Ask about this productRelated genes to: NEK9 antibody
- Gene:
- NEK9 NIH gene
- Name:
- NIMA related kinase 9
- Previous symbol:
- -
- Synonyms:
- Nek8, NERCC, DKFZp434D0935, MGC16714
- Chromosome:
- 14q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-05-08
- Date modifiied:
- 2016-10-05
Related products to: NEK9 antibody
Related articles to: NEK9 antibody
- The NIMA-related kinase (NEK) family comprises a group of serine/threonine kinases that play pivotal roles in cell cycle control. Emerging evidence has demonstrated that loss-of-function (LOF) mutations in NEK family members, particularly NEK1 and NEK9, cause skeletal and joint developmental abnormalities. - Source: PubMed
Publication date: 2026/07/13
Zhao YitongZheng YingChen QianYang YingZhang Liyu - Immune checkpoint inhibitors (ICIs) demonstrate limited efficacy in hepatocellular carcinoma (HCC), largely attributable to a profoundly immunosuppressive tumour microenvironment (TME). - Source: PubMed
Publication date: 2026/06/25
Lu GuofangDu RuiWan YueDong JiaqiangLi BoLiu MeiHan QingHe FaWang YuhaoJia LintaoAn YanxinLiu YanshengHan YingShang Yulong - Fibroblast-like synoviocytes (FLSs) are crucial in driving synovial inflammation and joint damage in rheumatoid arthritis (RA). This study explored the functions and underlying mechanisms of GALNT1-mediated O-glycosylation, which is markedly upregulated in RA FLSs, in synovial aggression and subsequent experimental joint damage. Targeted suppression of GALNT1 effectively curtailed migration and invasion in RA FLSs and mitigated arthritis severity in a collagen-induced arthritis model in rats. Mechanistically, NEK9 was identified as a pivotal substrate and downstream effector of GALNT1, affecting the aggressive phenotype of RA FLSs. In vitro experiments further demonstrated that O-glycosylation of NEK9, mediated by GALNT1, promotes the pathogenic phenotype of RA FLSs by promoting cytoskeleton reorganization and restraining excessive ER stress activation. Our study provides mechanistic insights into the activation of RA FLSs and identifies GALNT1 as a potential therapeutic target for RA. - Source: PubMed
Publication date: 2026/04/23
Zou YaoyaoLin HaoboSu JianlingWang JieyingZeng QinFeng TianxiaoLei YunxiaMa JiandaPan HudanXu HanshiDai LieLi Yang - The C-terminal to LisH (CTLH) complex is a modular multi-subunit E3 ligase with diverse biological functions, yet how its overall ubiquitylation activity is tuned remains unclear. Here, we identify CDK- and mTOR-dependent phosphorylation of the cognate E2 enzyme UBE2H as a key regulator of CTLH E3 catalytic capacity. Phosphorylation of two N-terminal serine residues (S3/S5) reduces UBE2H charging with ubiquitin, thereby limiting the pool of active E2 available to CTLH. Mitotic CDK activity inactivates UBE2H during mitosis, whereas mTOR restrains UBE2H charging in interphase to couple CTLH-dependent ubiquitylation to nutrient status. Preventing this phosphorylation maintains UBE2H charging, enhances CTLH-mediated substrate degradation, promotes CTLH subunit turnover, and causes proliferation and mitotic defects. Using hyperactive UBE2H, we identify two additional CTLH substrates, the mitotic kinase NEK9 and Angio-associated migratory cell protein (AAMP) and define a DR-like C-degron recognized by the CTLH subunit MKLN1. These findings reveal how regulation of an E2 enzyme by cell cycle and nutrient signaling pathways dynamically shape CTLH activity. - Source: PubMed
Publication date: 2026/03/09
Chen YingqianRossio ValentinaPaulo Joao AKarki MenukaManohar SandhyaOzimek NoelleFrizzi LauraGygi Steven PKing Randall W - Oral squamous cell carcinoma (OSCC) is a prevalent malignancy characterized by aggressive behavior, poor prognosis, and limited therapeutic options. Mutations in the NIMA-related kinase (NEK) family are increasingly implicated in tumorigenesis across various cancers. However, their contributions to OSCC pathogenesis remain largely unexplored. - Source: PubMed
Publication date: 2026/02/04
Nawab FouziaNaeem WafaFatima SadiaKhan Muhammad UzairMehmood AamirNawab SadiaKhan IshaqNawaz HaseenaAhmad HilalKhalil Ali TalhaKhan Ishtiaq AhmadIrfan MuhammadAlorini MohammedKhurram Syed AliAli Asif