AZI1
- Known as:
- AZI1
- Catalog number:
- 002336A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AZI1
Related genes to: AZI1
- Gene:
- CEP131 NIH gene
- Name:
- centrosomal protein 131
- Previous symbol:
- AZI1
- Synonyms:
- AZ1, KIAA1118
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-07-15
- Date modifiied:
- 2016-03-30
Related products to: AZI1
Related articles to: AZI1
- Messenger RNAs (mRNAs) accumulate at centrosomes in mitosis and interphase, yet the mechanisms governing their localization and their functional significance remain poorly understood. Here, we identify a centriolar satellite - RNA-binding protein (RBP) pathway that regulates CEP350 mRNA localization and stability to support centriole overduplication. We find that CEP350 mRNA localizes to centrosomes in S phase in a microtubule (MT)-dependent manner. The RBP, UNK and centriolar satellite protein, CEP131 stabilize CEP350 mRNA and promote its steady-state levels and centrosomal protein accumulation. CEP350 is required for PLK4-induced centriole overduplication but has limited effects on canonical centriole duplication. Disrupting the centriolar satellite - RBP pathway reduces centriole overduplication in triple-negative breast cancer cells, indicating CEP131 and UNK are potential therapeutic targets for reducing centriole overduplication. - Source: PubMed
Publication date: 2026/08/05
Martinez AbrahamPearson Chad G - The CCL5/CCR5 axis plays a pivotal role in tumor progression and metastasis. We previously reported CCR5 promoted melanoma EMT and metastasis by upregulating TGFβ1 expression via the PI3K/AKT/GSK3β pathway. However, the full spectrum of downstream events triggered by CCR5 activation remains poorly understood. - Source: PubMed
Publication date: 2026/06/22
Xie LifenZhu TianhuiHe AnWu QinZeng JinfengHuang LiqinZhang LingLiu Jie - Multiple morphological abnormalities of the sperm flagellum (MMAF) is a phenotypically severe but genetically heterogeneous subtype of asthenoteratozoospermia. The genetic etiology of MMAF patients is still largely unknown. - Source: PubMed
Publication date: 2026/06/16
Chen XuelingLi ZhuyuLiu WenshengZhao JindongLong ChaoxueChi KekeWang ShiyangWei XiaoliSha YanweiShan Lianhai - Vascular remodeling is crucial for establishing a functional vasculature and maintaining organ homeostasis. In the central nervous system (CNS), Wnt signaling plays a critical role in guiding endothelial cell (EC) behavior during vascular development and specialization. While canonical Wnt/β-catenin signaling regulates endothelial specification and blood-brain barrier formation, the non-canonical Wnt/Planar Cell Polarity (PCP) pathway orchestrates vascular remodeling and flow adaptation. However, how PCP signaling is transduced into intracellular polarity control remains unknown. Here, we identify MCC (Mutated in Colorectal Cancer) as a key regulator of endothelial polarity and migration downstream of the Wnt/PCP signaling pathway. Mechanistically, MCC interacts with the centriolar satellite protein CEP131 and promotes its turnover through proteasome- and autophagy-dependent pathways, thereby maintaining centrosome-associated organization required for directional polarity. MCC depletion disrupts directional polarity while preserving and enhancing flow-induced cytoskeletal elongation, revealing a functional dissociation between alignment and front-rear polarization. In vivo, endothelial-specific deletion of Mcc in the postnatal retina impairs vascular remodeling, reduces endothelial proliferation, and disrupts polarity at the angiogenic front. Notably, normalization of vascular density and regression by captopril does not restore polarity, indicating a cell-intrinsic role for MCC in endothelial organization. Together, these findings uncover an MCC-CEP131 axis linking Wnt/PCP signaling to centrosome-associated proteostasis and identify MCC as a key coordinator of endothelial polarity during vascular remodeling. - Source: PubMed
Publication date: 2026/06/15
Delobel ValentinJaspard BéatriceSalami MalvinaCamoin MarionPeghaire ClaireVaurs JulietteBoulestreau RomainKohonen-Corish MaijaDubrac AlexandreCouffinhal ThierryDuplàa Cécile - Messenger RNAs (mRNAs) accumulate at centrosomes in mitosis and interphase, yet the mechanisms governing their localization and the functional significance of centrosomal localization remain poorly understood. Here, we investigate the regulation and function of the centrosome-localized mRNA, . We find that mRNA localizes to centrosomes during S phase via the centriolar satellite protein CEP131 and the RNA binding protein (RBP) Unkempt (UNK), in a microtubule (MT)-dependent manner. CEP131 and UNK stabilize mRNA to maintain mRNA steady-state levels. Furthermore, CEP131 and UNK promote normal CEP350 protein levels at centrosomes. CEP350 is required for PLK4-induced centriole overduplication but is less important for canonical centriole duplication. Moreover, CEP131, UNK, and CEP350 are important for centrosome amplification in triple-negative breast cancer cells. Together, these findings reveal a centriolar satellite-RBP pathway regulating mRNA localization to centrosomes. - Source: PubMed
Publication date: 2026/03/26
Martinez AbrahamPearson Chad G