SIRT5 regulates protein substrates involved in glycolysis, TCA cycle, fatty acid oxidation, electron transport chain, ketone body formation, nitrogenous waste management, and ROS detoxification, among other processes.

Sirtuin (silent mating type information regulation 2 homolog) 5 (S. cerevisiae), also known as SIRT5 is a protein which in humans in encoded by the SIRT5 gene and in other species by the orthologous Sirt5 gene.

SIRT5 regulates protein substrates involved in glycolysis, the TCA cycle, fatty acid oxidation, electron transport chain, ketone body formation, nitrogenous waste management, and ROS detoxification, among other processes.

SIRT5 controls a wide range of aspects of myocardial energy metabolism and plays critical roles in heart physiology and stress responses. Moreover, SIRT5 has a protective function in the context of neurodegenerative diseases, while it acts as a …

Jun 5, 2022 · SIRT5 is thought to be closely related to some diseases such as cancer and neurodegenerative diseases. Herein, we present an overview of the structure and biological function of SIRT5 as well as the advances in SIRT5 inhibitors research.

Sirtuins are a class of deacylating enzymes involved in regulating a variety of processes, including epigenetic state, DNA damage response, and metabolism (21, 22). SIRT5 has specific deacylating activity toward succinyl, malonyl, and glutaryl …

Aug 15, 2024 · SIRT5 inhibited the trophoblast cell proliferation, invasion, and migration to promote PE through suppressing Notch and β-catenin signaling pathway activation via desuccinylating HOXB3. Preeclampsia (PE) is a pregnancy-specific syndrome with increasing maternal and perinatal morbidity and mortality.

Mar 10, 2018 · SIRT5 substrates include a number of proteins integral to metabolism. Recent Advances: New work has begun to elucidate the roles of SIRT5 in glycolysis, tricarboxylic acid cycle, fatty acid oxidation, nitrogen metabolism, pentose …

Jan 30, 2018 · SIRT5-mediated deglutarylation of glucose 6 phosphate dehydrogenase, the rate-limiting enzyme in the PPP, increases its activity and contributes to antioxidant defenses in brain (Zhou et al., 2016). This regulation might also affect purine metabolite levels.

Herein, with adoptive transfer of Sirt5 +/+ or Sirt5 −/− OT-1 cells and acute Listeria monocytogenes infection model, we demonstrate that SIRT5 deficiency does not affect CD8 + T cell effector function and that SIRT5 is not required for CD8 + T cell memory formation.