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akr1b10  (MedChemExpress)


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    Structured Review

    MedChemExpress akr1b10
    Reagents and antibodies used in the present study.
    Akr1b10, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 92/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/akr1b10/product/MedChemExpress
    Average 92 stars, based on 2 article reviews
    akr1b10 - by Bioz Stars, 2026-02
    92/100 stars

    Images

    1) Product Images from "AKR1B10 inhibits the proliferation and metastasis of hepatocellular carcinoma cells by regulating the PI3K/AKT pathway"

    Article Title: AKR1B10 inhibits the proliferation and metastasis of hepatocellular carcinoma cells by regulating the PI3K/AKT pathway

    Journal: Oncology Letters

    doi: 10.3892/ol.2023.14151

    Reagents and antibodies used in the present study.
    Figure Legend Snippet: Reagents and antibodies used in the present study.

    Techniques Used:

    AKR1B10 expression was screened out and found to be upregulated in hepatocellular carcinoma. (A-C) Flow chart of AKR1B10 filtering from the GSE146719 dataset (D-F) Amplification of AKR1B10 was common in the GDC-TCGA and ICGC provisional cohort. (G) Representative images of immunohistochemical staining for low/high expression of AKR1B10 in public tissue microarray datasets from The Human Protein Atlas database (upper image: magnification, ×100, scale bar, 200 µm; lower image: magnification, ×400; scale bar, 50 µm). (H-J) Prognostic significance of AKR1B10 in (H) GDC-TCGA-PANCAN, (I) GDC-TCGA-LIHC, and (J) ICGC-LIRI cohorts. AKR1B10, aldo-keto reductase family 1 member B10; GDC-TCGA, Genomic Data Commons-The Cancer Genome Atlas; ICGC, International Cancer Genome Consortium; PANCAN, Pan-Cancer Atlas; LIHC, liver hepatocellular carcinoma; LIRI, donor information of the liver cancer project; FPKM, Fragments Per Kilobase Million.
    Figure Legend Snippet: AKR1B10 expression was screened out and found to be upregulated in hepatocellular carcinoma. (A-C) Flow chart of AKR1B10 filtering from the GSE146719 dataset (D-F) Amplification of AKR1B10 was common in the GDC-TCGA and ICGC provisional cohort. (G) Representative images of immunohistochemical staining for low/high expression of AKR1B10 in public tissue microarray datasets from The Human Protein Atlas database (upper image: magnification, ×100, scale bar, 200 µm; lower image: magnification, ×400; scale bar, 50 µm). (H-J) Prognostic significance of AKR1B10 in (H) GDC-TCGA-PANCAN, (I) GDC-TCGA-LIHC, and (J) ICGC-LIRI cohorts. AKR1B10, aldo-keto reductase family 1 member B10; GDC-TCGA, Genomic Data Commons-The Cancer Genome Atlas; ICGC, International Cancer Genome Consortium; PANCAN, Pan-Cancer Atlas; LIHC, liver hepatocellular carcinoma; LIRI, donor information of the liver cancer project; FPKM, Fragments Per Kilobase Million.

    Techniques Used: Expressing, Amplification, Immunohistochemical staining, Staining, Microarray

    DepMap analysis of AKR1B10. (A and B) The Gene Effect CRISPR (DepMap Public 22Q4 + Score, Chronos) and (C and D) the expression of AKR1B10 in hepatocellular carcinoma cell lines with the DepMap dataset was validated. AKR1B10, aldo-keto reductase family 1 member B10.
    Figure Legend Snippet: DepMap analysis of AKR1B10. (A and B) The Gene Effect CRISPR (DepMap Public 22Q4 + Score, Chronos) and (C and D) the expression of AKR1B10 in hepatocellular carcinoma cell lines with the DepMap dataset was validated. AKR1B10, aldo-keto reductase family 1 member B10.

