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anti-Human KIF3A Antibodies:
anti-Mouse (Murine) KIF3A Antibodies:
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Human Monoclonal KIF3A Primary Antibody for IF, WB - ABIN968567
Hirokawa: Kinesin and dynein superfamily proteins and the mechanism of organelle transport. in Science (New York, N.Y.) 1998
Show all 3 Pubmed References
Inhibition of kif3a in the human dental follicle cells (hDFCs) and human dental pulp cells (hDPCs) is disrupted primary cilia formation and/or function, and it was shown that kif3a is important in the differentiation of hDFCs and hDPCs through the Wnt (show WNT2 Antibodies) pathway.
High KIF3A expression is associated with glioblastoma.
These data suggest that GLI (show GLI1 Antibodies) interactions with KIF3A-KIF3B (show KIF3B Antibodies)-KAP3 (show KIFAP3 Antibodies) complexes are essential for proper GLI (show GLI1 Antibodies) transcriptional activity.
KIF3A and OVOL1 (show OVOL1 Antibodies) 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 Antibodies) expression, suggesting that phosphorylation of KIF3A is the primary mechanism of viral suppression of CD1d (show CD1D Antibodies) expression.
Findings support the notion that upregulation of KIF3a is causal of aberrant activation of Wnt (show WNT2 Antibodies) signaling in advanced prostate cancer through the KIF3a-DVL2 (show DVL2 Antibodies)-beta-catenin (show CTNNB1 Antibodies) axis.
POPX2 (show PPM1F Antibodies) 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 Antibodies)) to the subdistal appendages of mother centrioles, critical for centrosomes to function as microtubule-organizing centres.
Cell senescence is a central feature in nephronophthisis type 7 and Kif3a is unexpectedly required for efficient DNA damage response and cell cycle arrest.
genetically ablated Kif3a, Ift88 (show IFT88 Antibodies), and Ttc21b (show TTC21B Antibodies) in a series of specific spatiotemporal domains. The resulting phenotypes allow us to draw several conclusions. First, we conclude that the Ttc21b (show TTC21B Antibodies) cortical phenotype is not due to the activity of Ttc21b (show TTC21B Antibodies) within the brain itself
Airway epithelial KIF3A suppresses Th2 pulmonary inflammation and airway hyperresponsiveness following aeroallergen exposure, implicating epithelial microtubular functions in the pathogenesis of Th2-mediated lung pathology.
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 Antibodies)/Kif3a/Trp53 (show TP53 Antibodies) mutant kidneys compared to Kif3a/Trp53 (show TP53 Antibodies) or Vhl (show VHL Antibodies)/Kif3a mutant kidneys.
Data suggest biocatalysis by Kif3a homodimer, Kif3c (show KIF3C Antibodies) homodimer, or Kif3a/Kif3c (show KIF3C Antibodies) heterodimer vary; microtubule interaction is very fast for Kif3a homodimer; Kif3c (show KIF3C Antibodies) homodimer interaction is much slower; Kif3a/Kif3c (show KIF3C Antibodies) heterodimer interaction is intermediate.
KIF1-binding protein (show KIAA1279 Antibodies) interacts with KIF3A in haploid male germ cells, promoting spermatid elongation.
Vhl (show VHL Antibodies) 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 Antibodies) in homeostatic synaptic plasticity.
The results demonstrate that visual pigments transport to the retinal outer segment despite removal of KIF3 and IFT88 (show IFT88 Antibodies), and KIF3-mediated anterograde IFT is responsible for photoreceptor transition zone and axoneme formation.
Processivity of the kinesin-2 (show KIF2A Antibodies) KIF3A results from rear head gating and not front head gating.
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