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Infection with Hepatitis C Virus Depends on TACSTD2, a Regulator of Claudin-1 and Occludin Highly Downregulated in Hepatocellular Carcinoma

ABSTRACT: Infection with Hepatitis C Virus Depends on TACSTD2, a Regulator of Claudin-1 and Occludin Highly Downregulated in Hepatocellular Carcinoma

PROVIDER: PRJNA313404 | ENA |

REPOSITORIES: ENA

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Infection with Hepatitis C Virus Depends on TACSTD2, a Regulator of Claudin-1 and Occludin Highly Downregulated in Hepatocellular Carcinoma [patient]

Project description:Our study identifies TACSTD2 as a novel regulator of two major HCV entry factors, CLDN1 and OCLN, which is strongly downregulated in malignant hepatocytes. These results provide new insights into the complex process of HCV entry into hepatocytes and may assist in the development of more efficient cellular systems for HCV propagation in vitro.

2018-03-01 | GSE69715 | GEO

Infection with Hepatitis C Virus Depends on TACSTD2, a Regulator of Claudin-1 and Occludin Highly Downregulated in Hepatocellular Carcinoma [cell line]

2018-03-01 | GSE78736 | GEO

Infection with hepatitis C virus depends on TACSTD2, a regulator of claudin-1 and occludin highly downregulated in hepatocellular carcinoma.

Project description: Not available

| S-EPMC5882150 | biostudies-literature

Infection with Hepatitis C Virus Depends on TACSTD2, a Regulator of Claudin-1 and Occludin Highly Downregulated in Hepatocellular Carcinoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-03-01 | GSE78737 | GEO

Claudin-7 in keratinocytes is downregulated by the inhibition of HMG-CoA reductase and is highly expressed in the stratum granulosum of the psoriatic epidermis

Project description:Background: Cholesterol is de novo synthesized in the upper epidermis and plays an important role in maintaining the normality of skin. Studying the impact of the inhibition of cholesterol de novo synthesis in the epidermis may help understand how skin homeostasis is regulated. Objective: In this study, we created a gene expression profile to investigate the effect of hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors on epidermal homeostasis. Methods: A microarray analysis was performed using normal keratinocytes with or without HMG-CoA reductase inhibitor (pitavastatin) treatment. Real-time PCR confirmed the reproducibility of genes with altered expression in keratinocytes treated with HMG-CoA reductase inhibitors. Among these genes, we focused on reduced expression of claudin 7 histologically confirmed by immunohistochemical staining, in situ hybridization, and immunoelectron microscopy. Results: Claudin-7 was highly expressed in the stratum granulosum of psoriatic lesions but was not expressed in the normal epidermis. Immunoelectron microscopy revealed that claudin-7 was localized in the keratohyalin granules of psoriatic lesions. Conclusion: These results indicate that claudin-7 expression was regulated by HMG-CoA reductase in the epidermis and might play a pathogenic role in the keratohyalin granules found in the epidermal granular layer of psoriasis.

2021-07-20 | GSE180418 | GEO

Highly metastatic claudin-low mammary cancers can originate from luminal epithelial cells

Project description:Claudin-low breast cancer represents an aggressive molecular subtype that is comprised of mostly triple-negative mammary tumor cells that possess stem cell-like and mesenchymal features. Little is known about the cellular origin and oncogenic drivers that promote claudin-low breast cancer. In this study, we show that persistent oncogenic RAS signaling causes highly metastatic triple-negative mammary tumors in mice. More importantly, the activation of endogenous mutant KRAS and expression of exogenous KRAS specifically in luminal epithelial cells in a continuous and differentiation stage-independent manner induces preneoplastic lesions that evolve into basal-like and claudin-low mammary cancers. Further investigations demonstrate that the continuous signaling of oncogenic RAS as well as regulators of EMT play a crucial role in the cellular plasticity and maintenance of the mesenchymal and stem cell characteristics of claudin-low mammary cancer cells.

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Gene expression profiling of hepatitis B- and hepatitis C-related hepatocellular carcinoma using graphical Gaussian modeling

Project description:Gene expression profiling of hepatocellular carcinoma (HCC) and background liver has been studied extensively; however, the relationship between the gene expression profiles of different lesions has not been assessed. We examined the expression profiles of 34 HCC specimens (17 hepatitis B virus [HBV]-related and 17 hepatitis C virus [HCV]-related) and 71 non-tumor liver specimens (36 chronic hepatitis B [CH-B] and 35 chronic hepatitis C [CH-C]) using an in-house cDNA microarray consisting of liver-predominant genes. Graphical Gaussian modeling (GGM) was applied to elucidate the interactions of gene clusters among the HCC and non-tumor lesions. Gene expression profiling of HCC and non-tumor lesions revealed the predisposing changes of gene expression in HCC. This approach has potential for the early diagnosis and possible prevention of HCC. We examined the expression profiles of 34 HCC specimens (17 hepatitis B virus [HBV]-related and 17 hepatitis C virus [HCV]-related) and 71 non-tumor liver specimens (36 chronic hepatitis B [CH-B] and 35 chronic hepatitis C [CH-C]) using an in-house cDNA microarray consisting of liver-predominant genes. Graphical Gaussian modeling (GGM) was applied to elucidate the interactions of gene clusters among the HCC and non-tumor lesions.

2013-11-14 | E-GEOD-44074 | biostudies-arrayexpress

Gene expression profiling of hepatitis B- and hepatitis C-related hepatocellular carcinoma using graphical Gaussian modeling

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Claudin-10a deficiency shifts proximal tubular Cl- permeability to cation selectivity via claudin-2 translocation

Project description:The tight junction (TJ) proteins claudin-2 and -10a form paracellular cation and anion channels, respectively, and have both been reported to be expressed in the proximal tubule (PT). However, the physiological role of claudin-10a in the kidney is yet obscure. Mice deficient in claudin-10a were generated and successful knockout was confirmed by Southern Blot, Western Blot and immunofluorescence staining. The functionality of isolated PTs was investigated electrophysiologically. Compensatory regulation was studied by pharmacological intervention, RNA-Seq analysis, Western Blot and immunofluorescence staining.

2021-03-02 | GSE167928 | GEO

Homo sapiens

Project description:Infection with Hepatitis C Virus Depends on TACSTD2, a Regulator of Claudin-1 and Occludin Highly Downregulated in Hepatocellular Carcinoma [cell line]

| PRJNA313407 | ENA

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