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

Kinesin family member 5C

KIF5C
Top mentioned proteins: KIF5B, ACID, CAN, GRIF-1, RAN
Papers on KIF5C
Kif5 Regulates Mitochondrial Movement, Morphology, Function And Neuronal Survival.
New
Rintoul et al., Canada. In Mol Cell Neurosci, Feb 2016
We evaluated the consequences of disrupted kif5c-mediated mitochondrial trafficking on mitochondrial form and function in primary rat cortical neurons.
A novel interstitial deletion of 2q22.3 q23.3 in a patient with dysmorphic features, epilepsy, aganglionosis, pure red cell aplasia, and skeletal malformations.
New
Esmer et al., San Luis Potosí, Mexico. In Am J Med Genet A, Aug 2015
Array-CGH revealed a 7.1 Mb deletion causing haploinsufficiency of several genes including MBD5, ACVR2, KIF5C, and EPC2.
X-ray and Cryo-EM structures reveal mutual conformational changes of Kinesin and GTP-state microtubules upon binding.
New
Hirokawa et al., Tokyo, Japan. In Embo J, Jun 2015
In neurons, kinesin-1/KIF5C preferentially binds to the GTP-state microtubules over GDP-state microtubules to selectively enter an axon among many processes; however, because the atomic structure of nucleotide-free KIF5C is unavailable, its molecular mechanism remains unresolved.
New approach to capture and characterize synaptic proteome.
Puthanveettil et al., Jupiter, United States. In Proc Natl Acad Sci U S A, 2014
We used this approach to identify and compare proteins transported to synapses by kinesin (Kif) complexes Kif5C and Kif3A in the mouse hippocampus and prefrontal cortex.
Somatic mutations in cerebral cortical malformations.
Impact
Walsh et al., Boston, United States. In N Engl J Med, 2014
We found potentially causal mutations in the candidate genes DYNC1H1, KIF5C, and other kinesin genes in persons with pachygyria.
Involvement of the kinesin family members KIF4A and KIF5C in intellectual disability and synaptic function.
Kleefstra et al., Nijmegen, Netherlands. In J Med Genet, 2014
METHODS: By applying next-generation sequencing (NGS) in ID patients, we identified likely pathogenic mutations in KIF4A and KIF5C.
Protrudin regulates endoplasmic reticulum morphology and function associated with the pathogenesis of hereditary spastic paraplegia.
Nakayama et al., Fukuoka, Japan. In J Biol Chem, 2014
Protrudin was found to interact with other HSP-related proteins including myelin proteolipid protein 1 (SPG2), atlastin-1 (SPG3A), REEP1 (SPG31), REEP5 (similar to REEP1), Kif5A (SPG10), Kif5B, Kif5C, and reticulon 1, 3, and 4 (similar to reticulon 2, SPG12).
Genetic modifiers and subtypes in schizophrenia: investigations of age at onset, severity, sex and family history.
Corvin et al., Boston, United States. In Schizophr Res, 2014
Family history positive analyses showed the greatest association with KIF5C (p=1.96×10(-8)),
Familial Alzheimer's disease-associated presenilin-1 alters cerebellar activity and calcium homeostasis.
Glatzel et al., In J Clin Invest, 2014
In PS1-E280A tissue, ER/mitochondria tethering was impaired, Ca2+ channels IP3Rs and CACNA1A were downregulated, and Ca2+-dependent mitochondrial transport proteins MIRO1 and KIF5C were reduced.
Beta tubulin isoforms are not interchangeable for rescuing impaired radial migration due to Tubb3 knockdown.
Chelly et al., Paris, France. In Hum Mol Genet, 2014
Inputs from genetic studies were provided through the identification of several mutated genes encoding either proteins associated with microtubules (DCX, LIS1, KIF2A, KIF5C, DYNC1H1) or tubulin subunits (TUBA1A, TUBB2B, TUBB5 and TUBG1), in malformations of cortical development (MCD).
Silencing BMI1 eliminates tumor formation of pediatric glioma CD133+ cells not by affecting known targets but by down-regulating a novel set of core genes.
Li et al., In Acta Neuropathol Commun, 2013
Importantly, we found that silencing BMI1 in CD133+ cells derived from 3 PDOX models did not affect most of the known genes previously associated with the activated BMI1, but modulated a novel set of core genes, including RPS6KA2, ALDH3A2, FMFB, DTL, API5, EIF4G2, KIF5c, LOC650152, C20ORF121, LOC203547, LOC653308, and LOC642489, to mediate the elimination of tumor formation.
Delineation of the TRAK binding regions of the kinesin-1 motor proteins.
Stephenson et al., London, United Kingdom. In Febs Lett, 2013
To refine the TRAK1/2 binding sites within the kinesin-1 cargo domain, rationally designed C-terminal truncations of KIF5A and KIF5C were generated and their co-association with TRAK1/2 determined by quantitative co-immunoprecipitations following co-expression in mammalian cells.
Temporal and tissue specific gene expression patterns of the zebrafish kinesin-1 heavy chain family, kif5s, during development.
Marlow et al., United States. In Gene Expr Patterns, 2013
KIF5A and KIF5C proteins are strictly neural in mouse whereas, KIF5B is ubiquitously expressed.
Role of kinesin-1 in the pathogenesis of SPG10, a rare form of hereditary spastic paraplegia.
Review
Kawaguchi, Chiba, Japan. In Neuroscientist, 2013
SPG10 is an autosomal dominant form of hereditary spastic paraplegia caused by mutations in KIF5A, which encodes one of the isoforms of kinesin-1 (KIF5A, KIF5B, and KIF5C).
Mutations in TUBG1, DYNC1H1, KIF5C and KIF2A cause malformations of cortical development and microcephaly.
Impact
Chelly et al., Paris, France. In Nat Genet, 2013
Here we report the discovery of multiple pathogenic missense mutations in TUBG1, DYNC1H1 and KIF2A, as well as a single germline mosaic mutation in KIF5C, in subjects with MCD.
Sunday Driver/JIP3 binds kinesin heavy chain directly and enhances its motility.
GeneRIF
Cavalli et al., Saint Louis, United States. In Embo J, 2011
syd activates KIF5C for transport and enhances its motility, increasing both its velocity and run length.
Preferential binding of a kinesin-1 motor to GTP-tubulin-rich microtubules underlies polarized vesicle transport.
GeneRIF
Hirokawa et al., Tokyo, Japan. In J Cell Biol, 2011
data suggest that the abundance of GTP-tubulin in axonal microtubules may underlie selective KIF5 localization and polarized axonal vesicular transport
Posttranslational modifications of tubulin and the polarized transport of kinesin-1 in neurons.
GeneRIF
Verhey et al., Ann Arbor, United States. In Mol Biol Cell, 2010
motility of Kinesin-1, preferential translocation of Kinesin-1 on axonal microtubules in polarized neurons is not determined by acetylation alone but probably specified by a combination of tubulin modifications
KIF5C: a new binding partner for protein kinase CK2 with a preference for the CK2alpha' subunit.
GeneRIF
Montenarh et al., Homburg, Germany. In Cell Mol Life Sci, 2009
Results identified the motor neuron protein KIF5C as a new binding partner for the protein kinase CK2alpha'.
The kinesin I family member KIF5C is a novel substrate for protein kinase CK2.
GeneRIF
Montenarh et al., Homburg, Germany. In Biochem Biophys Res Commun, 2008
KIF5C, a member of the kinesin 1 heavy chain family, is a substrate for protein kinase CK2.
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