quantitative PCR results confirmed the knockdown efficiency of Idi1 genes by siRNA in AML-12 cells. The changes in AML-12 cell viability following Idi1 siRNA transfection (24 h) were also assessed (n = 4). (C) Quantitative PCR results confirmed the overexpression efficiency of Idi1 genes via plasmid transfection in AML-12 cells. Changes in AML-12 cell viability following Idi1 plasmid transfection (24 h) were also evaluated (n = 4). (D) Changes in cell viability and apoptosis ratios were assessed in ethanol/PA-treated AML-12 cells, with or without 0.25 mg/ml MgIG, following Idi1 knockdown/overexpression (n = 4). (E, F) Western blot results for TNF-α, IL-6, Bax, and Bcl-2 and cell supernatant results for TNF-α and IL-6 in AML-12 cells treated with ethanol/PA and ethanol/PA + MgIG, with or without Idi1 knockdown/overexpression (n = 3). (G, H) Nile Red staining area (%) with corresponding representative cell staining images. Data are expressed as mean ± SD. For Western blot quantification: * P < 0.05, ** P < 0.01, *** P < 0.001. Scale bar: 20 μm.

Article Snippet: Antibodies against IDI1 (#11166-2-AP) and SREBP2 (#28212-1-AP) were obtained from Proteintech (Wuhan, China).

Techniques: Real-time Polymerase Chain Reaction, Biomarker Discovery, RNA Sequencing, Gene Expression, Knockdown, Transfection, Over Expression, Plasmid Preparation, Western Blot, Staining

(A) Quantitative PCR validation of RNA-seq results revealed changes in Hsd11b1 gene expression in AML-12 cells treated with ethanol/PA, with or without 0.25 mg/ml MgIG co-treatment (n = 4). (B, C) Quantitative PCR confirmed the knockdown efficiency of Hsd11b1 (siRNA) and the overexpression efficiency of Idi1 (plasmid) in AML-12 cells, and cell viability changes were assessed 48 h after transfection (n = 4). (D) Nile Red staining area (%) with corresponding representative cell staining images (n=4). (E, F) Western blot results for TNF-α, IL-6, Bax, and Bcl-2 and cell supernatant results for TNF-α and IL-6 in AML-12 cells treated with ethanol/PA and ethanol/PA + MgIG, with or without Hsd11b1 knockdown/overexpression (n = 3). Data are expressed as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001. Scale bar: 20 μm.

Journal: bioRxiv

Article Title: Magnesium isoglycyrrhizinate alleviates alcohol-associated liver disease through targeting HSD11B1

doi: 10.1101/2025.10.02.679991

Figure Lengend Snippet: (A) Quantitative PCR validation of RNA-seq results revealed changes in Hsd11b1 gene expression in AML-12 cells treated with ethanol/PA, with or without 0.25 mg/ml MgIG co-treatment (n = 4). (B, C) Quantitative PCR confirmed the knockdown efficiency of Hsd11b1 (siRNA) and the overexpression efficiency of Idi1 (plasmid) in AML-12 cells, and cell viability changes were assessed 48 h after transfection (n = 4). (D) Nile Red staining area (%) with corresponding representative cell staining images (n=4). (E, F) Western blot results for TNF-α, IL-6, Bax, and Bcl-2 and cell supernatant results for TNF-α and IL-6 in AML-12 cells treated with ethanol/PA and ethanol/PA + MgIG, with or without Hsd11b1 knockdown/overexpression (n = 3). Data are expressed as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001. Scale bar: 20 μm.

Article Snippet: Antibodies against IDI1 (#11166-2-AP) and SREBP2 (#28212-1-AP) were obtained from Proteintech (Wuhan, China).

Techniques: Real-time Polymerase Chain Reaction, Biomarker Discovery, RNA Sequencing, Gene Expression, Knockdown, Over Expression, Plasmid Preparation, Transfection, Staining, Western Blot

Journal: bioRxiv

Article Title: Magnesium isoglycyrrhizinate alleviates alcohol-associated liver disease through targeting HSD11B1

doi: 10.1101/2025.10.02.679991

Article Snippet: Antibodies against IDI1 (#11166-2-AP) and SREBP2 (#28212-1-AP) were obtained from Proteintech (Wuhan, China).

