SIRT5
- Known as:
- SIRT5
- Catalog number:
- 000470A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- SIRT5
Related genes to: SIRT5
- Gene:
- SIRT5 NIH gene
- Name:
- sirtuin 5
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 6p23
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-20
- Date modifiied:
- 2014-11-19
Related products to: SIRT5
Related articles to: SIRT5
- Ischemic tolerance is an inducible state in which the brain becomes transiently resistant to injury. Across models, conditioning recruits 3 coordinated modules: (1) rapid synaptic downscaling that lowers excitability and delays ischemic depolarization, (2) metabolic reprogramming that matches demand with reduced mitochondrial reactive oxygen species, and (3) a delayed consolidation phase that stabilizes the phenotype. A delayed window integrates nicotinamide adenine dinucleotide (NAD)/sirtuin pathways (PKCε [protein kinase C epsilon]→NAMPT [nicotinamide phosphoribosyltransferase]→NAD, SIRT1 [sirtuin 1] control of glycolysis, and SIRT5 [sirtuin 5] desuccinylation), maintenance of the malate-aspartate shuttle, and proteostasis/innate-immune programs (HSP70 [heat shock protein 70]/HSP27 [heat shock protein 27]/HO-1 [heme oxygenase-1]; interferon-biased signaling). These mechanisms exhibit similarities with evolutionary adaptations while preserving the capacity for plasticity via homeostatic scaling. Both preconditioning and postconditioning mitigate ischemia-induced cognitive impairment by limiting pathology in the septal nuclei. Specifically, physical exercise restores septohippocampal oscillatory coherence, which is linked to cognitive improvement. Clinically, the best scenarios for treatment are predictable ischemia and well-phenotyped high-risk cohorts. Future priorities are further elucidation of mechanisms of conditioning mimetics, rational combinations (eg, exercise or remote conditioning layered with these mimetics), and preclinical designs incorporating aging and comorbidities to derisk translation. - Source: PubMed
Publication date: 2026/04/27
Perez-Pinzon Miguel A - - Source: PubMed
Publication date: 2026/01/20
Xiao MinZhao JunchengDou ZixuanChen XiangyuXu SunyuntaoZhang YuFan HongxuanChen XudongZhang PingHuang ZhenZhou BodaWei Taotao - Triple-negative breast cancer (TNBC) is characterized by aggressive progression and poor prognosis, partly due to abnormal angiogenesis. While the metabolic reprogramming of tumor cells is well characterized, the metabolic regulation of tumor-associated endothelial cells (ECs) remains unclear. Here, we identified the mitochondrial deacylase SIRT5, which has established tumor-promoting roles in TNBC cells, as a key regulator of endothelial metabolic homeostasis and tumor angiogenesis. SIRT5-deficient host mice showed significant defects in supporting the growth of orthotopic SIRT5-proficient mammary tumor transplants, and the resulting neoplasms showed defects in tumor vascularization. In a 3D microfluidic vessel-on-chip model, loss compromised vascular barrier integrity and EC sprouting. Mechanistically, -deficient ECs exhibited diminished mitochondrial respiratory capacity but apparently normal glycolysis. SIRT5 loss also caused increased mitochondrial reactive oxygen species levels, and a mitochondrial antioxidant rescued the endothelial cell defects following SIRT5 loss, indicating that SIRT5-mediated mitochondrial redox homeostasis in the tumor microenvironment is necessary to maintain vascular function. Orthotopic co-transplantation of TNBC and EC cells with or without SIRT5 knockdown demonstrated that endothelial SIRT5 promotes increased tumor growth . These results suggest that targeting SIRT5 offers a potential therapeutic strategy to disrupt tumor angiogenesis and suppress TNBC progression by targeting the metabolic vulnerabilities of the tumor endothelium. - Source: PubMed
Publication date: 2026/04/13
Chen Anthony MCano IssahyZhao QianTsai Pei-YinBacchus Elijah AJana SadhanFernandez Irma RNwosu Zeribe CMiller AndrewBarrow JoevaLin HeningLee EsakWeiss Robert S - The sirtuin (SIRT) family is an NAD-dependent class III histone deacetylase protein that comprises seven members (SIRT1-7). SIRTs are involved in many cellular pathways, which enable them to act as significant regulators of critical diseases such as cancer, cardiovascular disease, respiratory disease, and diabetes. Despite extensive research conducted to understand SIRT biology, many areas remain unexplored, such as the lack of SIRT isoform selectivity and specificity, restrained potency, limited bioavailability, poor pharmacokinetic and pharmacodynamic properties, and insufficient clinical and preclinical trials. Our study focused on one of the major research gaps, i.e., "lack of SIRT isoform selectivity and specificity," through extensive computational exploration. - Source: PubMed
Publication date: 2026/04/10
Sharma DeepakMuniyan Rajiniraja - Azadirachtin, a major botanical insecticide, is widely recognized as a sustainable alternative to synthetic pesticides, yet the molecular mechanisms underlying its effects on insect hosts remain poorly understood. Transcriptomic analysis, RT-PCR, and qPCR revealed significant upregulation of Sirt5 in the midgut following azadirachtin exposure. In the present study, we investigated the role of Sirt5, a key regulator of metabolic and stress responses, in mediating midgut damage in Spodoptera litura under azadirachtin stress. Functional assays showed that overexpression of Sirt5 in SpLi-221 cells suppressed lysosomal activity under stress, whereas CRISPR/Cas9-mediated knockout (KO) of Sirt5 led to elevated expression of autophagy-related genes (Atg6, Atg16, Atg101) and the apoptosis marker caspase-1. Compared with the wild-type control group, the mortality of the larvae lacking Sirt5 increased from 49% to 95% when fed with the median lethal dose of azadirachtin. These findings indicate that Sirt5 mitigates azadirachtin-induced midgut damage by modulating autophagy and apoptosis pathways. The present study provides the first experimental evidence linking Sirt5 to host responses against azadirachtin, offering new mechanistic insights into botanical insecticide action and identifying a potential target for enhancing sustainable pest management strategies. - Source: PubMed
Publication date: 2026/04/05
Yang XueXiao YingdanHao ShaopengLiu JianqiuGuo HuizhenXu YajingGoldsmith Marian RSmagghe GuyXia QingyouMita Kazuei