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anti echdc2 (Bioss)

Name: anti echdc2
Brand: Bioss
Rating: 94 (3 reviews)

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Bioss anti echdc2

<t>ECHDC2</t> is downregulated in GC tissues. ( A-C ) Heatmaps depict the differential expression of various enoyl-CoA hydratase/isomerases in GC versus normal tissues in the TCGA-STAD, GSE27342, and GSE54129 datasets. ( D ) Relative expression levels of ECHDC2 in 20 GC tissues and their corresponding adjacent non-cancerous tissues. ( E ) Representative images of tissue microarrays. Scale bar, 50 μm. ( F ) Quantitative analysis of ECHDC2 protein expression. ( G ) Kaplan-Meier survival curve analysis explores the relationship between ECHDC2 expression levels in tissue microarrays and overall survival (OS) in patients with GC. ( H ) Analysis of the relationship between ECHDC2 expression and GC patient OS based on the Kaplan-Meier Plotter database. ( I–J ) Univariate and multivariate Cox regression analyses of GC patients in tissue microarrays. * P < 0.05, ** P < 0.01, *** P < 0.001

Anti Echdc2, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti echdc2/product/Bioss
Average 94 stars, based on 3 article reviews

anti echdc2 - by Bioz Stars, 2026-02

94/100 stars

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1) Product Images from "ECHDC2 inhibits the proliferation of gastric cancer cells by binding with NEDD4 to degrade MCCC2 and reduce aerobic glycolysis"

Article Title: ECHDC2 inhibits the proliferation of gastric cancer cells by binding with NEDD4 to degrade MCCC2 and reduce aerobic glycolysis

Journal: Molecular Medicine

doi: 10.1186/s10020-024-00832-9

ECHDC2 is downregulated in GC tissues. ( A-C ) Heatmaps depict the differential expression of various enoyl-CoA hydratase/isomerases in GC versus normal tissues in the TCGA-STAD, GSE27342, and GSE54129 datasets. ( D ) Relative expression levels of ECHDC2 in 20 GC tissues and their corresponding adjacent non-cancerous tissues. ( E ) Representative images of tissue microarrays. Scale bar, 50 μm. ( F ) Quantitative analysis of ECHDC2 protein expression. ( G ) Kaplan-Meier survival curve analysis explores the relationship between ECHDC2 expression levels in tissue microarrays and overall survival (OS) in patients with GC. ( H ) Analysis of the relationship between ECHDC2 expression and GC patient OS based on the Kaplan-Meier Plotter database. ( I–J ) Univariate and multivariate Cox regression analyses of GC patients in tissue microarrays. * P < 0.05, ** P < 0.01, *** P < 0.001

Figure Legend Snippet: ECHDC2 is downregulated in GC tissues. ( A-C ) Heatmaps depict the differential expression of various enoyl-CoA hydratase/isomerases in GC versus normal tissues in the TCGA-STAD, GSE27342, and GSE54129 datasets. ( D ) Relative expression levels of ECHDC2 in 20 GC tissues and their corresponding adjacent non-cancerous tissues. ( E ) Representative images of tissue microarrays. Scale bar, 50 μm. ( F ) Quantitative analysis of ECHDC2 protein expression. ( G ) Kaplan-Meier survival curve analysis explores the relationship between ECHDC2 expression levels in tissue microarrays and overall survival (OS) in patients with GC. ( H ) Analysis of the relationship between ECHDC2 expression and GC patient OS based on the Kaplan-Meier Plotter database. ( I–J ) Univariate and multivariate Cox regression analyses of GC patients in tissue microarrays. * P < 0.05, ** P < 0.01, *** P < 0.001

Techniques Used: Expressing

ECHDC2 inhibits GC cell proliferation in vivo and in vitro. ( A ) qRT-PCR was used to detect the relative mRNA expression levels of ECHDC2 in GES-1 and four GC cell lines. ( B ) Western blotting was performed to detect the protein expression of ECHDC2 in GES-1 and four GC cell lines. ( C ) Western blotting was used to detect transfection efficiency after overexpression of ECHDC2. ( D ) GC cells was detected by CCK-8 assay to cell viability. ( E–F ) Colony formation assay and EDU assay were performed to assess the cell proliferation capacity. Scale bar, 20 μm. ( G ) Typical images of subcutaneous xenograft tumor. ( H–I ) The volume and weight of subcutaneous xenograft tumors ( n = 5). ( J ) Intensity of IHC staining in different groups of subcutaneous xenograft tumor. Scale bar, 50 μm. * P < 0.05, ** P < 0.01, *** P < 0.001