Techniques: Co-Immunoprecipitation Assay, Binding Assay, Knockdown, Over Expression, Staining, Expressing, Luciferase, Mutagenesis, Plasmid Preparation, Control

Journal: bioRxiv

Article Title: Magnesium isoglycyrrhizinate alleviates alcohol-associated liver disease through targeting HSD11B1

doi: 10.1101/2025.10.02.679991

Article Snippet: Antibodies against IDI1 (#11166-2-AP) and SREBP2 (#28212-1-AP) were obtained from Proteintech (Wuhan, China).

Techniques: Staining, Knockdown, Over Expression, Activity Assay

Expression analyses of transcription or protein levels of selected genes. (A) Expression analyses of selected genes by qRT–PCR. The data represent the means ± SDs from six biological replicates with three technical replicates. (B–D) FCJ/RCJ upregulated ABCC3, IDI1, and APOA2 expression in the liver. FCJ and RCJ significantly upregulated hepatic ABCC3 (B) and IDI1 (C) expression, and RCJ significantly upregulated hepatic APOA2 (D) expression in T2DM rats. The data represent the means ± SDs from three biological replicates with three technical replicates. * p < 0.05, *** p < 0.001, **** p < 0.0001.

Journal: Frontiers in Nutrition

Article Title: Prevention of high-fat/high-sugar diet-induced type 2 diabetes mellitus-associated non-alcoholic fatty liver disease in rats with fermented and raw Rosa roxburghii Tratt (Cili) juice

doi: 10.3389/fnut.2025.1584551

Figure Lengend Snippet: Expression analyses of transcription or protein levels of selected genes. (A) Expression analyses of selected genes by qRT–PCR. The data represent the means ± SDs from six biological replicates with three technical replicates. (B–D) FCJ/RCJ upregulated ABCC3, IDI1, and APOA2 expression in the liver. FCJ and RCJ significantly upregulated hepatic ABCC3 (B) and IDI1 (C) expression, and RCJ significantly upregulated hepatic APOA2 (D) expression in T2DM rats. The data represent the means ± SDs from three biological replicates with three technical replicates. * p < 0.05, *** p < 0.001, **** p < 0.0001.

Article Snippet: The western blotting antibodies used included APOA2 (BM5624, BOSTER, China), IDI1 (A07892-1, BOSTER, China), ABCC3 (DF3874, Affinity, United States), β-tubulin (Solarbio, China), goat anti-rabbit (BS13278, Bioworld, United States), and goat anti-mouse (BS12478, Bioworld, United States) antibodies.

Techniques: Expressing, Quantitative RT-PCR

Upregulation of IDI1 in liver cancer. (A) IDI1 expression in normal liver cells and liver cancer cells, as measured by Western blotting. (B) Protein levels of IDI1 in adjacent tissues (N) and liver cancer tissues (C), as measured by Western blotting; the relative protein levels of IDI1 were analyzed statistically. (C–E) Protein levels of IDI1 in adjacent tissues (Normal) and liver cancer tissues (Cancer), as evaluated by IHC staining; the pie chart was generated and statistical analysis was performed. ****, P < 0.0001. Scale bar, 50 μm. (F) Analysis of the relationship between IDI1 expression and the survival of liver cancer patients using the Human Protein Atlas (HPA) database.

Journal: Heliyon

Article Title: IDI1 inhibits the cGAS-Sting signaling pathway in hepatocellular carcinoma

doi: 10.1016/j.heliyon.2024.e27205

Figure Lengend Snippet: Upregulation of IDI1 in liver cancer. (A) IDI1 expression in normal liver cells and liver cancer cells, as measured by Western blotting. (B) Protein levels of IDI1 in adjacent tissues (N) and liver cancer tissues (C), as measured by Western blotting; the relative protein levels of IDI1 were analyzed statistically. (C–E) Protein levels of IDI1 in adjacent tissues (Normal) and liver cancer tissues (Cancer), as evaluated by IHC staining; the pie chart was generated and statistical analysis was performed. ****, P < 0.0001. Scale bar, 50 μm. (F) Analysis of the relationship between IDI1 expression and the survival of liver cancer patients using the Human Protein Atlas (HPA) database.

Article Snippet: The tissue sections were then washed with PBS 1–2 times and incubated overnight at 4 °C with an anti-IDI1 antibody (Abcam, ab97448, 1:300) or anti-ki67 antibody (Proteintech, 27309-1-AP, 1:8000).

