Proteomics

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Hepatic Huwe1 loss protects mice from non-alcoholic fatty liver disease through lipid metabolic rewiring

ABSTRACT: Non-alcoholic fatty liver disease (NAFLD) is the most prevalent form of liver disease worldwide and is estimated to affect nearly a third of the population. Huwe1, also known as ARF-BP1, MULE, and HectH9, is a HECT (homology to E6-APC terminus)-domain E3 ubiquitin ligase originally identified as a binding partner of the tumor suppressor ARF, as well as a direct negative regulator of the tumor suppressor p53. To further elucidate the in vivo role of Huwe1, we generated a liver-specific Huwe1 (Huwe1LKO) knockout mouse model. Surprisingly, liver-specific knockout of Huwe1 protected mice from the development of age-induced hepatic steatosis. To elucidate the mechanism underlying this phenotype, mass spectrometry analysis was performed on liver tissues from 1-year-old Huwe1LKO and Huwe1WT mice.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Liver

SUBMITTER: William Feng  

LAB HEAD: Manabu Kurokawa

PROVIDER: PXD045279 | Pride | 2024-01-26

REPOSITORIES: Pride

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Publications

Non-alcoholic fatty liver disease (NAFLD) is the most pervasive liver pathology worldwide. Here, we demonstrate that the ubiquitin E3 ligase Huwe1 is vital in NAFLD pathogenesis. Using mass spectrometry and RNA sequencing, we reveal that liver-specific deletion of Huwe1 (<i>Huwe1</i><sup><i>LKO</i></sup>) in 1-year-old mice (approximately middle age in humans) elicits extensive lipid metabolic reprogramming that involves downregulation of <i>de novo</i> lipogenesis and fatty acid uptake, upregul  ...[more]

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