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Proteintech antibody against snd1

A The immunescore was found to be significantly different between the high and low PARG expression groups in TCGA breast cancer databse. B The correlation between the expression of PARG and the infiltration of immune cells in TCGA breast cancer databse. C Differences in immune cell infiltration between the high expression group and low expression group of PARG in breast cancer patients. D Representative IHC images of the relationship of PARG expression and CD8 + T cells infiltration in patients with breast cancer. Scale bar, 50μm. E GSEA anlysis of PARG high- and low-expressed differential genes. F Immunofluorescence analysis of MTDH and <t>SND1</t> expression and co-localization of MTDH (green) and SND1 (red) in infiltrating breast cancer. Scale bar, 10 μm. G , H Fresh breast cancer tissues were lysed and immunoprecipitated with an antibody specific for SND1 or MTDH. Subsequently, Western blot analysis was conducted using an antibody directed against MTDH or SND1. I , J To ascertain the content of the SND1-MTDH complex in cells transfected with shPARG or vector, CO-IP was employed using an anti-SND1 antibody, both in MCF-7 cells and MDA-MB-231 cells. K , L In order to determine the quantity of SND1-bound TAP1/2 mRNA present in cells transfected with shPARG or vector, a RIP assay was performed using an anti-SND1 antibody(RIP represents RNA-binding immunoprecipitation). M , N TAP1/2 expression was analyzed using a western blot with PARG knockdown in both MCF-7 cells and MDA-MB-231 cells. O The experimental process for co-culturing tumor cells and CD8 + T cells. Co-culture experiments of tumor cells and CD8 + T cells were conducted, including a PBS treatment group(PBS) and a CD8 + T cell treatment group(CTL). P Co-culture experiments of tumor cells and CD8 + T cells when PARG is knocked down in MCF-7 and MDA-MB-231 cells. Scale bar, 10 μm Statistical comparison of fluoresence intensity of the indicated groups. Data are presented as mean ± SD. Student’s t test was used to determine the significance of the observed differences. Q In the TCGA database, the relationship of CD8 + T cell infiltration and overall survival in ductal breast cancer, and the progression-free interval in LumB and Basal breast cancer. R Schematic mechanism: PARG inhibition destabilizes the MTDH-SND1 complex and releases TAP1/2 mRNA, thereby enhancing TAP1/2 expression and promoting MHC-I antigen presentation and CD8 + T cell recruitment. Statistical comparison of the number of cells in the indicated groups. Significance was determined by Student’s t test.* p < 0.05,** p < 0.01, *** p < 0.001.

Antibody Against Snd1, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 15 article reviews

antibody against snd1 - by Bioz Stars, 2026-03

93/100 stars

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1) Product Images from "PARG inhibition suppresses breast cancer progression and potentiates immunoresponse through MTDH degradation mediated by E3 ligase ITCH-dependent ubiquitination"

Article Title: PARG inhibition suppresses breast cancer progression and potentiates immunoresponse through MTDH degradation mediated by E3 ligase ITCH-dependent ubiquitination

Journal: NPJ Breast Cancer

doi: 10.1038/s41523-025-00847-3

Figure Legend Snippet: A The immunescore was found to be significantly different between the high and low PARG expression groups in TCGA breast cancer databse. B The correlation between the expression of PARG and the infiltration of immune cells in TCGA breast cancer databse. C Differences in immune cell infiltration between the high expression group and low expression group of PARG in breast cancer patients. D Representative IHC images of the relationship of PARG expression and CD8 + T cells infiltration in patients with breast cancer. Scale bar, 50μm. E GSEA anlysis of PARG high- and low-expressed differential genes. F Immunofluorescence analysis of MTDH and SND1 expression and co-localization of MTDH (green) and SND1 (red) in infiltrating breast cancer. Scale bar, 10 μm. G , H Fresh breast cancer tissues were lysed and immunoprecipitated with an antibody specific for SND1 or MTDH. Subsequently, Western blot analysis was conducted using an antibody directed against MTDH or SND1. I , J To ascertain the content of the SND1-MTDH complex in cells transfected with shPARG or vector, CO-IP was employed using an anti-SND1 antibody, both in MCF-7 cells and MDA-MB-231 cells. K , L In order to determine the quantity of SND1-bound TAP1/2 mRNA present in cells transfected with shPARG or vector, a RIP assay was performed using an anti-SND1 antibody(RIP represents RNA-binding immunoprecipitation). M , N TAP1/2 expression was analyzed using a western blot with PARG knockdown in both MCF-7 cells and MDA-MB-231 cells. O The experimental process for co-culturing tumor cells and CD8 + T cells. Co-culture experiments of tumor cells and CD8 + T cells were conducted, including a PBS treatment group(PBS) and a CD8 + T cell treatment group(CTL). P Co-culture experiments of tumor cells and CD8 + T cells when PARG is knocked down in MCF-7 and MDA-MB-231 cells. Scale bar, 10 μm Statistical comparison of fluoresence intensity of the indicated groups. Data are presented as mean ± SD. Student’s t test was used to determine the significance of the observed differences. Q In the TCGA database, the relationship of CD8 + T cell infiltration and overall survival in ductal breast cancer, and the progression-free interval in LumB and Basal breast cancer. R Schematic mechanism: PARG inhibition destabilizes the MTDH-SND1 complex and releases TAP1/2 mRNA, thereby enhancing TAP1/2 expression and promoting MHC-I antigen presentation and CD8 + T cell recruitment. Statistical comparison of the number of cells in the indicated groups. Significance was determined by Student’s t test.* p < 0.05,** p < 0.01, *** p < 0.001.

