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Inhibition of kif3a in the human dental follicle cells (hDFCs) and human dental pulp cells (hDPCs) is disrupted primary cilia formation (show PIFO Proteins) and/or function, and it was shown that kif3a is important in the differentiation of hDFCs and hDPCs through the Wnt (show WNT2 Proteins) pathway.
High KIF3A expression is associated with glioblastoma.
These data suggest that GLI (show GLI1 Proteins) interactions with KIF3A-KIF3B (show KIF3B Proteins)-KAP3 (show KIFAP3 Proteins) complexes are essential for proper GLI (show GLI1 Proteins) transcriptional activity.
KIF3A and OVOL1 (show OVOL1 Proteins) are involved in the development of Atopic dermatitis in the Chinese pediatric population.
both motor domains of KIF3A/B coordinate for processive motility and move at different speeds
Ablation of this phosphorylation abolished herpes simplex virus 1 US3-mediated downregulation of CD1d (show CD1D Proteins) expression, suggesting that phosphorylation of KIF3A is the primary mechanism of viral suppression of CD1d (show CD1D Proteins) expression.
Findings support the notion that upregulation of KIF3a is causal of aberrant activation of Wnt (show WNT2 Proteins) signaling in advanced prostate cancer through the KIF3a-DVL2 (show DVL2 Proteins)-beta-catenin (show CTNNB1 Proteins) axis.
POPX2 (show PPM1F Proteins) affects trafficking by determining the phosphorylation status of KIF3A at serine 690.
Association of KIF3A, but not OVOL1 and ACTL9, with atopic eczema in Italian patients
in addition to its ciliogenic roles, Kif3a recruits p150(Glued (show DCTN1 Proteins)) to the subdistal appendages of mother centrioles, critical for centrosomes to function as microtubule-organizing centres.
Longitudinal microcomputed tomography (muCT) imaging and histopathological analyses revealed an increased rate of cyst formation, increased proportion of cysts with proliferating cells, higher frequency of atypical cysts as well as the development of neoplasms in Vhl (show VHL Proteins)/Kif3a/Trp53 (show TP53 Proteins) mutant kidneys compared to Kif3a/Trp53 (show TP53 Proteins) or Vhl (show VHL Proteins)/Kif3a mutant kidneys.
Data suggest biocatalysis by Kif3a homodimer, Kif3c (show KIF3C Proteins) homodimer, or Kif3a/Kif3c (show KIF3C Proteins) heterodimer vary; microtubule interaction is very fast for Kif3a homodimer; Kif3c (show KIF3C Proteins) homodimer interaction is much slower; Kif3a/Kif3c (show KIF3C Proteins) heterodimer interaction is intermediate.
KIF1-binding protein (show KIAA1279 Proteins) interacts with KIF3A in haploid male germ cells, promoting spermatid elongation.
Vhl (show VHL Proteins) and Kif3a deletion accelerates renal cyst formation
The results of this study suggested thatactivity-dependent cargo loading, in which phosphorylation of the KIF3A C terminus upregulates the loading and transport of N-cadherin (show CDH2 Proteins) in homeostatic synaptic plasticity.
The results demonstrate that visual pigments transport to the retinal outer segment despite removal of KIF3 and IFT88 (show IFT88 Proteins), and KIF3-mediated anterograde IFT is responsible for photoreceptor transition zone and axoneme formation.
Processivity of the kinesin-2 (show KIF2A Proteins) KIF3A results from rear head gating and not front head gating.
A ciliopathy with hydrocephalus, isolated craniosynostosis, hypertelorism, and clefting caused by deletion of Kif3a
KIF3AB exhibits novel ATPase activity.
single-molecule motility from different kinesin-1 and kinesin-2 (show KIF2A Proteins) neck-linker chimeras stepping along microtubules, was studied.
mouse homolog is a molecular motor protein involved in the development of primary cilia
kinesin family protein 3A
, kinesin-like protein KIF3A
, microtubule plus end-directed kinesin motor 3A
, DNA sequence AF180004
, DNA sequence AF180009
, N-4 kinesin
, kinesin-II subunit