Ask about this productRelated genes to: PMVK antibody
- Gene:
- PMVK NIH gene
- Name:
- phosphomevalonate kinase
- Previous symbol:
- -
- Synonyms:
- PMK, PMKA, HUMPMKI
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-09
- Date modifiied:
- 2014-11-19
Related products to: PMVK antibody
Related articles to: PMVK antibody
- To evaluate clinical outcomes (performance-based tests and patient-reported outcome measures [PROMs]) and biomechanical measures of movement smoothness, and explore their associations with molecular markers in individuals with knee osteoarthritis (KOA). - Source: PubMed
Publication date: 2026/07/30
Gawelowicz KarolSimonsen Morten BildeHedström MargaretaBroström EvaAulin CeciliaNaili Josefine E - Metabolic reprogramming is a hallmark of cancer, yet the critical drivers and mechanisms in hepatocellular carcinoma (HCC) remain incompletely understood. Through a metabolism-focused CRISPR screen, we identified phosphomevalonate kinase (PMVK), a mevalonate pathway enzyme, as a key regulator of HCC stemness and progression. PMVK directly phosphorylates the transcription factor SP1 at Thr, which enhances SP1's DNA binding affinity and promotes its interaction with the master lipid regulator SREBP1/2, driving a transcriptional program essential for de novo cholesterol and fatty acid synthesis. Clinically, PMVK levels are positively correlated with phospho-SP1 (Thr) levels and predicate poor prognosis in patients with HCC. Functionally, we demonstrate that genetic or pharmacologic inhibition of the PMVK-SP1 axis, including using the SP1 inhibitor mithramycin A (MTA), significantly suppresses HCC tumorigenesis. In conclusion, our findings uncover the PMVK-SP1 axis as a central driver of lipid metabolic reprogramming and hepatocarcinogenesis, highlighting it as a compelling therapeutic target in HCC. - Source: PubMed
Publication date: 2026/06/26
Liu RuiyangHuang CainiXu ZhijieXu FuyuanWen XinyiZhao ZhijuXiao Fei - Major depressive disorder (MDD) is a highly prevalent and disabling neuropsychiatric condition, its underlying molecular mechanisms remain incompletely understood. This study aimed to systematically characterize proteomic alterations in the prefrontal cortex associated with depression-like behaviors induced by chronic stress. Depression-like behaviors in mice were evaluated using standardized behavioral tests and confirmed by Digital Western blotting. Quantitative proteomic analysis of prefrontal cortex tissues was performed to compare chronic social defeat stress (CSDS) and control groups, identifying differentially expressed proteins (DEPs). These DEPs were subsequently subjected to bioinformatic analyses, including Gene Ontology (GO) enrichment and construction of protein-protein interaction (PPI) networks. Key DEPs were further validated by parallel reaction monitoring (PRM) and Western blotting. We found that CSDS mice displayed robust depression-like phenotypes, including decreased sucrose preference and increased immobility. Western blot analysis confirmed the dysregulation of ER stress markers, proinflammatory factors, and proteins related to synaptic plasticity. Proteomic analysis identified 95 differentially expressed proteins, with GO enrichment revealing predominant associations with gene regulation, mitochondrial, metabolic, and synaptic function. PPI network analysis highlighted hub proteins involved in mitochondrial, endoplasmic reticulum, and synaptic regulation. PRM and Western blot validation confirmed dysregulation in four functional modules: 1) Mitochondrial function (Mrpl17, Mrpl41)；2) Signal transduction (Rigi, Pbrm1, Plppr5, Glyr1)；3) Metabolic regulation(Pmvk, Rpl13a, Ubtd2, Tmem63b)；4) Synaptic plasticity (Kif21b, Klc4, Lama2, Col4a2). Our results demonstrate that chronic stress disrupts prefrontal cortical pathways that govern gene regulation, mitochondrial metabolism, and synaptic function, suggesting their concerted contribution to the pathophysiology of depression. - Source: PubMed
Publication date: 2026/02/27
Zhang YiLi LeiZhang XiaoweiXu JiyiKan WeijingWang TianyiDu Jing - Porokeratosis (PK) is an autosomal dominant inherited disorder characterized by abnormal epidermal keratinization, primarily resulting from mutations in four genes associated with the mevalonate pathway: mevalonate decarboxylase (), mevalonate kinase (), phosphomevalonate kinase (), and farnesyl diphosphate synthase (). - Source: PubMed
Publication date: 2026/01/29
He YangZhu ShengcaiWei QuanYe FanZhu YunxiaOuyang XiaoliangWu LiangLi Chunming - Pyroptotic inflammation has been shown to contribute to neuronal injury after stroke. Uncoordinated-5 homolog B (UNC5B) is implicated in neuroinflammation, and its downstream kinase death-associated protein kinase 3 (DAPK3) is predicted to interact with mevalonate kinase (MVK). To examine the role of UNC5B in post-stroke pyroptosis, we used a photothrombosis (PT) stroke model in mice and an oxygen-glucose deprivation (OGD) model in BV-2 microglia. Knockdown of Unc5b or Mvk and pharmacological inhibition of DAPK3 were performed, followed by detection of pyroptosis-associated proteins and cell viability. Interactions between DAPK3 and MVK were assessed using transwell coculture and co-immunoprecipitation. PT or OGD induced neuronal injury and increased expression of pyroptosis-related proteins. Knockdown of Unc5b or Mvk in microglia protected neurons by suppressing pyroptosis and disrupting the DAPK3-MVK protein complex. Upregulation of p-MVK was prevented by either Unc5b knockdown or DAPK3 inhibition, whereas DAPK3 upregulation was blocked only by Unc5b knockdown and not by Mvk knockdown. Our results suggest that UNC5B promotes post-stroke microglial pyroptosis in part through the DAPK3/MVK pathway. - Source: PubMed
Publication date: 2026/01/07
Luo YingLiao SongjieYao MeilingWang RuiYu Jian