Techniques Used: Expressing, Immunofluorescence, Immunoprecipitation, Western Blot, Transfection, Plasmid Preparation, Co-Immunoprecipitation Assay, RNA Binding Assay, Knockdown, Co-Culture Assay, Comparison, Inhibition, Immunopeptidomics

A , B MTDH protein stability was measured in MCF-7 cells ( A ) and MDA-MB-231 cells ( B ) with or without COH34. After treatment with 20 mM CHX, cells were lysed at the indicated time points and analyzed by Western blot. Data are expressed as mean ± SD (CHX represents cycloheximide). C MTDH and TAP1/2 expression was tested by western blot after treated with HU or COH34 (HU represents hydroxyurea inducing cell cycle arrest). D Structural modeling using DMFold predicted several potential interaction interfaces between PARG and ITCH. E Cells were lysed and immunoprecipitated with an antibody specific for ITCH or MTDH in MCF-7 cells. Western blot analysis was performed using an antibody directed against MTDH or ITCH. F Cells were lysed and immunoprecipitated with an antibody specific for ITCH or MTDH in MDA-MB-231 cells. Western blot analysis was performed using an antibody directed against ITCH or MTDH. G IF analysis of MTDH and ITCH expression and co-localization of MTDH (green) and ITCH (red) in MCF-7 and MDA-MB-231 cells.Scale bar, 10 μm. H , I Western blot analysis was performed on cells that transfected with either an ITCH knockdown plasmid or an MTDH overexpression plasmid. J , K After MG-132 treating cells for 6 hours, CO-IP experiments were performed with MTDH specific antibody showing that PARG inhibition promoted MTDH ubiquitination. L , M RIP experiments were conducted to verify the effect of ITCH knockout or MTDH overexpression on the binding of SND1 to TAP1/2 mRNA. N , O CO-IP experiments were performed before and after ITCH knockdown using a plasmid in both MCF-7 and MDA-MB-231 cells. The detection of ubiquitination levels was conducted following a 6-hour treatment period with 10 µM MG-132. P , Q MCF-7 and MDA-MB-231 cells stably transfected with shPARG were treated with 10 µM MG-132 for 6 hours, and the expression of PARG and MTDH was detected by western blot (shP represents shPARG). The bar graph represents relative protein expression. The statistical significance of the observed differences was determined using Student’s t test. ** p < 0.01, *** p < 0.001.

Figure Legend Snippet: A , B MTDH protein stability was measured in MCF-7 cells ( A ) and MDA-MB-231 cells ( B ) with or without COH34. After treatment with 20 mM CHX, cells were lysed at the indicated time points and analyzed by Western blot. Data are expressed as mean ± SD (CHX represents cycloheximide). C MTDH and TAP1/2 expression was tested by western blot after treated with HU or COH34 (HU represents hydroxyurea inducing cell cycle arrest). D Structural modeling using DMFold predicted several potential interaction interfaces between PARG and ITCH. E Cells were lysed and immunoprecipitated with an antibody specific for ITCH or MTDH in MCF-7 cells. Western blot analysis was performed using an antibody directed against MTDH or ITCH. F Cells were lysed and immunoprecipitated with an antibody specific for ITCH or MTDH in MDA-MB-231 cells. Western blot analysis was performed using an antibody directed against ITCH or MTDH. G IF analysis of MTDH and ITCH expression and co-localization of MTDH (green) and ITCH (red) in MCF-7 and MDA-MB-231 cells.Scale bar, 10 μm. H , I Western blot analysis was performed on cells that transfected with either an ITCH knockdown plasmid or an MTDH overexpression plasmid. J , K After MG-132 treating cells for 6 hours, CO-IP experiments were performed with MTDH specific antibody showing that PARG inhibition promoted MTDH ubiquitination. L , M RIP experiments were conducted to verify the effect of ITCH knockout or MTDH overexpression on the binding of SND1 to TAP1/2 mRNA. N , O CO-IP experiments were performed before and after ITCH knockdown using a plasmid in both MCF-7 and MDA-MB-231 cells. The detection of ubiquitination levels was conducted following a 6-hour treatment period with 10 µM MG-132. P , Q MCF-7 and MDA-MB-231 cells stably transfected with shPARG were treated with 10 µM MG-132 for 6 hours, and the expression of PARG and MTDH was detected by western blot (shP represents shPARG). The bar graph represents relative protein expression. The statistical significance of the observed differences was determined using Student’s t test. ** p < 0.01, *** p < 0.001.