    Techniques Used: CRISPR, Expressing

    AKR1B10 promoted the proliferation, migration, and invasion in HCC cells. (A) AKR1B10 expression was knocked down in Huh7 cells and confirmed by western blotting. (B-F) AKR1B10 knockdown inhibits the proliferation, migration, and invasion of Huh7 cells. (G) AKR1B10 expression was overexpressed in Hep3B cells and confirmed by western blotting. (H-I) AKR1B10 overexpression promoted the proliferation, migration, and invasion of Hep3B cells. Cell proliferation was evaluated using a CCK-8 assay (B and H) and colony formation assays (C). Cell migration and invasion were investigated using Transwell assays (D, E, and I). **P<0.01 and ****P<0.0001. AKR1B10, aldo-keto reductase family 1 member B10; sh, short hairpin; oe, overexpression; NC, negative control; OD, optical density.
    Figure Legend Snippet: AKR1B10 promoted the proliferation, migration, and invasion in HCC cells. (A) AKR1B10 expression was knocked down in Huh7 cells and confirmed by western blotting. (B-F) AKR1B10 knockdown inhibits the proliferation, migration, and invasion of Huh7 cells. (G) AKR1B10 expression was overexpressed in Hep3B cells and confirmed by western blotting. (H-I) AKR1B10 overexpression promoted the proliferation, migration, and invasion of Hep3B cells. Cell proliferation was evaluated using a CCK-8 assay (B and H) and colony formation assays (C). Cell migration and invasion were investigated using Transwell assays (D, E, and I). **P<0.01 and ****P<0.0001. AKR1B10, aldo-keto reductase family 1 member B10; sh, short hairpin; oe, overexpression; NC, negative control; OD, optical density.

    Techniques Used: Migration, Expressing, Western Blot, Knockdown, Over Expression, CCK-8 Assay, Negative Control

    GDC-TCGA and DepMap analysis of the AKR1B10, CCND1, and EMT-related co-expressed genes. (A) Pearson correlation of AKR1B10 and CCND1 gene expression in the GDC-TCGA models. (B-E) Pearson correlation analysis of AKR1B10 and EMT-related gene expression in the GDC-TCGA models. (F) Pearson correlation analysis of AKR1B10 and CCND1 gene expression in the DepMap Public 22Q4 models. (G-J) Pearson correlation analysis of AKR1B10 and EMT-related gene expression in the DepMap Public 22Q4 models. AKR1B10, aldo-keto reductase family 1 member B10; EMT, epithelial-mesenchymal transition; GDC-TCGA, Genomic Data Commons-The Cancer Genome Atlas.
    Figure Legend Snippet: GDC-TCGA and DepMap analysis of the AKR1B10, CCND1, and EMT-related co-expressed genes. (A) Pearson correlation of AKR1B10 and CCND1 gene expression in the GDC-TCGA models. (B-E) Pearson correlation analysis of AKR1B10 and EMT-related gene expression in the GDC-TCGA models. (F) Pearson correlation analysis of AKR1B10 and CCND1 gene expression in the DepMap Public 22Q4 models. (G-J) Pearson correlation analysis of AKR1B10 and EMT-related gene expression in the DepMap Public 22Q4 models. AKR1B10, aldo-keto reductase family 1 member B10; EMT, epithelial-mesenchymal transition; GDC-TCGA, Genomic Data Commons-The Cancer Genome Atlas.

    Techniques Used: Gene Expression

    AKR1B10 promoted the expression of CCND1 and EMT-related genes and activate the PI3K/AKT pathway. (A) AKR1B10 knockdown inhibited the expression of CCND1 in Huh7 cells. (B) AKR1B10 knockdown disturbs cell cycle distribution in Huh7 cells. (C) AKR1B10 knockdown impairs the EMT of Huh7 cells. (D and E) Western blotting showed that the PI3K signal pathway was regulated by AKR1B10. AKR1B10-overexpressing Huh7 cells were incubated with 40 nM PI3K inhibitor GDC-0941 for 48 h, after which the expression of the PI3K signal pathway genes was measured using western blotting. *P<0.05 and **P<0.01. AKR1B10, aldo-keto reductase family 1 member B10; EMT, epithelial-mesenchymal transition; GDC-TCGA, Genomic Data Commons-The Cancer Genome Atlas; LIHC, liver hepatocellular carcinoma; TPM, transcripts per million; FPKM-UQ, the upper quartile Fragments Per Kilobase Million.
    Figure Legend Snippet: AKR1B10 promoted the expression of CCND1 and EMT-related genes and activate the PI3K/AKT pathway. (A) AKR1B10 knockdown inhibited the expression of CCND1 in Huh7 cells. (B) AKR1B10 knockdown disturbs cell cycle distribution in Huh7 cells. (C) AKR1B10 knockdown impairs the EMT of Huh7 cells. (D and E) Western blotting showed that the PI3K signal pathway was regulated by AKR1B10. AKR1B10-overexpressing Huh7 cells were incubated with 40 nM PI3K inhibitor GDC-0941 for 48 h, after which the expression of the PI3K signal pathway genes was measured using western blotting. *P<0.05 and **P<0.01. AKR1B10, aldo-keto reductase family 1 member B10; EMT, epithelial-mesenchymal transition; GDC-TCGA, Genomic Data Commons-The Cancer Genome Atlas; LIHC, liver hepatocellular carcinoma; TPM, transcripts per million; FPKM-UQ, the upper quartile Fragments Per Kilobase Million.

