KIF3A antibody - C-terminal region (ARP33917_P050)
- Known as:
- KIF3A (anti-) - C-terminal region (ARP33917_P050)
- Catalog number:
- arp33917_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- KIF3A antibody - C-terminal region (ARP33917_P050)
Related genes to: KIF3A antibody - C-terminal region (ARP33917_P050)
- Gene:
- KIF3A NIH gene
- Name:
- kinesin family member 3A
- Previous symbol:
- -
- Synonyms:
- FLA10, KLP-20
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-07
- Date modifiied:
- 2016-10-05
Related products to: KIF3A antibody - C-terminal region (ARP33917_P050)
Related articles to: KIF3A antibody - C-terminal region (ARP33917_P050)
- Intracellular transport is essential for neuronal organization, yet how motor proteins achieve cargo selectivity remains incompletely understood. Kinesin-2 motors transport diverse cargos through the heterotrimeric KIF3/KAP3 complex, but whether variations in assembly composition contribute to functional specificity has been unclear. This study provides evidence for heterogeneity in neuronal KIF3/KAP3 assemblies, including a KIF3B-enriched, KAP3-associated population in addition to the canonical KIF3A/B/KAP3 complex. Biochemical and cellular analyses support a preferential association between this KIF3B-enriched assembly and TRIM46, a protein required for axon initial segment organization. Structural analyses further suggest that differences in tail conformation accompany distinct assembly states and may underlie cargo selectivity. Together, these findings support a model in which compositional and structural diversity within kinesin-2 complexes contributes to spatially regulated transport during neuronal development. - Source: PubMed
Publication date: 2026/03/30
Jiang XuguangIchinose SotaroOgawa TadayukiYonezawa KentoShimizu NobutakaHirokawa Nobutaka - Disruption of the locus in epithelial and endocrine tissues fails to generate the full spectrum of gastroenteropancreatic neuroendocrine tumors (GEP-NETs), raising the possibility of a potential stromal source for these cancers. Neural crest-derived glial cells were previously implicated in neuroendocrine tumors arising in the pituitary and pancreas, yet these studies lacked a clear mechanism for these events. Here, we investigated the hypothesis that -driven Hedgehog (HH) signaling redirects the glial cell fate to give rise to neuroendocrine tumors in the gastrointestinal tract. - Source: PubMed
Publication date: 2026/02/21
Duan SuzannTwer AnneLeigh BZinkeng AtehNaciri IkrameMoore Juliette WGentry Rebeca GSontz Ricky AAyabe Reed ITapia EdgarSawyer Travis WMerchant Juanita L - Liver cancer ranks sixth in incidence and third in mortality worldwide, with hepatocellular carcinoma (HCC) accounting for 90% of cases. Kinesin family genes (KIFs) have been implicated in HCC progression, but their specific roles remain unclear. Here, using multiple transcriptomic datasets and machine learning, we systematically screened KIF genes in HCC and identified nine key differentially expressed KIFs (KIF3A, KIF3B, KIF5B, KIF11, KIF13A, KIF13B, KIF20A, KIFC3, KLC2) as diagnostic biomarkers. A logistic regression model showed excellent diagnostic accuracy (AUC = 0.992) in the GSE121248 dataset. Six genes (KIF3A, KIF5B, KIF11, KIF13B, KIF20A, KLC2) were validated in TCGA, several correlating with prognosis. Notably, KIF20A was an independent prognostic factor, validated across cohorts. Single-cell and experimental data revealed high KIF20A expression in HCC cells, promoting proliferation and migration. Mechanistically, KIF20A drives tumor growth and metastasis via Wnt/β-catenin signaling and epithelial-mesenchymal transition (EMT) proteins such as N-cadherin, Slug, Snail, and Twist1/2. Wnt pathway activator SKL2001 and inhibitor LGK974 confirmed KIF20A's role in tumor progression. Upstream, the transcription factor FOXK1 was identified as a key positive regulator of KIF20A. FOXK1 is overexpressed in HCC, strongly correlates with KIF20A, and predicts poor prognosis. ChIP-seq and promoter assays verified FOXK1's direct binding to the KIF20A promoter, activating its transcription. In conclusion, KIF20A serves as a diagnostic and prognostic biomarker promoting HCC progression via Wnt/β-catenin signaling, regulated by FOXK1, offering new therapeutic targets. - Source: PubMed
Publication date: 2026/02/19
Liu JiaxuanZhang MengLi JialingTian YuZhao JinyanLiu Xue - Intracellular transport relies on motor proteins such as kinesins to deliver cargo along microtubules, yet how they recognize cargo remains unclear. Here, we present high-resolution cryo-electron microscopy structures of the heterotrimeric kinesin-2 complex (KIF3A/KIF3B/KAP3) bound to the cargo protein APC. Our findings reveal a previously uncharacterized KIF3 tail hook-like motif, termed the "HAC" domain, which mediates binding to both KAP3 adaptor and APC cargo. Within this domain, the KIF3A helical regions ensure cargo specificity, while a β-hairpin and KIF3B provide structural support. Biochemical and neuronal experiments confirm its functional importance. Notably, the HAC/KAP3 structure resembles hook-like architectures seen in kinesin-1 and dynein, suggesting a shared cargo recognition framework. These findings also shed light on kinesin-2 cargo specificity and offer a structural framework for understanding related neuronal transport mechanisms. - Source: PubMed
Publication date: 2025/10/24
Jiang XuguangDanev RadostinIchinose SotaroNiu BaichunOhtsuki SumioYanagisawa HaruakiNagatoishi SatoruTsumoto KouheiHirokawa NobutakaKikkawa Masahide - Kinesin superfamily proteins (KIFs) are driver proteins used by microtubules for intracellular transport, cellular homeostasis, and mitosis. Reportedly, the aberration in the expression of these proteins has been found to mediate sensitivity to chemotherapy. KIF5A, KIF11, and KIF20A are consistently involved in resistance to paclitaxel and docetaxel in breast, lung, and prostate cancers, while KIF14 overexpression is a prognostic marker for poor outcomes in paclitaxel-treated triple-negative breast and cervical cancer. KIF14 and KIF23 in HCC enhance sorafenib and cisplatin resistance, while suppression of KIF5B or KIF20A increases sensitivity to oxaliplatin in colorectal cancer. Clinic-applied fusions of KIF5B with ALK or EGFR have made it possible to use targeted therapy in non-small cell lung cancer. From a mechanistic point of view, PI3K/Akt, JAK/STAT, and NF-κB activation, metabolic reprogramming, and inhibition of cellular programmed death are involved in KIF-mediated resistance. KIF3A or KIF11 silencing increases chemosensitivity, suggesting a dual role here. Present approaches-small-molecule inhibitors, microRNA modulation, and KIF20A peptide vaccines-are hopeful but are beset by issues of toxicity and specificity. Overall, KIFs are context-dependent regulators of chemoresistance and are multifunctional but promising precision oncology targets. - Source: PubMed
Publication date: 2025/09/27
Owida Hamza AbuMohammad Suleiman IbrahimVasudevan AsokanBishoyi Ashok KumarRenukaJyothi SPanigrahi RajashreeAbosaoda Munthar KadhimGarg GunjanPargaien Amrita