Figure Legend Snippet: ECHDC2 inhibits GC cell proliferation in vivo and in vitro. ( A ) qRT-PCR was used to detect the relative mRNA expression levels of ECHDC2 in GES-1 and four GC cell lines. ( B ) Western blotting was performed to detect the protein expression of ECHDC2 in GES-1 and four GC cell lines. ( C ) Western blotting was used to detect transfection efficiency after overexpression of ECHDC2. ( D ) GC cells was detected by CCK-8 assay to cell viability. ( E–F ) Colony formation assay and EDU assay were performed to assess the cell proliferation capacity. Scale bar, 20 μm. ( G ) Typical images of subcutaneous xenograft tumor. ( H–I ) The volume and weight of subcutaneous xenograft tumors ( n = 5). ( J ) Intensity of IHC staining in different groups of subcutaneous xenograft tumor. Scale bar, 50 μm. * P < 0.05, ** P < 0.01, *** P < 0.001

Techniques Used: In Vivo, In Vitro, Quantitative RT-PCR, Expressing, Western Blot, Transfection, Over Expression, CCK-8 Assay, Colony Assay, EdU Assay, Immunohistochemistry

ECHDC2 inhibits aerobic glycolysis in GC cells. ( A ) GSEA results of the TCGA-STAD dataset show that ECHDC2 is associated with glycolysis. ( B–C ) qRT-PCR was used to detect the mRNA expression of GLUT1, PKM2, SDHA and G6PD after overexpression of ECHDC2. ( D ) Effect of ECHDC2 expression on proteins related to aerobic oxidation, aerobic glycolysis, and pentose phosphate pathway detected by western blotting. ( E–F ) Glucose uptake rate and lactic acid production rate of GC cells were measured after ECHDC2 overexpression. ( G ) IHC analysis of subcutaneous xenograft tumor was performed with anti-GLUT1 antibody and anti-PKM2 antibody. Scale bar, 50 μm. ns P > 0.05, ** P < 0.01, *** P < 0.001

Figure Legend Snippet: ECHDC2 inhibits aerobic glycolysis in GC cells. ( A ) GSEA results of the TCGA-STAD dataset show that ECHDC2 is associated with glycolysis. ( B–C ) qRT-PCR was used to detect the mRNA expression of GLUT1, PKM2, SDHA and G6PD after overexpression of ECHDC2. ( D ) Effect of ECHDC2 expression on proteins related to aerobic oxidation, aerobic glycolysis, and pentose phosphate pathway detected by western blotting. ( E–F ) Glucose uptake rate and lactic acid production rate of GC cells were measured after ECHDC2 overexpression. ( G ) IHC analysis of subcutaneous xenograft tumor was performed with anti-GLUT1 antibody and anti-PKM2 antibody. Scale bar, 50 μm. ns P > 0.05, ** P < 0.01, *** P < 0.001

Techniques Used: Quantitative RT-PCR, Expressing, Over Expression, Western Blot

ECHDC2 inhibits aerobic glycolysis and cell proliferation via the P38 MAPK pathway. ( A ) Western blotting was used to detect the effect of ECHDC2 on PI3K-AKT/mTOR pathway, Myc pathway, and P38-MAPK pathway. ( B-E ) Glucose uptake rate and lactic acid production rate of GC cells were measured after ECHDC2 overexpression and/or P38 MAPK overexpression. ( F ) The protein expression of GLUT1, PKM2, P38 MAPK were detected in GC cells transfected with vector, ECHDC2 or ECHDC2 plus P38 MAPK by western blotting. ( G-I ) CCK-8 assay, colony formation assay and EDU assay were performed to assess the cell viability and cell proliferation capacity following ECHDC2 overexpression and/or P38 MAPK overexpression. Scale bar, 20 μm. ** P < 0.01, *** P < 0.001

Figure Legend Snippet: ECHDC2 inhibits aerobic glycolysis and cell proliferation via the P38 MAPK pathway. ( A ) Western blotting was used to detect the effect of ECHDC2 on PI3K-AKT/mTOR pathway, Myc pathway, and P38-MAPK pathway. ( B-E ) Glucose uptake rate and lactic acid production rate of GC cells were measured after ECHDC2 overexpression and/or P38 MAPK overexpression. ( F ) The protein expression of GLUT1, PKM2, P38 MAPK were detected in GC cells transfected with vector, ECHDC2 or ECHDC2 plus P38 MAPK by western blotting. ( G-I ) CCK-8 assay, colony formation assay and EDU assay were performed to assess the cell viability and cell proliferation capacity following ECHDC2 overexpression and/or P38 MAPK overexpression. Scale bar, 20 μm. ** P < 0.01, *** P < 0.001

