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Effect of knockdown Tbl1xr1 on gene expression after 2/3 hepatectomy

ABSTRACT: Our spatiotemporal data confirmed activation of Tbl1xr1 in hepatocytes after 2/3 hepatectomy. TBL1XR1 is a transcriptional cofactor inducing ubiquitination and degradation of NCoR/SMRT co-repressors and NCoR is a negative regulator of hepatocyte proliferation acting through histone deacetylases (HDACs). We have examined the role of TBL1XR1 in liver regeneration through in vivo shRNA knockdown using adeno-associated viruses (shNC and shTbl1xr1) specifically targeting hepatocytes. The knockdown of Tbl1xr1 results in impair hepatocyte proliferation.To investigate the downstream targets of TBL1XR1 during liver regenration, we here perform the bulk RNA-seq for shNC and shTbl1xr1 at D2 after hepatectomy. Our data show demonstrated that Tbl1xr1 knockdown not only led to reduced cell cycle genes but also to impaired fatty acid β-oxidation as the most obviously affected liver function.

ORGANISM(S): Mus musculus

PROVIDER: GSE254481 | GEO | 2024/02/05

REPOSITORIES: GEO

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Expression data from rat hepatocyte during liver regeneration after partial hepatectomy

2014-02-28 | GSE55434 | GEO

Expression data from rat hepatocyte during liver regeneration after partial hepatectomy

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2014-02-28 | E-GEOD-55434 | biostudies-arrayexpress

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Project description:TBL1XR1 gene is associated with multiple developmental disorders presenting several neurological aspects. The relative protein is involved in regulation of important cellular pathways and master regulators of transcriptional output including nuclear receptor repressors, Wnt signaling, and MECP2 protein. However, TBL1XR1 mutations (including complete loss of its functions) have not been experimentally studied in neurological context, leaving a lack of knowledge in the mechanisms at the basis of the diseases. We show that Tbl1xr1 knock-out mice exhibit behavioral and neuronal abnormalities. Either the absence of TBL1XR1, or point mutations interfering with stability/regulation of NCOR complex induced decreased proliferation and increased differentiation in neural progenitors. We suggest that this developmental unbalance is due to the failure in the regulation of MAPK cascade. Together, our results broaden the molecular and functional aftermath of TBL1XR1 deficiency associated with human disorders.

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Real-time quantitative PCR analysis of the effects of chronic ethanol feeding and partial hepatectomy on gene expression in single rat hepatocytes

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2009-05-01 | E-GEOD-13864 | biostudies-arrayexpress

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