    Techniques Used: Expressing, Knockdown, Western Blot, Incubation



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    akr1b10  (MedChemExpress)
    92
    MedChemExpress akr1b10
    Reagents and antibodies used in the present study.
    Akr1b10, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/akr1b10/product/MedChemExpress
    Average 92 stars, based on 1 article reviews
    akr1b10 - by Bioz Stars, 2026-02
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    		  Buy from Supplier

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    Reagents and antibodies used in the present study.

    Journal: Oncology Letters

    Article Title: AKR1B10 inhibits the proliferation and metastasis of hepatocellular carcinoma cells by regulating the PI3K/AKT pathway

    doi: 10.3892/ol.2023.14151

    Figure Lengend Snippet: Reagents and antibodies used in the present study.

    Article Snippet: Meanwhile, although cells transfected with AKR1B10 were subsequently treated with GDC-0941 (100 nM; PI3K/AKT pathway antagonist; MedChemExpress) for 24 h, western blotting showed that the protein content of AKR1B10 failed to be significantly altered ( ).

    Techniques:

    AKR1B10 expression was screened out and found to be upregulated in hepatocellular carcinoma. (A-C) Flow chart of AKR1B10 filtering from the GSE146719 dataset (D-F) Amplification of AKR1B10 was common in the GDC-TCGA and ICGC provisional cohort. (G) Representative images of immunohistochemical staining for low/high expression of AKR1B10 in public tissue microarray datasets from The Human Protein Atlas database (upper image: magnification, ×100, scale bar, 200 µm; lower image: magnification, ×400; scale bar, 50 µm). (H-J) Prognostic significance of AKR1B10 in (H) GDC-TCGA-PANCAN, (I) GDC-TCGA-LIHC, and (J) ICGC-LIRI cohorts. AKR1B10, aldo-keto reductase family 1 member B10; GDC-TCGA, Genomic Data Commons-The Cancer Genome Atlas; ICGC, International Cancer Genome Consortium; PANCAN, Pan-Cancer Atlas; LIHC, liver hepatocellular carcinoma; LIRI, donor information of the liver cancer project; FPKM, Fragments Per Kilobase Million.

    Journal: Oncology Letters

    Article Title: AKR1B10 inhibits the proliferation and metastasis of hepatocellular carcinoma cells by regulating the PI3K/AKT pathway

    doi: 10.3892/ol.2023.14151

    Figure Lengend Snippet: AKR1B10 expression was screened out and found to be upregulated in hepatocellular carcinoma. (A-C) Flow chart of AKR1B10 filtering from the GSE146719 dataset (D-F) Amplification of AKR1B10 was common in the GDC-TCGA and ICGC provisional cohort. (G) Representative images of immunohistochemical staining for low/high expression of AKR1B10 in public tissue microarray datasets from The Human Protein Atlas database (upper image: magnification, ×100, scale bar, 200 µm; lower image: magnification, ×400; scale bar, 50 µm). (H-J) Prognostic significance of AKR1B10 in (H) GDC-TCGA-PANCAN, (I) GDC-TCGA-LIHC, and (J) ICGC-LIRI cohorts. AKR1B10, aldo-keto reductase family 1 member B10; GDC-TCGA, Genomic Data Commons-The Cancer Genome Atlas; ICGC, International Cancer Genome Consortium; PANCAN, Pan-Cancer Atlas; LIHC, liver hepatocellular carcinoma; LIRI, donor information of the liver cancer project; FPKM, Fragments Per Kilobase Million.

