KIF21A antibody - N-terminal region (ARP33932_P050)
- Known as:
- KIF21A (anti-) - N-terminal region (ARP33932_P050)
- Catalog number:
- arp33932_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- KIF21A antibody - N-terminal region (ARP33932_P050)
Related genes to: KIF21A antibody - N-terminal region (ARP33932_P050)
- Gene:
- KIF21A NIH gene
- Name:
- kinesin family member 21A
- Previous symbol:
- FEOM1
- Synonyms:
- FLJ20052
- Chromosome:
- 12q12
- Locus Type:
- gene with protein product
- Date approved:
- 2002-10-08
- Date modifiied:
- 2016-11-10
Related products to: KIF21A antibody - N-terminal region (ARP33932_P050)
Related articles to: KIF21A antibody - N-terminal region (ARP33932_P050)
- Kinesin tails are structurally diverse and mediate a range of functions, including autoinhibition, cargo binding, and microtubule regulation. Within the kinesin-4 family, KIF21A and KIF21B have emerged as key regulators of microtubule network organization and dynamics in neurons and immune cells, yet the molecular basis of this activity has remained unclear. Here, we combined single-particle cryo-electron microscopy (cryo-EM) and cryo-electron tomography (cryo-ET) to examine how the KIF21B tail engages microtubules. We find that conserved residues in the WD40 β-propeller and an adjacent N-terminal linker contact successive tubulin dimers along a single protofilament, forming an extended longitudinal binding mode that spans both the intradimer and interdimer interfaces. Cryo-EM 3D classification further revealed two distinct engagement states, a tilted state, in which the β-propeller makes partial contacts with the microtubule while the linker remains anchored, and a flat state, in which the β-propeller lies flush with the lattice surface. Cryo-ET of full-length KIF21B reveals multiple binding configurations on the microtubule lattice, including orientations consistent with crosslinking adjacent microtubules. Together, these findings provide a structural framework for tail-mediated microtubule attachment by a neuronal kinesin-4 and suggest how its distinctive WD40 domain may contribute to microtubule regulation and organization of microtubule arrays. - Source: PubMed
Publication date: 2026/07/30
Taheri AryanLaFrance BenjaminPeukes JuliaRai AnkitAkhmanova AnnaNogales Eva - KIF21A, a member of the Kinesin-4 family of motor proteins, is involved in the regulation of microtubule dynamics and intracellular transport, with emerging evidence suggesting its potential role in cancer progression. In this study, we performed an integrative analysis of over 3825 human phosphoproteomics studies to characterize site-specific phosphorylation of KIF21A. Three predominant phosphosites were identified in KIF21A (S853, S1212, and S1239) with the highest detection frequency across phosphoproteomics studies, and were analyzed for co-regulation patterns to identify potential kinase associations and functional networks. Phosphosite S853 showed a strong association with cytoskeletal organization and cortical microtubule stabilization complexes (CMSCs) components, including KANK1 (S186), PHLDB2 (S513, S42) and CLASP1 (S600, S572, S646), indicating its role in cytoskeletal organization. Upstream kinase analysis identified potential regulators, such as PAK2, RPS6KA1/A3, RPS6KB1, CHEK1/2 and CDK18/16 with site-specific variability in their associations with KIF21A predominant sites. Interestingly, phosphosite-specific correlation analysis between KIF21A and candidate kinases revealed that the KIF21A S1239 phosphosite exhibited tumor-specific correlations with CDK18 across multiple cancer types. Functional enrichment revealed that co-regulated phosphoproteins were involved in cytoskeleton regulation, cell cycle regulation, and carcinogenesis. Pan-cancer analysis demonstrated dysregulated expression of KIF21A in multiple tumor types, with stage-associated upregulation in selected cancers. Gene-level validation further supported these findings, showing consistent positive correlations between KIF21A and key regulators such as CTNND1 and PTK2, as well as other cytoskeleton and cancer-associated genes. Overall, this study highlights site-specific phosphorylation as a key regulatory mechanism of KIF21A and suggests its involvement in cytoskeleton-associated signaling networks in cancer. - Source: PubMed
