Ask about this productRelated genes to: ITGB1BP3 antibody
- Gene:
- NMRK2 NIH gene
- Name:
- nicotinamide riboside kinase 2
- Previous symbol:
- ITGB1BP3
- Synonyms:
- MIBP, NRK2
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-15
- Date modifiied:
- 2014-11-19
Related products to: ITGB1BP3 antibody
Related articles to: ITGB1BP3 antibody
- Precocious puberty in chickens is an important biological trait regulated by the hypothalamic-pituitary-gonadal (HPG) axis. The comb height of roosters is an indicator of precocious puberty in breeding. However, the underlying mechanisms of precocious puberty, particularly in roosters, remain underexplored. - Source: PubMed
Publication date: 2026/05/25
Xiang HaiLi XiangkunSun XiaoxuZhang ZhengfenWei JixiangLiu ZhijieMa ZhengChen SiyuGou JunweiYe FeiLi Hua - Glucocorticoid-induced myopathy is characterized by progressive muscle atrophy and impaired regeneration, yet effective microbiota-oriented interventions for preserving muscle homeostasis remain largely unexplored. Here, we demonstrate that dietary chondroitin sulfate (DCS) restores muscle mass and function through a microbiota-dependent gut-muscle metabolic axis. DCS failed to confer protection in germ-free or antibiotic-treated mice, establishing gut microbiota as a prerequisite for its efficacy. Microbiota transplantation and mono-colonization experiments identified Z-RW as a functionally relevant mediator capable of recapitulating muscle protection under controlled microbial conditions. Integrated metagenomic, metabolomic, and proteomic analyses revealed coordinated reprogramming of intestinal sugar utilization and bile acid metabolism following DCS administration. Notably, DCS promoted bile acid deconjugation and enrichment of secondary bile acids, coinciding with restoration of muscle regenerative and energetic programs, including upregulation of NMRK2, PAX7, and SIRT1. Metabolite supplementation further implicated bile acids as candidate mediators linking microbial metabolism to muscle phenotypes. To quantitatively integrate these shifts, we introduce the sugar-bile acid ratio as a systems-level descriptor of microbiota-driven metabolic remodeling. Our findings delineate a microbiota-dependent metabolic framework through which a functional polysaccharide reshapes intestinal biochemistry to influence distal muscle physiology. This work highlights bile acid-associated signaling as a central relay within the gut-muscle axis and provides a conceptual foundation for microbiota-targeted strategies to mitigate muscle wasting. - Source: PubMed
Publication date: 2026/03/12
Wu RuiyunWen TaoShang NanXie PenghaoWang ZhenyuLi HangLi ShaoboZhang Dequan - Substantial oxidative stress during myocardial ischemia/reperfusion (I/R) injury precipitates cell death and heart failure, for which translatable redox therapies remain scarce. Here, we show that nicotinamide riboside kinase 2 (NMRK2) is rapidly upregulated after reperfusion and exerts redox protection by a previously unrecognized mechanism. We established myocardial I/R injury in mice and hypoxia/reoxygenation (H/R) injury in cardiomyocytes. By elevating NADPH, restoring NAD/NADH, increasing GSH/GSSG and activating Trx1, NMRK2 overexpression enhanced cellular antioxidant capacity and reduced oxidative damage during both myocardial I/R and cellular H/R injury. Knockdown of NAD kinase (NADK) abolished these protective effects. Mechanistically, nucleocytoplasmic fractionation and immunofluorescence confirmed robust Yes-associated protein (YAP) nuclear entry in NMRK2-overexpressing cells; Co-IP revealed NMRK2-induced disruption of the integrin β-YAP interaction; knockdown of integrin β reduced NADK expression and increased YAP phosphorylation at Ser127; and ChIP-qPCR and luciferase assays demonstrated that YAP directly binds the NADK promoter (-1500 to -1000 bp) for its transcriptional activation. In conclusion, NMRK2 sustains redox protection by disrupting the integrin β-YAP complex and driving YAP-dependent NADK transcription, providing a readily translatable therapy against myocardial I/R injury. - Source: PubMed
