NEK3 antibody Polyclonal Antibodies Primary antibodies
- Known as:
- NEK3 (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100342
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- NEK3 antibody Polyclonal Antibodies Primary antibodies
Related genes to: NEK3 antibody Polyclonal Antibodies Primary antibodies
- Gene:
- NEK3 NIH gene
- Name:
- NIMA related kinase 3
- Previous symbol:
- -
- Synonyms:
- HSPK36, MGC29949
- Chromosome:
- 13q14.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-08-26
- Date modifiied:
- 2016-10-05
Related products to: NEK3 antibody Polyclonal Antibodies Primary antibodies
Related articles to: NEK3 antibody Polyclonal Antibodies Primary antibodies
- Bisphenol TMC (BPTMC) is a novel substitute for bisphenol A (BPA) and is increasingly detected in the environment and in human tissues. Despite its potent estrogenic activity, BPTMC's impact on mammalian oocyte quality remains poorly understood. In this study, we examined whether BPTMC exposure affected oocyte maturation in vitro by screening the first polar body and spindle morphology. The results showed that BPTMC significantly reduced the rate of polar body extrusion (MII oocytes) in a dose-dependent manner. Furthermore, BPTMC exposure disrupted cytoplasmic maturation, evidenced by abnormal mitochondrial distribution, elevated reactive oxygen species (ROS) accumulation, and increased apoptosis. These cytoplasmic defects correlated with lower fertilization ability and impaired embryonic development, indicated by reduced percentages of pronuclei and 2-cell embryo formation. Mechanistic analysis showed that BPTMC caused abnormal spindle assembly due to reduced microtubule acetylation, which was mediated by downregulation of the NEK3 protein. Collectively, our findings first demonstrated that BPTMC impaired oocyte maturation through oxidative stress and NEK3-dependent disruption of the cytoskeleton, providing important evidence for risk assessment of emerging bisphenol substitutes. - Source: PubMed
Publication date: 2026/06/03
Liu HuageSun ZhendongXu YongfangXiang LifengYang XiaoxiShi JianboZhou QunfangJiang Guibin - NIMA-related kinases (NEKs) are conserved protein kinases in eukaryotes that regulate cell division and elongation. In Arabidopsis thaliana, NEK6 has been shown to control anisotropic growth through cortical microtubule depolymerization, but the functions of other NEK family members remain largely unknown. Here, we show that Arabidopsis NEKs redundantly regulate organ growth and flowering through phosphorylation-dependent mechanisms. Expression analyses revealed overlapping promoter activities of NEK genes in meristems, vascular tissues, and floral organs. While most single mutants showed no obvious phenotype, multiple mutants exhibited defects in root growth direction, leaf elongation, vascular formation, and floral transition. Biochemical analysis showed that NEK3 and NEK6 phosphorylate both β-tubulin and γ-tubulin, indicating a conserved role in microtubule regulation. In addition, several NEKs interacted with the florigen FLOWERING LOCUS T (FT), and NEK3 phosphorylated FT in vitro and inhibited FT-FD interaction in transient assays, suggesting a role in flowering regulation. These findings show that Arabidopsis NEKs redundantly coordinate vegetative and reproductive development through phosphorylation-dependent regulation of microtubules and flowering pathway. - Source: PubMed
Publication date: 2026/04/28
Takatani ShogoKanazawa MaiSakamoto KotaroTomita YukiKawamoto NozomiSakai TatsuyaAraki TakashiMotose Hiroyasu - Congenital heart disease (CHD) is the most common birth defect, and its pathogenesis is closely related to the abnormal establishment of the left-right (LR) bod axis, which highly depends on the ciliary function of the left-right organizer (LRO). This review systematically expounds the molecular pathways by which ciliary structural and functional abnormalities cause cardiac malformations by integrating multi-species model evidence. We believe that defects in multiple conserved genes (including , , , , , and microRNAs) disrupt ciliary assembly, motility, or signaling capacity, leading to the disappearance of the leftward nodal flow or mechanical sensing failure within the LRO. This further interrupts the left-specific calcium ion flicker and the activation of the Nodal-Pitx2 signaling cascade, ultimately resulting in failed cardiac looping and structural defects (such as ventricular septal defect and transposition of the great arteries). This review integrates transcriptional regulation, protein stability, miRNA-mediated fine regulation, and the planar cell polarity (PCP) pathway into a unified "cilia-LRO-heart" network and explores the molecular mechanisms of cilia in valve diseases and cardiac fibrosis. This not only deepens the understanding of the fundamental biological processes of heart development but also provides new molecular targets and theoretical frameworks for the genetic diagnosis and counseling of related congenital heart diseases. - Source: PubMed
Publication date: 2026/02/17
Ma WenqiZhang ZhuofengMa YunMa Chengxu - 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 - The progression of spermatogenesis is under dynamic transcriptional regulation. As a subunit of the transcription-export complex 2 (TREX-2), PCI domain-containing protein 2 (PCID2), participates in RNA processing. However, the physiological functions of PCID2 in spermatogenesis remain poorly understood. Here, we generate germline conditional knockout (Pcid2-SKO) mice using Stra8-Cre, and it is found that Pcid2-SKO mice are infertile, exhibit extensive germ cell apoptosis, impaired spermatogonial differentiation, and failure of meiosis initiation. Single-cell transcriptome analysis reveals developmental arrest at the transition from type A to type B spermatogonia in Pcid2-SKO mice. Gene Set Enrichment Analysis (GSEA) demonstrates a significant decrease in the enrichment of mRNA splicing pathway in Pcid2-SKO germ cells. IP-MS results indicate candidate proteins interacting with PCID2 are significantly enriched in RNA splicing pathway. Co-IP results indicate that PCID2 interacts with SNRPG, hnRNPH1 and SF3B1 to modulate alternative splicing in germ cells. Combining RNA sequencing and PCR identifies four key genes (Prpf3, Nek3, Dvl2, and Slc30a9) as splicing targets of PCID2. Collectively, PCID2 is essential for normal spermatogenesis and male fertility by regulating the alternative splicing (AS) of genes critical for cell cycle progression, spliceosome assembly, and mitochondrial homeostasis. This study provides novel insights into the molecular mechanisms underlying spermatogenesis and highlights the importance of AS in germ cell development. - Source: PubMed
Publication date: 2026/01/13
Zhu FeiyinZhang YingXi YuGong ChenjiaTang YanlinChen YidongYan LiyingQiao JieLiu Qiang