Techniques: Expressing, Western Blot, Immunohistochemistry, Generated

The expression of IDI1 has no significant impact on the growth or invasion of liver cancer cells but promotes the occurrence of liver cancer in mice. (A) Overexpression of exogenous IDI1 (Flag-IDI1) and knockdown of endogenous IDI1 in liver cancer cells were evaluated by Western blotting. (B) The impact of IDI1 overexpression on the in vitro growth of liver cancer cells was evaluated by a CCK-8 assay. (C–D) The impact of IDI1 knockdown on the invasion of liver cancer cells was evaluated by a Transwell assay. Statistical analysis was performed. (E) The effect of IDI1 knockdown on the in vitro growth of Huh7 cells was evaluated by a CCK-8 assay. (F–H) The impact of IDI1 overexpression in the liver on the occurrence of liver cancer in mice was evaluated using a model established via hydrodynamic injection, and the tumor area percentage and the proportion of Ki67-positive cells were quantified. **, P < 0.01.

Journal: Heliyon

Article Title: IDI1 inhibits the cGAS-Sting signaling pathway in hepatocellular carcinoma

doi: 10.1016/j.heliyon.2024.e27205

Figure Lengend Snippet: The expression of IDI1 has no significant impact on the growth or invasion of liver cancer cells but promotes the occurrence of liver cancer in mice. (A) Overexpression of exogenous IDI1 (Flag-IDI1) and knockdown of endogenous IDI1 in liver cancer cells were evaluated by Western blotting. (B) The impact of IDI1 overexpression on the in vitro growth of liver cancer cells was evaluated by a CCK-8 assay. (C–D) The impact of IDI1 knockdown on the invasion of liver cancer cells was evaluated by a Transwell assay. Statistical analysis was performed. (E) The effect of IDI1 knockdown on the in vitro growth of Huh7 cells was evaluated by a CCK-8 assay. (F–H) The impact of IDI1 overexpression in the liver on the occurrence of liver cancer in mice was evaluated using a model established via hydrodynamic injection, and the tumor area percentage and the proportion of Ki67-positive cells were quantified. **, P < 0.01.

Techniques: Expressing, Over Expression, Western Blot, In Vitro, CCK-8 Assay, Transwell Assay, Injection

IDI1 inhibits the cGAS-STING signaling pathway (A) The effect of IDI1 overexpression on the phosphorylation of TBK1 at S172 was evaluated by Western blotting. (B) The effect of IDI1 knockdown on the phosphorylation of TBK1 at S172 upon IR treatment was evaluated by Western blotting. (C–D) The effect of IDI1 knockdown on the phosphorylation of TBK1 (S172) and IRF3 (S386) was evaluated in Huh7 and QGY7701 cells upon stimulation with HT-DNA. (E) The effect of IDI1 overexpression on the expression of CCL5 and CXCL10 was evaluated by qPCR. ***, P < 0.01.

Journal: Heliyon

Article Title: IDI1 inhibits the cGAS-Sting signaling pathway in hepatocellular carcinoma

doi: 10.1016/j.heliyon.2024.e27205

Figure Lengend Snippet: IDI1 inhibits the cGAS-STING signaling pathway (A) The effect of IDI1 overexpression on the phosphorylation of TBK1 at S172 was evaluated by Western blotting. (B) The effect of IDI1 knockdown on the phosphorylation of TBK1 at S172 upon IR treatment was evaluated by Western blotting. (C–D) The effect of IDI1 knockdown on the phosphorylation of TBK1 (S172) and IRF3 (S386) was evaluated in Huh7 and QGY7701 cells upon stimulation with HT-DNA. (E) The effect of IDI1 overexpression on the expression of CCL5 and CXCL10 was evaluated by qPCR. ***, P < 0.01.

Techniques: Over Expression, Western Blot, Expressing

Interaction between cGAS and IDI1. (A) An immunoprecipitation assay was performed to detect the interaction between exogenously expressed cGAS (HA-cGAS) and IDI1 (Flag-IDI1). (B) A GST pulldown assay was conducted to evaluate the interaction between the GST-cGAS fusion protein and endogenously expressed IDI1 in liver cancer cells. (C) An immunoprecipitation assay was used to investigate the interaction between endogenously expressed cGAS and IDI1 in liver cancer cells. (D) Immunoprecipitation was performed to determine the effect of HT-DNA stimulation or IR (4 Gy) treatment on the interaction between cGAS and IDI1. Cells were transfected with HT-DNA (4 μg) or treated with IR (4 Gy), and after 4 h, the cell lysates were collected and subjected to immunoprecipitation using an anti-IDI1 antibody. (E) Schematic diagram of full-length (FL) cGAS and the cGAS truncations. (F) Immunoprecipitation was used to identify the region in the cGAS protein that is responsible for the interaction between the cGAS protein and IDI1. The N-terminus and C-terminus of cGAS were cloned and cotransfected with Flag-IDI1 into 293T cells. Forty-eight hours later, coimmunoprecipitation was performed.