Techniques Used: Western Blot, Over Expression, Expressing, Transfection, Plasmid Preparation, CCK-8 Assay, Colony Assay, EdU Assay

ECHDC2 promotes the degradation of MCCC2 through the ubiquitin-proteasome pathway. ( A ) STRING predicts the interacting proteins of ECHDC2. ( B–C ) qRT-PCR and western blotting were employed to detect the mRNA and protein expression of ECHDC2 and MCCC2 after overexpression of ECHDC2. ( D ) IHC was performed to detect the protein expression of MCCC2 and P38 MAPK in subcutaneous xenograft tumor. Scale bar, 50 μm. ( E ) Western blotting was used to detect the effect of ECHDC2 overexpression on MCCC2 protein stability after treatment with CHX. ( F–G ) MCCC2 protein levels were detected in ECHDC2 overexpressing GC cells treated with MG132 or CQ. ( H ) The effect of ECHDC2 on the ubiquitination level of MCCC2 was detected in GC cells treated with/without MG132. ns P > 0.05, *** P < 0.001

Figure Legend Snippet: ECHDC2 promotes the degradation of MCCC2 through the ubiquitin-proteasome pathway. ( A ) STRING predicts the interacting proteins of ECHDC2. ( B–C ) qRT-PCR and western blotting were employed to detect the mRNA and protein expression of ECHDC2 and MCCC2 after overexpression of ECHDC2. ( D ) IHC was performed to detect the protein expression of MCCC2 and P38 MAPK in subcutaneous xenograft tumor. Scale bar, 50 μm. ( E ) Western blotting was used to detect the effect of ECHDC2 overexpression on MCCC2 protein stability after treatment with CHX. ( F–G ) MCCC2 protein levels were detected in ECHDC2 overexpressing GC cells treated with MG132 or CQ. ( H ) The effect of ECHDC2 on the ubiquitination level of MCCC2 was detected in GC cells treated with/without MG132. ns P > 0.05, *** P < 0.001

Techniques Used: Quantitative RT-PCR, Western Blot, Expressing, Over Expression

ECHDC2 ubiquitinates MCCC2 via NEDD4. ( A ) UbiBrowser was used to predict the E3 ubiquitin ligase of MCCC2. ( B ) Co-IP were used to validate the binding between ECHDC2, MCCC2 and NEDD4. ( C ) IF assays was used to detect co-localization of ECHDC2, MCCC2 and NEDD4 in GC cells, GC tissues and subcutaneous xenograft tumors. Scale bar, 10 μm. ( D ) Molecular docking models of ECHDC2 with NEDD4 and NEDD4 with MCCC2. Green: NEDD4; cyan: MCCC2; Orange: ECHDC2; Yellow: the docking region. ( E ) The effect of NEDD4 on ECHDC2-induced ubiquitination of MCCC2 was detected in GC cells

Figure Legend Snippet: ECHDC2 ubiquitinates MCCC2 via NEDD4. ( A ) UbiBrowser was used to predict the E3 ubiquitin ligase of MCCC2. ( B ) Co-IP were used to validate the binding between ECHDC2, MCCC2 and NEDD4. ( C ) IF assays was used to detect co-localization of ECHDC2, MCCC2 and NEDD4 in GC cells, GC tissues and subcutaneous xenograft tumors. Scale bar, 10 μm. ( D ) Molecular docking models of ECHDC2 with NEDD4 and NEDD4 with MCCC2. Green: NEDD4; cyan: MCCC2; Orange: ECHDC2; Yellow: the docking region. ( E ) The effect of NEDD4 on ECHDC2-induced ubiquitination of MCCC2 was detected in GC cells

Techniques Used: Co-Immunoprecipitation Assay, Binding Assay

ECHDC2 inhibits the proliferation of GC cells by binding with NEDD4 to degrade MCCC2 and reduce aerobic glycolysis. The schematic of the mechanism of action of ECHDC2 in GC cells. In GC tissues with ECHDC2 overexpression, ECHDC2 binds to NEDD4 to degrade MCCC2. This reduces the activation of P38 MAPK and its downstream targets GLUT1 and PKM2, thereby inhibiting aerobic glycolysis and proliferation in GC cells

Figure Legend Snippet: ECHDC2 inhibits the proliferation of GC cells by binding with NEDD4 to degrade MCCC2 and reduce aerobic glycolysis. The schematic of the mechanism of action of ECHDC2 in GC cells. In GC tissues with ECHDC2 overexpression, ECHDC2 binds to NEDD4 to degrade MCCC2. This reduces the activation of P38 MAPK and its downstream targets GLUT1 and PKM2, thereby inhibiting aerobic glycolysis and proliferation in GC cells