Techniques Used: Western Blot, Expressing, Immunoprecipitation, Transfection, Knockdown, Plasmid Preparation, Over Expression, Co-Immunoprecipitation Assay, Inhibition, Ubiquitin Proteomics, Knock-Out, Binding Assay, Stable Transfection

There is a two-axis regulatory network. The first axis is nuclear PARG inhibition, which impairs DNA repair via PAR chain accumulation and cell cycle disruption. Secondly, cytoplasmic PARG inactivation promotes ITCH PARylation, inducing ITCH autoubiquitination and subsequently activating its E3 ligase activity. This ultimately triggers the proteasomal degradation of MTDH, destabilizing the MTDH-SND1 complex and then upregulating TAP1/2 expression. This enhances MHC-I antigen presentation and CD8 + T cell-mediated tumor clearance.

Figure Legend Snippet: There is a two-axis regulatory network. The first axis is nuclear PARG inhibition, which impairs DNA repair via PAR chain accumulation and cell cycle disruption. Secondly, cytoplasmic PARG inactivation promotes ITCH PARylation, inducing ITCH autoubiquitination and subsequently activating its E3 ligase activity. This ultimately triggers the proteasomal degradation of MTDH, destabilizing the MTDH-SND1 complex and then upregulating TAP1/2 expression. This enhances MHC-I antigen presentation and CD8 + T cell-mediated tumor clearance.

Techniques Used: Inhibition, Disruption, Activity Assay, Expressing, Immunopeptidomics

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Journal: NPJ Breast Cancer

Article Title: PARG inhibition suppresses breast cancer progression and potentiates immunoresponse through MTDH degradation mediated by E3 ligase ITCH-dependent ubiquitination

doi: 10.1038/s41523-025-00847-3

Figure Lengend Snippet: A The immunescore was found to be significantly different between the high and low PARG expression groups in TCGA breast cancer databse. B The correlation between the expression of PARG and the infiltration of immune cells in TCGA breast cancer databse. C Differences in immune cell infiltration between the high expression group and low expression group of PARG in breast cancer patients. D Representative IHC images of the relationship of PARG expression and CD8 + T cells infiltration in patients with breast cancer. Scale bar, 50μm. E GSEA anlysis of PARG high- and low-expressed differential genes. F Immunofluorescence analysis of MTDH and SND1 expression and co-localization of MTDH (green) and SND1 (red) in infiltrating breast cancer. Scale bar, 10 μm. G , H Fresh breast cancer tissues were lysed and immunoprecipitated with an antibody specific for SND1 or MTDH. Subsequently, Western blot analysis was conducted using an antibody directed against MTDH or SND1. I , J To ascertain the content of the SND1-MTDH complex in cells transfected with shPARG or vector, CO-IP was employed using an anti-SND1 antibody, both in MCF-7 cells and MDA-MB-231 cells. K , L In order to determine the quantity of SND1-bound TAP1/2 mRNA present in cells transfected with shPARG or vector, a RIP assay was performed using an anti-SND1 antibody(RIP represents RNA-binding immunoprecipitation). M , N TAP1/2 expression was analyzed using a western blot with PARG knockdown in both MCF-7 cells and MDA-MB-231 cells. O The experimental process for co-culturing tumor cells and CD8 + T cells. Co-culture experiments of tumor cells and CD8 + T cells were conducted, including a PBS treatment group(PBS) and a CD8 + T cell treatment group(CTL). P Co-culture experiments of tumor cells and CD8 + T cells when PARG is knocked down in MCF-7 and MDA-MB-231 cells. Scale bar, 10 μm Statistical comparison of fluoresence intensity of the indicated groups. Data are presented as mean ± SD. Student’s t test was used to determine the significance of the observed differences. Q In the TCGA database, the relationship of CD8 + T cell infiltration and overall survival in ductal breast cancer, and the progression-free interval in LumB and Basal breast cancer. R Schematic mechanism: PARG inhibition destabilizes the MTDH-SND1 complex and releases TAP1/2 mRNA, thereby enhancing TAP1/2 expression and promoting MHC-I antigen presentation and CD8 + T cell recruitment. Statistical comparison of the number of cells in the indicated groups. Significance was determined by Student’s t test.* p < 0.05,** p < 0.01, *** p < 0.001.

