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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Kinesin family member 3A

mouse homolog is a molecular motor protein involved in the development of primary cilia [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: KIF3B, CAN, ACID, HAD, ROD
Papers on KIF3A
Disruption of KIF3A in patient-derived glioblastoma cells: effects on ciliogenesis, hedgehog sensitivity, and tumorigenesis.
Sarkisian et al., Gainesville, United States. In Oncotarget, Feb 2016
UNASSIGNED: KIF3A, a component of the kinesin-2 motor, is necessary for the progression of diverse tumor types.
Kinesin-2 KIF3AC: Fast or Slow Either Head Can Start the Processive Run.
Gilbert et al., United States. In J Biol Chem, Jan 2016
The hypothesis tested was whether there is an intrinsic bias within KIF3AC such that either KIF3A or KIF3C initiates the processive run.
Kinesin family 17 (osmotic avoidance abnormal-3) is dispensable for photoreceptor morphology and function.
Baehr et al., Salt Lake City, United States. In Faseb J, Dec 2015
In Caenorhabditis elegans, homodimeric [kinesin family (KIF) 17, osmotic avoidance abnormal-3 (OSM-3)] and heterotrimeric (KIF3) kinesin-2 motors are required to establish sensory cilia by intraflagellar transport (IFT) where KIF3 and KIF17 cooperate to build the axoneme core and KIF17 builds the distal segments.
Mechanism of Activity-Dependent Cargo Loading via the Phosphorylation of KIF3A by PKA and CaMKIIa.
Hirokawa et al., Tokyo, Japan. In Neuron, Oct 2015
To elucidate this mechanism, we investigated the activity-dependent transport of N-cadherin via its transporter, KIF3A.
KIF1-binding protein interacts with KIF3A in haploid male germ cells.
Sironen et al., Turku, Finland. In Reproduction, Sep 2015
Previously, we have demonstrated that a microtubule-based anterograde transport motor protein KIF3A is required for the sperm tail formation and nuclear shaping during spermatogenesis.
Meta-analysis identifies seven susceptibility loci involved in the atopic march.
Lee et al., Berlin, Germany. In Nat Commun, 2014
IL4/KIF3A (5q31.1),
Kinesin-2 family motors in the unusual photoreceptor cilium.
Besharse et al., Sheffield, United Kingdom. In Vision Res, 2013
This is thought to occur because both kif3b or kif3c can dimerize with kif3a and function redundantly.
Genome-wide association study identifies eight new susceptibility loci for atopic dermatitis in the Japanese population.
Tamari et al., Yokohama, Japan. In Nat Genet, 2012
We also replicated the associations of the FLG, C11orf30, TMEM232-SLC25A46, TNFRSF6B-ZGPAT, OVOL1, ACTL9 and KIF3A-IL13 loci that were previously reported in GWAS of European and Chinese individuals and a meta-analysis of GWAS for atopic dermatitis.
Meta-analysis of genome-wide association studies identifies three new risk loci for atopic dermatitis.
EArly Genetics & Lifecourse Epidemiology (EAGLE) Consortium et al., Bristol, United Kingdom. In Nat Genet, 2012
P = 7.1 × 10(-9)), both of which are near genes that have been implicated in epidermal proliferation and differentiation, as well as rs2897442 in KIF3A within the cytokine cluster at 5q31.1 (OR = 1.11,
Cilia, KIF3 molecular motor and nodal flow.
Okada et al., Tokyo, Japan. In Curr Opin Cell Biol, 2012
The establishment of left-right asymmetry during development of vertebrate embryos depends on leftward flow in the nodal cavity.
Association of the testis-specific TRIM/RBCC protein RNF33/TRIM60 with the cytoplasmic motor proteins KIF3A and KIF3B.
Chang et al., Taipei, Taiwan. In Mol Cell Biochem, 2012
our data suggest that RNF33 most likely interacts with KIF3A-KIF3B independent of the adaptor kinesin-associated protein KAP3
Mechanosensing by the primary cilium: deletion of Kif3A reduces bone formation due to loading.
Jacobs et al., Palo Alto, United States. In Plos One, 2011
Deletion of Kif3A reduces bone formation due to loading.
TMJ development and growth require primary cilia function.
Koyama et al., Philadelphia, United States. In J Dent Res, 2011
Kif3a and primary cilia are required for coordination of chondrocyte maturation, intramembranous bone formation, and chondrogenic condylar growth
Kif3a regulates planar polarization of auditory hair cells through both ciliary and non-ciliary mechanisms.
Lu et al., Charlottesville, United States. In Development, 2011
show that the microtubule motor subunit Kif3a regulates hair cell polarization through both ciliary and non-ciliary mechanisms
Identification of KIF3A as a novel candidate gene for childhood asthma using RNA expression and population allelic frequencies differences.
Hershey et al., Cincinnati, United States. In Plos One, 2010
KIF3A is a novel candidate gene for childhood asthma
Ciliary entry of the kinesin-2 motor KIF17 is regulated by importin-beta2 and RanGTP.
Verhey et al., Ann Arbor, United States. In Nat Cell Biol, 2010
The biogenesis, maintenance and function of primary cilia are controlled through intraflagellar transport (IFT) driven by two kinesin-2 family members, the heterotrimeric KIF3A/KIF3B/KAP complex and the homodimeric KIF17 motor.
Left-right determination: involvement of molecular motor KIF3, cilia, and nodal flow.
Okada et al., Tokyo, Japan. In Cold Spring Harb Perspect Biol, 2009
KIF3, cilia, and nodal flow have roles in left-right determination [review]
Gardner's syndrome (familial adenomatous polyposis): a cilia-related disorder.
Knoers et al., Maastricht, Netherlands. In Lancet Oncol, 2009
Other candidates for the common link between Gardner's syndrome and cilia-related disorders are the APC-binding proteins: end-binding protein 1 (EB1) and kinesin-family-member 3a (KIF3a), both of which are ciliary proteins involved in intraflagellar transport.
Beta-arrestin-mediated localization of smoothened to the primary cilium.
Lefkowitz et al., Durham, United States. In Science, 2008
findings indicate that, together, beta-arrestins and Kif3A may mediate the transport of Smo to the primary cilium
Nodal flow and the generation of left-right asymmetry.
Takeda et al., Tokyo, Japan. In Cell, 2006
These cilia are built by transport via the KIF3 motor complex.
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