Proteomics

Dataset Information

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TST knockout liver proteome iTRAQ and persulfidome


ABSTRACT: Impaired hepatic glucose and lipid metabolism are hallmarks of type–2 diabetes. Increased sulfide production or sulfide–donor compounds may beneficially regulate hepatic metabolism. Disposal of sulfide through the sulfide oxidation pathway (SOP) is critical for maintaining sulfide within a safe physiological range. We show that mice lacking the liver–enriched mitochondrial SOP enzyme thiosulfate sulfur–transferase (Tst—/— mice) exhibit high circulating sulfide, increased gluconeogenesis, hypertriglyceridemia and fatty liver. Unexpectedly, hepatic sulfide levels are normal in Tst—/— mice due to exaggerated induction of sulfide disposal, with an associated suppression of global protein persulfidation and nuclear respiratory factor–2 target protein levels. Hepatic proteomic and persulfidomic profiles converge on gluconeogenesis and lipid metabolism, revealing a selective deficit in medium–chain fatty acid oxidation in Tst—/— mice. We reveal a critical role for TST in hepatic metabolism that has implications for sulfide-donor strategies in the context of metabolic disease.

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Liver

SUBMITTER: Pauline Ward  

LAB HEAD: Nik Morton

PROVIDER: PXD028909 | Pride | 2021-11-11

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
150622_o2_05_mo_i1_4.raw Raw
150622_o2_06_mo_i1_5-6.raw Raw
150622_o2_07_mo_i1_7-12.raw Raw
150622_o2_08_mo_i1_13.raw Raw
150622_o2_09_mo_i1_14.raw Raw
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