Publication date: 2026/07/18
Rai Shanmitha BSujina AyadathilAhmed MukhtarKammarambath Sreeshma RavindranSubair SuhailGopalakrishnan Athira PerunellyKalasa Anil Kumar Apoorva PaiJohn LevinRaju RajeshPalollathil Akhina - Neuromuscular disorders (NMDs) affect approximately 1 in 1,000 individuals and are clinically and genetically heterogeneous. Despite advances in genomic diagnostics, many cases remain unsolved after initial sequencing. Bioinformatic reanalysis approaches provide opportunities to identify missed variants and establish novel disease genes. - Source: PubMed
Publication date: 2026/07/20
Malaichamy SivasankarPolavarapu KiranThompson RachelIdoux RomaneSpendiff SallyKarcagi VeronikaHerczegfalvi AgnesAlmomen MomenScola Rosana HerminiaLorenzoni Paulo JoséZanoteli EdmarZambon Antonio AlbertoCamelo Clara GontijoEstephan Eduardo de PaulaGeetha Thenral SRamprasad Vedam LVengalil SeenaNashi SaraswatiKeerthipriya MuddassuBaskar DiptiPreethish-Kumar VeeramaniKotambail AnanthapadmanabhaMuhmann DavidSchara-Schmidt UlrikeLaurie StevenMatalonga LeslieBeltran SergiRoos AndreasBarić IvoNalini AtchayaramLochmüller Hanns - The β cells in the pancreatic endocrine islets preferentially secrete insulin in specific subdomains of the plasma membrane adjacent to the vasculature (i.e., hot spots). Impaired insulin secretion and β -cell dysfunction are central features of Type-2 Diabetes, yet the cytoskeletal machinery that supports directional secretion and secretory hot spots remains incompletely defined. KIF21A is a plus-end-directed kinesin-4 motor protein that anchors microtubule plus ends to the cell cortex. However, the role of KIF21A in pancreatic islet endocrine cells and potential link to type 2 diabetes (T2D) remain unexplored. - Source: PubMed
Publication date: 2026/06/23
Barmaver Syed NHamilton NalaGu GuoqiangKaverina Irina - Osteosarcoma remains aggressive with poor prognosis, particularly in chemotherapy-resistant cases. This study aimed to characterize transcriptional features of chemoresistant osteosarcoma cells, establish a prognostic resistance signature, and identify therapeutic vulnerabilities. Single-cell RNA sequencing (scRNA-seq) was performed on paired pre- and post-neoadjuvant chemotherapy (NAC) specimens from three patients (6 samples; 16,272 cells). Resistance trajectories were reconstructed using Monocle 3 pseudotime analysis. A nine-gene resistance score was validated in the Peking University People's Hospital (PKPH) bulk RNA-seq cohort ( = 70) and Therapeutically Applicable Research to Generate Effective Treatments (TARGET) database ( = 87), with drug sensitivities predicted via oncoPredict. Chemotherapy reduced the malignant cell fraction but triggered expansion of cancer-associated fibroblasts and endothelial cells, creating a stromal-dominant, immune-sparse residual niche. Surviving tumor cells upregulated a nine-gene module along the resistance trajectory: , , , , , , , , and . In an independent unpaired scRNA-seq cohort (two pre- and three post-chemotherapy samples), this signature remained associated with features of chemotherapy resistance. Higher scores correlated with poorer histopathologic response (r = -0.35, = 0.006) and shorter progression-free survival [PKPH: hazard ratio (HR) = 2.4, 95% confidence interval (CI) 1.2-4.8, = 0.01; TARGET: HR = 2.1, 95%CI 1.1-4.0, = 0.02]. Of 198 compounds screened, only Pictilisib, a phosphoinositide 3-kinase (PI3K) inhibitor, showed lower predicted IC50 in the high-score subset across both datasets. However, the paired discovery cohort warrant further validation. Our paired scRNA-seq approach identifies a nine-gene signature linking pre-treatment tumor biology to NAC response and outcome. The enhanced Pictilisib sensitivity in chemoresistant tumors positions PI3K blockade as a strategy meriting prospective testing in refractory osteosarcoma. - Source: PubMed
Publication date: 2026/04/21
Hu LiZhang YaxinWang BoyangLiu QianQi FeiyangLiu HuiminLi QinghuaZhao ZhiqingLiang HaijieLiu XingyuDu ZhiyeWang Jichuan