KIF9 antibody - N-terminal region (ARP33966_P050)
- Known as:
- KIF9 (anti-) - N-terminal region (ARP33966_P050)
- Catalog number:
- arp33966_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- KIF9 antibody - N-terminal region (ARP33966_P050)
Related genes to: KIF9 antibody - N-terminal region (ARP33966_P050)
- Gene:
- KIF9 NIH gene
- Name:
- kinesin family member 9
- Previous symbol:
- -
- Synonyms:
- MGC104186
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-24
- Date modifiied:
- 2014-11-19
Related products to: KIF9 antibody - N-terminal region (ARP33966_P050)
Related articles to: KIF9 antibody - N-terminal region (ARP33966_P050)
- This study elucidates the molecular pathogenesis of neurodevelopmental deficits in Chinese Allan-Herndon-Dudley syndrome (AHDS) patients caused by pathogenic SLC16A2 mutations. Genetic analysis of three Han Chinese patients with severe intellectual disability and global developmental delay identified two novel truncating mutations (c.1093del [p.A365Lfs35] and c.270_271del [p.G91Lfs28]) and a hemizygous de novo splice-site mutation (c.1026 + 1G > A). Structural modeling predicted that the c.1093del variant causes C-terminal truncation of transmembrane helix 12, which is likely to disrupt the T3-binding pocket by impairing the critical Arg445–His415 hydrogen bond. Functional studies confirmed significantly reduced SLC16A2 expression ( < 0.05) accompanied by dysregulated thyroid metabolism (increased and ; < 0.01) and downregulated neurodevelopmental genes ( and ; < 0.001). Mechanistically, MCT8 deficiency impaired cerebral thyroid hormone uptake, driving synaptic and axonal defects through dysregulation of both transcriptional and cytoskeletal programs: T3-dependent transcriptional suppression via inactivation of the promoter thyroid response element, and disruption of the signaling axis. These findings establish novel genotype-phenotype correlations in Chinese AHDS patients and provide a mechanistic framework for understanding the neurodevelopmental consequences of impaired thyroid hormone transport, with patient-derived iPSCs serving as a valuable resource for future therapeutic development. - Source: PubMed
Publication date: 2026/03/01
Sun XiaoangWang ChaoLin LonglongLan XiaopingWu ShengnanChen XuqinCai Cheng - Centriolar satellites are cytoplasmic granules that are localized near centrosomes and regulate centrosome and cilia function. A new study identifies a kinesin that contributes to the establishment and maintenance of their pericentrosomal distribution. - Source: PubMed
Fang Chieh-TingPelletier Laurence - Centrosomes are the principal microtubule-organizing centers of the cell, are cellular hubs for protein degradation, and play an essential role in mitotic spindle function that ultimately regulates chromosome segregation during mitosis. Centrosome maturation is achieved by strict control of protein acquisition and phosphorylation prior to mitosis. Defects in this process during interphase promote fragmentation of pericentriolar material once cells enter mitosis due to the increased forces exerted over the centrosome by the mitotic spindle, finally culminating in multipolar spindles and chromosome missegregation. Centriolar satellites, membrane-less assemblies of proteins involved in the trafficking of proteins toward and away from the centrosome, are thought to contribute to centrosome biogenesis. Moreover, centriolar satellites also regulate the quantity of proteolytic factors reaching the centrosome. Here, we show that the microtubule plus-end-directed kinesin motor Kif9 localizes to centriolar satellites and regulates their pericentrosomal localization during interphase. Lack of Kif9 leads to aggregation of satellites closer to the centrosome and increased centrosomal protein degradation that disrupts centrosome maturation and results in chromosome congression and segregation defects during mitosis. Our data show that the kinesin Kif9 controls the position of centriolar satellites relative to the centrosome and reveal roles for Kif9 and centriolar satellites in the regulation of cellular proteostasis and mitosis. - Source: PubMed
Publication date: 2025/09/19
Vicente Juan JesusWagenbach MichaelDecarreau JustinZelter AlexMacCoss Michael JDavis Trisha NWordeman Linda - Primary cilia are nonmotile, microtubule-based structures on the surface of most vertebrate cells, acting as sensory hubs to regulate cellular responses. Their formation, maintenance, and disassembly are tightly regulated, with dysfunction linked to diseases like ciliopathies, cancer, and neurological disorders. Centriolar satellites (CS), membrane-less granules around the centrosome, are involved in protein trafficking to and from the centrosome and centrosomal function, and regulate primary cilia. We show that Kif9 loss causes CS aggregation near the centrosome, leading to defects in cilia length and altering the levels of key primary cilia proteins like TALPID3, CEP131, CEP170, and CEP290. - Source: PubMed
Vicente Juan JesusWeiss JacobWagenbach MichaelWordeman Linda - Hepatocellular carcinoma (HCC) is a highly lethal malignancy with limited treatment options, particularly for patients with advanced stages of the disease. Sorafenib, the standard first-line therapy, faces significant challenges due to the development of drug resistance. Yu explored the mechanisms by which lncRNA KIF9-AS1 regulates the stemness and sorafenib resistance in HCC using a combination of cell culture, transfection, RNA immunoprecipitation, co-immunoprecipitation, and xenograft tumor models. They demonstrate that N6-methyladenosine-modified long non-coding RNA KIF9-AS1 acts as an oncogene in HCC. This modification involves methyltransferase-like 3 and insulin-like growth factor 2 mRNA-binding protein 1, which play critical roles in regulating KIF9-AS1. Furthermore, KIF9-AS1 stabilizes and upregulates short stature homeobox 2 by promoting its deubiquitination through ubiquitin-specific peptidase 1, thereby enhancing stemness and contributing to sorafenib resistance in HCC cells. These findings provide a theoretical basis for KIF9-AS1 as a diagnostic marker and therapeutic target for HCC, highlighting the need for further investigation into its clinical application potential. - Source: PubMed
Wang NingMin Fei-TianWen Wei-BoCui Huan-Tian