Journal: Heliyon

Article Title: IDI1 inhibits the cGAS-Sting signaling pathway in hepatocellular carcinoma

doi: 10.1016/j.heliyon.2024.e27205

Figure Lengend Snippet: Interaction between cGAS and IDI1. (A) An immunoprecipitation assay was performed to detect the interaction between exogenously expressed cGAS (HA-cGAS) and IDI1 (Flag-IDI1). (B) A GST pulldown assay was conducted to evaluate the interaction between the GST-cGAS fusion protein and endogenously expressed IDI1 in liver cancer cells. (C) An immunoprecipitation assay was used to investigate the interaction between endogenously expressed cGAS and IDI1 in liver cancer cells. (D) Immunoprecipitation was performed to determine the effect of HT-DNA stimulation or IR (4 Gy) treatment on the interaction between cGAS and IDI1. Cells were transfected with HT-DNA (4 μg) or treated with IR (4 Gy), and after 4 h, the cell lysates were collected and subjected to immunoprecipitation using an anti-IDI1 antibody. (E) Schematic diagram of full-length (FL) cGAS and the cGAS truncations. (F) Immunoprecipitation was used to identify the region in the cGAS protein that is responsible for the interaction between the cGAS protein and IDI1. The N-terminus and C-terminus of cGAS were cloned and cotransfected with Flag-IDI1 into 293T cells. Forty-eight hours later, coimmunoprecipitation was performed.

Techniques: Immunoprecipitation, GST Pulldown Assay, Transfection, Clone Assay

IDI1 promotes the degradation of cGAS through the ubiquitination pathway. (A) Western blot analysis of the effect of exogenously overexpressed IDI1 (Flag-IDI1) on the level of the endogenous cGAS protein. (B) Prediction of the E3 ligase for cGAS using the UbiBrowser database, revealing TRIM41 as a potential candidate. (C) An immunoprecipitation assay was performed to detect the interaction between exogenously expressed TRIM41 (myc-TRIM41) and cGAS (Flag-cGAS). (D) A GST pull-down experiment was performed to evaluate the interaction between the GST-cGAS fusion protein and endogenously expressed TRIM41 in liver cancer cells. (E) An immunoprecipitation assay with an anti-cGAS antibody was performed to detect the interaction between endogenously expressed cGAS and TRIM41 in liver cancer cells. (F) An immunoprecipitation assay was performed to assess the effect of overexpressed IDI1 (HA-IDI1) on the interaction between exogenously expressed cGAS (Flag-cGAS) and TRIM41 (myc-TRIM41). (G) A ubiquitination assay was performed to investigate the impact of IDI1 expression on the ubiquitination of cGAS. (H) The protein levels of cGAS and IDI1 in HCC clinical samples (C) and adjacent tissues (N) were measured using Western blotting.

Journal: Heliyon

Article Title: IDI1 inhibits the cGAS-Sting signaling pathway in hepatocellular carcinoma

doi: 10.1016/j.heliyon.2024.e27205

Figure Lengend Snippet: IDI1 promotes the degradation of cGAS through the ubiquitination pathway. (A) Western blot analysis of the effect of exogenously overexpressed IDI1 (Flag-IDI1) on the level of the endogenous cGAS protein. (B) Prediction of the E3 ligase for cGAS using the UbiBrowser database, revealing TRIM41 as a potential candidate. (C) An immunoprecipitation assay was performed to detect the interaction between exogenously expressed TRIM41 (myc-TRIM41) and cGAS (Flag-cGAS). (D) A GST pull-down experiment was performed to evaluate the interaction between the GST-cGAS fusion protein and endogenously expressed TRIM41 in liver cancer cells. (E) An immunoprecipitation assay with an anti-cGAS antibody was performed to detect the interaction between endogenously expressed cGAS and TRIM41 in liver cancer cells. (F) An immunoprecipitation assay was performed to assess the effect of overexpressed IDI1 (HA-IDI1) on the interaction between exogenously expressed cGAS (Flag-cGAS) and TRIM41 (myc-TRIM41). (G) A ubiquitination assay was performed to investigate the impact of IDI1 expression on the ubiquitination of cGAS. (H) The protein levels of cGAS and IDI1 in HCC clinical samples (C) and adjacent tissues (N) were measured using Western blotting.

Techniques: Western Blot, Immunoprecipitation, Ubiquitin Assay, Expressing

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