    Article Snippet: Meanwhile, although cells transfected with AKR1B10 were subsequently treated with GDC-0941 (100 nM; PI3K/AKT pathway antagonist; MedChemExpress) for 24 h, western blotting showed that the protein content of AKR1B10 failed to be significantly altered ( ).

    Techniques: Expressing, Amplification, Immunohistochemical staining, Staining, Microarray

    DepMap analysis of AKR1B10. (A and B) The Gene Effect CRISPR (DepMap Public 22Q4 + Score, Chronos) and (C and D) the expression of AKR1B10 in hepatocellular carcinoma cell lines with the DepMap dataset was validated. AKR1B10, aldo-keto reductase family 1 member B10.

    Journal: Oncology Letters

    Article Title: AKR1B10 inhibits the proliferation and metastasis of hepatocellular carcinoma cells by regulating the PI3K/AKT pathway

    doi: 10.3892/ol.2023.14151

    Figure Lengend Snippet: DepMap analysis of AKR1B10. (A and B) The Gene Effect CRISPR (DepMap Public 22Q4 + Score, Chronos) and (C and D) the expression of AKR1B10 in hepatocellular carcinoma cell lines with the DepMap dataset was validated. AKR1B10, aldo-keto reductase family 1 member B10.

    Article Snippet: Meanwhile, although cells transfected with AKR1B10 were subsequently treated with GDC-0941 (100 nM; PI3K/AKT pathway antagonist; MedChemExpress) for 24 h, western blotting showed that the protein content of AKR1B10 failed to be significantly altered ( ).

    Techniques: CRISPR, Expressing

    AKR1B10 promoted the proliferation, migration, and invasion in HCC cells. (A) AKR1B10 expression was knocked down in Huh7 cells and confirmed by western blotting. (B-F) AKR1B10 knockdown inhibits the proliferation, migration, and invasion of Huh7 cells. (G) AKR1B10 expression was overexpressed in Hep3B cells and confirmed by western blotting. (H-I) AKR1B10 overexpression promoted the proliferation, migration, and invasion of Hep3B cells. Cell proliferation was evaluated using a CCK-8 assay (B and H) and colony formation assays (C). Cell migration and invasion were investigated using Transwell assays (D, E, and I). **P<0.01 and ****P<0.0001. AKR1B10, aldo-keto reductase family 1 member B10; sh, short hairpin; oe, overexpression; NC, negative control; OD, optical density.

    Journal: Oncology Letters

    Article Title: AKR1B10 inhibits the proliferation and metastasis of hepatocellular carcinoma cells by regulating the PI3K/AKT pathway

    doi: 10.3892/ol.2023.14151

    Figure Lengend Snippet: AKR1B10 promoted the proliferation, migration, and invasion in HCC cells. (A) AKR1B10 expression was knocked down in Huh7 cells and confirmed by western blotting. (B-F) AKR1B10 knockdown inhibits the proliferation, migration, and invasion of Huh7 cells. (G) AKR1B10 expression was overexpressed in Hep3B cells and confirmed by western blotting. (H-I) AKR1B10 overexpression promoted the proliferation, migration, and invasion of Hep3B cells. Cell proliferation was evaluated using a CCK-8 assay (B and H) and colony formation assays (C). Cell migration and invasion were investigated using Transwell assays (D, E, and I). **P<0.01 and ****P<0.0001. AKR1B10, aldo-keto reductase family 1 member B10; sh, short hairpin; oe, overexpression; NC, negative control; OD, optical density.

    Article Snippet: Meanwhile, although cells transfected with AKR1B10 were subsequently treated with GDC-0941 (100 nM; PI3K/AKT pathway antagonist; MedChemExpress) for 24 h, western blotting showed that the protein content of AKR1B10 failed to be significantly altered ( ).

    Techniques: Migration, Expressing, Western Blot, Knockdown, Over Expression, CCK-8 Assay, Negative Control

    GDC-TCGA and DepMap analysis of the AKR1B10, CCND1, and EMT-related co-expressed genes. (A) Pearson correlation of AKR1B10 and CCND1 gene expression in the GDC-TCGA models. (B-E) Pearson correlation analysis of AKR1B10 and EMT-related gene expression in the GDC-TCGA models. (F) Pearson correlation analysis of AKR1B10 and CCND1 gene expression in the DepMap Public 22Q4 models. (G-J) Pearson correlation analysis of AKR1B10 and EMT-related gene expression in the DepMap Public 22Q4 models. AKR1B10, aldo-keto reductase family 1 member B10; EMT, epithelial-mesenchymal transition; GDC-TCGA, Genomic Data Commons-The Cancer Genome Atlas.

