Ask about this productRelated genes to: VRK3 antibody
- Gene:
- VRK3 NIH gene
- Name:
- VRK serine/threonine kinase 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2003-08-18
- Date modifiied:
- 2018-08-16
Related products to: VRK3 antibody
Related articles to: VRK3 antibody
- Vaccinia-Related Kinase 3 (VRK3) is increasingly recognized as a crucial signaling modulator in both normal and pathological processes. This kinase was long thought of as a catalytically inactive pseudokinase, until recently it was established to phosphorylate Barrier to Autointegration Factor (BAF) proteins through its extracatalytic domain. VRK3 regulates diverse cellular pathways through scaffold interactions and context-dependent phosphorylation. This review is centered around the phosphoregulatory network that modulates VRK3 phosphorylation with implications in its abundance and function. A large-scale phosphoproteomic data integration was performed by combining phosphoproteomics profiling and differential phosphorylation from 115 mass spectrometry studies, identifying 32 high-confidence phosphorylation sites on VRK3. Notably, VRK3 (S59), (S82), and (S83) were predominantly observed highlighting plausible functional significance. These phosphorylation sites share 33 potential upstream kinases, and multiple interactor proteins, which in combination are known to regulate ERK, Hippo, and GPCR pathways. These insights advance the understanding of phosphorylation control by kinases and highlight opportunities to target VRK3-associated networks for therapeutic intervention in diseases such as glioma and liver cancer. - Source: PubMed
Publication date: 2026/03/18
Sujina AyadathilFahma AmalSubair SuhailRaju RajeshRamesh Poornima - SLE is a multifactorial autoimmune disease with complex genetic architecture and immune cell involvement. While genome-wide association studies (GWAS) have identified numerous risk loci, most are non-coding, making it challenging to pinpoint causal eGenes [genes with expression quantitative trait loci (eQTLs)] and therapeutic targets. - Source: PubMed
Hong YanggangYe JianiHua Chunyan - Alzheimer's disease (AD) continues to be the sixth leading cause of death in the United States. Significant efforts are spent researching etiology and potential management strategies. Although minorities face a higher disease burden and are anticipated to make up 43% of the US population by 2060, most literature on inherited AD risk has been derived from studying European ancestry. Here we evaluate frequencies of top AD risk alleles for late-onset AD (LOAD) in African- (AA), Mexican- (MA) and non-Hispanic White (NHW)-American participants enrolled in the Health & Aging Brain Study-Health Disparities (HABS-HD) cohort to determine ethnicity-specific differential genetic architecture. - Source: PubMed
Publication date: 2025/06/19
Housini MohammadZhou ZhengyangAbdullah LubnaaPathak GitaAyoub ReemGutierrez JohnAndrews SheaPhillips NicoleO'Bryant SidBarber Robert - Periodontitis is considered to be one of the major risk factors associated with cancers of the oral cavity. Periodontogenic pathogens such as and are the important pathogens associated with periodontitis. Chronic exposure to bacterial components induces changes in the nearby cells. Hence, the present study has been designed to identify the molecular mechanisms that could be associated with the two disease conditions periodontitis and head and neck cancer. - Source: PubMed
Publication date: 2024/12/05
M DakshinyaP AnithaSmiline Girija A SA ParamasivamPriyadharsini J Vijayashree - We previously identified VRK3 as a specific vulnerability in DMG-H3K27M cells in a synthetic lethality screen targeting the whole kinome. The aim of the present study was to elucidate the mechanisms by which VRK3 depletion impact DMG-H3K27M cell fitness. Gene expression studies after knockdown emphasized the inhibition of genes involved in G1/S transition of the cell cycle resulting in growth arrest in G1. Additionally, a massive modulation of genes involved in chromosome segregation was observed, concomitantly with a reduction in the level of phosphorylation of serine 10 and serine 28 of histone H3 supporting the regulation of chromatin condensation during cell division. This last effect could be partly due to a concomitant decrease of the chromatin kinase VRK1 in DMG following knockdown. Furthermore, a metabolic switch specific to VRK3 function was observed towards increased oxidative phosphorylation without change in mitochondria content, that we hypothesized would represent a cell rescue mechanism. This study further explored the vulnerability of DMG-H3K27M cells to VRK3 depletion suggesting potential therapeutic combinations, with the mitochondrial ClpP protease activator ONC201. - Source: PubMed
Publication date: 2023/10/10
Menez VirginieKergrohen ThomasShasha TalSilva-Evangelista ClaudiaLe Dret LudivineAuffret LucieSubecz ChloéLancien ManonAjlil YassineVilchis Irma SegovianoBeccaria KévinBlauwblomme ThomasOberlin EstelleGrill JacquesCastel DavidDebily Marie-Anne