Techniques Used: Binding Assay, Over Expression, Activation Assay

Figure Legend Snippet: Correlation between ECHDC2 expression in GC tissue and clinicopathological Features of GC patients

Techniques Used: Expressing

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Journal: Molecular Medicine

Article Title: ECHDC2 inhibits the proliferation of gastric cancer cells by binding with NEDD4 to degrade MCCC2 and reduce aerobic glycolysis

doi: 10.1186/s10020-024-00832-9

Figure Lengend Snippet: ECHDC2 is downregulated in GC tissues. ( A-C ) Heatmaps depict the differential expression of various enoyl-CoA hydratase/isomerases in GC versus normal tissues in the TCGA-STAD, GSE27342, and GSE54129 datasets. ( D ) Relative expression levels of ECHDC2 in 20 GC tissues and their corresponding adjacent non-cancerous tissues. ( E ) Representative images of tissue microarrays. Scale bar, 50 μm. ( F ) Quantitative analysis of ECHDC2 protein expression. ( G ) Kaplan-Meier survival curve analysis explores the relationship between ECHDC2 expression levels in tissue microarrays and overall survival (OS) in patients with GC. ( H ) Analysis of the relationship between ECHDC2 expression and GC patient OS based on the Kaplan-Meier Plotter database. ( I–J ) Univariate and multivariate Cox regression analyses of GC patients in tissue microarrays. * P < 0.05, ** P < 0.01, *** P < 0.001

Article Snippet: The primary antibody used were as follows: anti-ECHDC2 (bs-13049R, Bioss, China); anti-GLUT1 (21829-1-AP, Proteintech, China); anti-PKM2 (15822-1-AP, Proteintech, China); anti-Ki67 (ab15580, Abcam, UK).

Techniques: Expressing

Journal: Molecular Medicine

Article Title: ECHDC2 inhibits the proliferation of gastric cancer cells by binding with NEDD4 to degrade MCCC2 and reduce aerobic glycolysis

doi: 10.1186/s10020-024-00832-9

Figure Lengend Snippet: ECHDC2 inhibits GC cell proliferation in vivo and in vitro. ( A ) qRT-PCR was used to detect the relative mRNA expression levels of ECHDC2 in GES-1 and four GC cell lines. ( B ) Western blotting was performed to detect the protein expression of ECHDC2 in GES-1 and four GC cell lines. ( C ) Western blotting was used to detect transfection efficiency after overexpression of ECHDC2. ( D ) GC cells was detected by CCK-8 assay to cell viability. ( E–F ) Colony formation assay and EDU assay were performed to assess the cell proliferation capacity. Scale bar, 20 μm. ( G ) Typical images of subcutaneous xenograft tumor. ( H–I ) The volume and weight of subcutaneous xenograft tumors ( n = 5). ( J ) Intensity of IHC staining in different groups of subcutaneous xenograft tumor. Scale bar, 50 μm. * P < 0.05, ** P < 0.01, *** P < 0.001

Techniques: In Vivo, In Vitro, Quantitative RT-PCR, Expressing, Western Blot, Transfection, Over Expression, CCK-8 Assay, Colony Assay, EdU Assay, Immunohistochemistry

Journal: Molecular Medicine

Article Title: ECHDC2 inhibits the proliferation of gastric cancer cells by binding with NEDD4 to degrade MCCC2 and reduce aerobic glycolysis

doi: 10.1186/s10020-024-00832-9

Figure Lengend Snippet: ECHDC2 inhibits aerobic glycolysis in GC cells. ( A ) GSEA results of the TCGA-STAD dataset show that ECHDC2 is associated with glycolysis. ( B–C ) qRT-PCR was used to detect the mRNA expression of GLUT1, PKM2, SDHA and G6PD after overexpression of ECHDC2. ( D ) Effect of ECHDC2 expression on proteins related to aerobic oxidation, aerobic glycolysis, and pentose phosphate pathway detected by western blotting. ( E–F ) Glucose uptake rate and lactic acid production rate of GC cells were measured after ECHDC2 overexpression. ( G ) IHC analysis of subcutaneous xenograft tumor was performed with anti-GLUT1 antibody and anti-PKM2 antibody. Scale bar, 50 μm. ns P > 0.05, ** P < 0.01, *** P < 0.001