Publication date: 2026/02/23
Zhang ChaoWang JieChi JingLiu Su-TingMeng Xiao-WenLi Lin-GuiDong ShunliCao HuiZhou Xing-GenZhang YangSun Hai-YanKang Pei-PeiPeng KeJi Fu-Hai - Disuse-induced muscle atrophy commonly occurs following illness, injury, or falls and becomes increasingly frequent with ageing. Whether skeletal muscle retains a "memory" of repeated disuse remains unknown. We investigated repeated lower-limb immobilization in young adults and a refined aged rat model, integrating physiological, multi-omic, immunohistochemical, biochemical, and primary human muscle stem cell (MuSC) analyses. To enable robust age comparisons, we integrated previously published young rat data with newly generated aged rat data. In young human muscle, repeated disuse elicited attenuated transcriptional perturbations in oxidative and mitochondrial pathways, suggestive of a protective molecular memory, despite similar atrophy to initial disuse. In contrast, aged muscle exhibited a detrimental memory, characterized by greater atrophy, exaggerated suppression of aerobic metabolism genes despite recovery after initial disuse, NAD and mitochondrial DNA depletion, and activation of proteasomal, extracellular-matrix, and DNA-damage pathways. Whereas young rats recovered muscle mass after initial disuse, aged rats failed to do so. Across species, repeated disuse induced DNA hypermethylation and downregulation of aerobic metabolism and mitochondrial gene networks. NR4A1 and NR4A3 were among the strongest disuse-suppressed genes; NR4A1 acquired recovery-phase hypermethylation that maintained its transcriptional repression, while NR4A3 was the most downregulated gene after initial atrophy and remained persistently suppressed into recovery. Acetylcholine receptor subunit genes (CHRNA1, CHRND) were epigenetically primed, demonstrating hypomethylation and strong upregulation after disuse, and further amplification after repeated atrophy, while CHRNG was selectively induced after repeated atrophy only. NMRK2, an NAD biosynthesis gene, was the most downregulated gene across both atrophy periods, and supplementation with its substrate, nicotinamide riboside (NR), improved myotube size in MuSCs derived post-atrophy. Overall, repeated disuse atrophy imprints a molecular memory in skeletal muscle shaping transcriptional resilience in young adults and exaggerated susceptibility in aged muscle. - Source: PubMed
Publication date: 2026/02/25
Turner Daniel CRaastad TrulsUllrich MaxChristiansen Stian FSutherland HazelBoot JamesWozniak EvaMein CharlesDalbram EmilieTreebak Jonas TOwens Daniel JHughes David CBodine Sue CJarvis Jonathan CSharples Adam P - PRCC-TFE3 rearrangement renal cell carcinoma (rRCC) is an independent subtype of rRCC caused by chromosomal translocation and rearrangement. Previous studies have revealed that nicotinamide riboside kinase 2 (NMRK2), which is transcriptionally upregulated by PRCC-TFE3 fusion protein, as a pivotal molecule in the energy metabolism remodeling of PRCC-TFE3 rRCC. However, the molecular mechanism by which NMRK2-mediated enhancement of nicotinamide adenine dinucleotide (NAD) synthesis contributes to tumor progression in PRCC-TFE3 rRCC remains unclear. In this study, utilizing immune system-humanized mice model and in vitro cell models, we demonstrated that elevated expression of NMRK2 impaired the cytotoxic functions of CD8T cells, leading to the emergence of immune-ignorant phenotypes in PRCC-TFE3 rRCC. Furthermore, it was shown that the increased NAD metabolism driven by NMRK2 enhanced the stability of CD38 protein through SIRT1-mediated deacetylation, which underlines impairment of CD8T cells and the development of an immunosuppressive state in PRCC-TFE3 rRCC. Our findings not only elucidated a mechanism underlying immunological ignorance in PRCC-TFE3 rRCC but also propose potential therapeutic targets. - Source: PubMed
Publication date: 2025/09/17
Chen YiLiu XuwentaiWu MengmengDong XiangMa WenliangFeng FanDing YibingDong PingDing WeidongZhang LuqingLiu NingGan WeidongLi Dongmei