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
- 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 rat collagen-induced arthritis (CIA) model. 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 endoplasmic reticulum (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 - EML4-ALK is a common oncogenic driver of non-small cell lung cancer. Distinct EML4-ALK variants cause different rates of disease progression, with patients expressing variant 3 (V3) exhibiting accelerated metastasis. Cells expressing EML4-ALK V3 develop a mesenchymal-like morphology and enhanced migration that is dependent on the NEK9 and NEK7 kinases. However, downstream substrates of these kinases relevant to these phenotypes are largely unknown. Here, we show that the actin-binding protein cortactin is phosphorylated by NEK7 within the F-actin-binding region (ABR) and that depletion of cortactin abrogates the morphological and migration phenotypes induced by EML4-ALK V3. Expression of constitutively active mutants of NEK9 or NEK7 causes similar cortactin-dependent morphological and migration changes. Cortactin co-localises with NEK7 and EML4-ALK V3 at branched filopodia-like extensions that are also generated upon expression of a cortactin protein with phospho-mimetic mutations in the ABR. In contrast, phospho-null mutations dissociate cortactin from F-actin. We propose that EML4-ALK V3 alters cell morphology and promotes directed cell migration by modulating the actin cytoskeleton via NEK7-mediated phosphorylation of cortactin within its ABR. - Source: PubMed
Publication date: 2026/01/27
Richardson Emily LKnebel AxelStraatman Kees RGourlay RobertLamont DouglasHardy TaraTurnbull Robert ERobinson Susan WO'Regan LauraBayliss RichardFry Andrew M - There are few reports on the comprehensive surgical management of extensive nevus comedonicus, and the genetic mechanism of this rare disease is not yet fully understood. - Source: PubMed
Publication date: 2025/12/20
Cheng HuiLi XiaojingLi XinyiBai YunZhang WeiZhao BoaoYang TaoLi PingYao Wende