Article Snippet: An antibody against SND1 (Proteintech, catalog number 60265-1-Ig) or an IgG antibody (provided in the kit) was added to each tube at a concentration of 5 μg and incubated overnight at 4 °C.

Techniques: Expressing, Immunofluorescence, Immunoprecipitation, Western Blot, Transfection, Plasmid Preparation, Co-Immunoprecipitation Assay, RNA Binding Assay, Knockdown, Co-Culture Assay, Comparison, Inhibition, Immunopeptidomics

Journal: NPJ Breast Cancer

Article Title: PARG inhibition suppresses breast cancer progression and potentiates immunoresponse through MTDH degradation mediated by E3 ligase ITCH-dependent ubiquitination

doi: 10.1038/s41523-025-00847-3

Figure Lengend Snippet: A , B MTDH protein stability was measured in MCF-7 cells ( A ) and MDA-MB-231 cells ( B ) with or without COH34. After treatment with 20 mM CHX, cells were lysed at the indicated time points and analyzed by Western blot. Data are expressed as mean ± SD (CHX represents cycloheximide). C MTDH and TAP1/2 expression was tested by western blot after treated with HU or COH34 (HU represents hydroxyurea inducing cell cycle arrest). D Structural modeling using DMFold predicted several potential interaction interfaces between PARG and ITCH. E Cells were lysed and immunoprecipitated with an antibody specific for ITCH or MTDH in MCF-7 cells. Western blot analysis was performed using an antibody directed against MTDH or ITCH. F Cells were lysed and immunoprecipitated with an antibody specific for ITCH or MTDH in MDA-MB-231 cells. Western blot analysis was performed using an antibody directed against ITCH or MTDH. G IF analysis of MTDH and ITCH expression and co-localization of MTDH (green) and ITCH (red) in MCF-7 and MDA-MB-231 cells.Scale bar, 10 μm. H , I Western blot analysis was performed on cells that transfected with either an ITCH knockdown plasmid or an MTDH overexpression plasmid. J , K After MG-132 treating cells for 6 hours, CO-IP experiments were performed with MTDH specific antibody showing that PARG inhibition promoted MTDH ubiquitination. L , M RIP experiments were conducted to verify the effect of ITCH knockout or MTDH overexpression on the binding of SND1 to TAP1/2 mRNA. N , O CO-IP experiments were performed before and after ITCH knockdown using a plasmid in both MCF-7 and MDA-MB-231 cells. The detection of ubiquitination levels was conducted following a 6-hour treatment period with 10 µM MG-132. P , Q MCF-7 and MDA-MB-231 cells stably transfected with shPARG were treated with 10 µM MG-132 for 6 hours, and the expression of PARG and MTDH was detected by western blot (shP represents shPARG). The bar graph represents relative protein expression. The statistical significance of the observed differences was determined using Student’s t test. ** p < 0.01, *** p < 0.001.

Techniques: Western Blot, Expressing, Immunoprecipitation, Transfection, Knockdown, Plasmid Preparation, Over Expression, Co-Immunoprecipitation Assay, Inhibition, Ubiquitin Proteomics, Knock-Out, Binding Assay, Stable Transfection

Journal: NPJ Breast Cancer

Article Title: PARG inhibition suppresses breast cancer progression and potentiates immunoresponse through MTDH degradation mediated by E3 ligase ITCH-dependent ubiquitination

doi: 10.1038/s41523-025-00847-3

Figure Lengend Snippet: There is a two-axis regulatory network. The first axis is nuclear PARG inhibition, which impairs DNA repair via PAR chain accumulation and cell cycle disruption. Secondly, cytoplasmic PARG inactivation promotes ITCH PARylation, inducing ITCH autoubiquitination and subsequently activating its E3 ligase activity. This ultimately triggers the proteasomal degradation of MTDH, destabilizing the MTDH-SND1 complex and then upregulating TAP1/2 expression. This enhances MHC-I antigen presentation and CD8 + T cell-mediated tumor clearance.

Techniques: Inhibition, Disruption, Activity Assay, Expressing, Immunopeptidomics

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