    Journal: Oncology Letters

    Article Title: AKR1B10 inhibits the proliferation and metastasis of hepatocellular carcinoma cells by regulating the PI3K/AKT pathway

    doi: 10.3892/ol.2023.14151

    Figure Lengend Snippet: GDC-TCGA and DepMap analysis of the AKR1B10, CCND1, and EMT-related co-expressed genes. (A) Pearson correlation of AKR1B10 and CCND1 gene expression in the GDC-TCGA models. (B-E) Pearson correlation analysis of AKR1B10 and EMT-related gene expression in the GDC-TCGA models. (F) Pearson correlation analysis of AKR1B10 and CCND1 gene expression in the DepMap Public 22Q4 models. (G-J) Pearson correlation analysis of AKR1B10 and EMT-related gene expression in the DepMap Public 22Q4 models. AKR1B10, aldo-keto reductase family 1 member B10; EMT, epithelial-mesenchymal transition; GDC-TCGA, Genomic Data Commons-The Cancer Genome Atlas.

    Article Snippet: Meanwhile, although cells transfected with AKR1B10 were subsequently treated with GDC-0941 (100 nM; PI3K/AKT pathway antagonist; MedChemExpress) for 24 h, western blotting showed that the protein content of AKR1B10 failed to be significantly altered ( ).

    Techniques: Gene Expression

    AKR1B10 promoted the expression of CCND1 and EMT-related genes and activate the PI3K/AKT pathway. (A) AKR1B10 knockdown inhibited the expression of CCND1 in Huh7 cells. (B) AKR1B10 knockdown disturbs cell cycle distribution in Huh7 cells. (C) AKR1B10 knockdown impairs the EMT of Huh7 cells. (D and E) Western blotting showed that the PI3K signal pathway was regulated by AKR1B10. AKR1B10-overexpressing Huh7 cells were incubated with 40 nM PI3K inhibitor GDC-0941 for 48 h, after which the expression of the PI3K signal pathway genes was measured using western blotting. *P<0.05 and **P<0.01. AKR1B10, aldo-keto reductase family 1 member B10; EMT, epithelial-mesenchymal transition; GDC-TCGA, Genomic Data Commons-The Cancer Genome Atlas; LIHC, liver hepatocellular carcinoma; TPM, transcripts per million; FPKM-UQ, the upper quartile Fragments Per Kilobase Million.

    Journal: Oncology Letters

    Article Title: AKR1B10 inhibits the proliferation and metastasis of hepatocellular carcinoma cells by regulating the PI3K/AKT pathway

    doi: 10.3892/ol.2023.14151

    Figure Lengend Snippet: AKR1B10 promoted the expression of CCND1 and EMT-related genes and activate the PI3K/AKT pathway. (A) AKR1B10 knockdown inhibited the expression of CCND1 in Huh7 cells. (B) AKR1B10 knockdown disturbs cell cycle distribution in Huh7 cells. (C) AKR1B10 knockdown impairs the EMT of Huh7 cells. (D and E) Western blotting showed that the PI3K signal pathway was regulated by AKR1B10. AKR1B10-overexpressing Huh7 cells were incubated with 40 nM PI3K inhibitor GDC-0941 for 48 h, after which the expression of the PI3K signal pathway genes was measured using western blotting. *P<0.05 and **P<0.01. AKR1B10, aldo-keto reductase family 1 member B10; EMT, epithelial-mesenchymal transition; GDC-TCGA, Genomic Data Commons-The Cancer Genome Atlas; LIHC, liver hepatocellular carcinoma; TPM, transcripts per million; FPKM-UQ, the upper quartile Fragments Per Kilobase Million.

    Article Snippet: Meanwhile, although cells transfected with AKR1B10 were subsequently treated with GDC-0941 (100 nM; PI3K/AKT pathway antagonist; MedChemExpress) for 24 h, western blotting showed that the protein content of AKR1B10 failed to be significantly altered ( ).

    Techniques: Expressing, Knockdown, Western Blot, Incubation