Techniques: Quantitative RT-PCR, Expressing, Over Expression, Western Blot

Journal: Molecular Medicine

Article Title: ECHDC2 inhibits the proliferation of gastric cancer cells by binding with NEDD4 to degrade MCCC2 and reduce aerobic glycolysis

doi: 10.1186/s10020-024-00832-9

Figure Lengend Snippet: ECHDC2 inhibits aerobic glycolysis and cell proliferation via the P38 MAPK pathway. ( A ) Western blotting was used to detect the effect of ECHDC2 on PI3K-AKT/mTOR pathway, Myc pathway, and P38-MAPK pathway. ( B-E ) Glucose uptake rate and lactic acid production rate of GC cells were measured after ECHDC2 overexpression and/or P38 MAPK overexpression. ( F ) The protein expression of GLUT1, PKM2, P38 MAPK were detected in GC cells transfected with vector, ECHDC2 or ECHDC2 plus P38 MAPK by western blotting. ( G-I ) CCK-8 assay, colony formation assay and EDU assay were performed to assess the cell viability and cell proliferation capacity following ECHDC2 overexpression and/or P38 MAPK overexpression. Scale bar, 20 μm. ** P < 0.01, *** P < 0.001

Techniques: Western Blot, Over Expression, Expressing, Transfection, Plasmid Preparation, CCK-8 Assay, Colony Assay, EdU Assay

Journal: Molecular Medicine

Article Title: ECHDC2 inhibits the proliferation of gastric cancer cells by binding with NEDD4 to degrade MCCC2 and reduce aerobic glycolysis

doi: 10.1186/s10020-024-00832-9

Figure Lengend Snippet: ECHDC2 promotes the degradation of MCCC2 through the ubiquitin-proteasome pathway. ( A ) STRING predicts the interacting proteins of ECHDC2. ( B–C ) qRT-PCR and western blotting were employed to detect the mRNA and protein expression of ECHDC2 and MCCC2 after overexpression of ECHDC2. ( D ) IHC was performed to detect the protein expression of MCCC2 and P38 MAPK in subcutaneous xenograft tumor. Scale bar, 50 μm. ( E ) Western blotting was used to detect the effect of ECHDC2 overexpression on MCCC2 protein stability after treatment with CHX. ( F–G ) MCCC2 protein levels were detected in ECHDC2 overexpressing GC cells treated with MG132 or CQ. ( H ) The effect of ECHDC2 on the ubiquitination level of MCCC2 was detected in GC cells treated with/without MG132. ns P > 0.05, *** P < 0.001

Techniques: Quantitative RT-PCR, Western Blot, Expressing, Over Expression

Journal: Molecular Medicine

Article Title: ECHDC2 inhibits the proliferation of gastric cancer cells by binding with NEDD4 to degrade MCCC2 and reduce aerobic glycolysis

doi: 10.1186/s10020-024-00832-9

Figure Lengend Snippet: ECHDC2 ubiquitinates MCCC2 via NEDD4. ( A ) UbiBrowser was used to predict the E3 ubiquitin ligase of MCCC2. ( B ) Co-IP were used to validate the binding between ECHDC2, MCCC2 and NEDD4. ( C ) IF assays was used to detect co-localization of ECHDC2, MCCC2 and NEDD4 in GC cells, GC tissues and subcutaneous xenograft tumors. Scale bar, 10 μm. ( D ) Molecular docking models of ECHDC2 with NEDD4 and NEDD4 with MCCC2. Green: NEDD4; cyan: MCCC2; Orange: ECHDC2; Yellow: the docking region. ( E ) The effect of NEDD4 on ECHDC2-induced ubiquitination of MCCC2 was detected in GC cells

Techniques: Co-Immunoprecipitation Assay, Binding Assay

Journal: Molecular Medicine

Article Title: ECHDC2 inhibits the proliferation of gastric cancer cells by binding with NEDD4 to degrade MCCC2 and reduce aerobic glycolysis

doi: 10.1186/s10020-024-00832-9

Figure Lengend Snippet: ECHDC2 inhibits the proliferation of GC cells by binding with NEDD4 to degrade MCCC2 and reduce aerobic glycolysis. The schematic of the mechanism of action of ECHDC2 in GC cells. In GC tissues with ECHDC2 overexpression, ECHDC2 binds to NEDD4 to degrade MCCC2. This reduces the activation of P38 MAPK and its downstream targets GLUT1 and PKM2, thereby inhibiting aerobic glycolysis and proliferation in GC cells

Techniques: Binding Assay, Over Expression, Activation Assay

Journal: Molecular Medicine

Article Title: ECHDC2 inhibits the proliferation of gastric cancer cells by binding with NEDD4 to degrade MCCC2 and reduce aerobic glycolysis

doi: 10.1186/s10020-024-00832-9

Figure Lengend Snippet: Correlation between ECHDC2 expression in GC tissue and clinicopathological Features of GC patients

Techniques: Expressing

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