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Kinesin family member 1C

KIF1C, Ltxs1, KIF1D
microtubule-based molecular motor which is responsible for transporting membrane-bound organelles [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: CAN, ACID, Actin, KIF5B, HAD
Papers on KIF1C
Positioning of AMPA Receptor-Containing Endosomes Regulates Synapse Architecture.
Hoogenraad et al., Utrecht, Netherlands. In Cell Rep, Dec 2015
By using chemically induced dimerization systems to recruit kinesin (KIF1C) or myosin (MyosinV/VI) motors to Rab11-positive recycling endosomes, we controlled their trafficking and found that induced removal of recycling endosomes from spines decreases surface AMPAR expression and PSD-95 clusters at synapses.
Podosome-regulating kinesin KIF1C translocates to the cell periphery in a CLASP-dependent manner.
Kaverina et al., Nashville, United States. In J Cell Sci, 2015
The kinesin KIF1C is known to regulate podosomes, actin-rich adhesion structures that remodel the extracellular matrix during physiological processes.
Rab6 regulation of the kinesin family KIF1C motor domain contributes to Golgi tethering.
Pfeffer et al., Stanford, United States. In Elife, 2014
We report here a novel function for KIF1C: it transports Rab6A-vesicles and can influence Golgi complex organization.
Microtubule acetylation regulates dynamics of KIF1C-powered vesicles and contact of microtubule plus ends with podosomes.
Linder et al., Hamburg, Germany. In Eur J Cell Biol, 2014
We show that microtubule acetylation influences the subcellular distribution of vesicles associated with the kinesin KIF1C, as well as their directionality, velocity and run length.
Motor protein mutations cause a new form of hereditary spastic paraplegia.
Schüle et al., Tübingen, Germany. In Neurology, 2014
RESULTS: In 2 families, we identified compound heterozygous or homozygous mutations in the kinesin gene KIF1C to cause hereditary spastic paraplegia type 58 (SPG58).
Kinesin family deregulation coordinated by bromodomain protein ANCCA and histone methyltransferase MLL for breast cancer cell growth, survival, and tamoxifen resistance.
Chen et al., Sacramento, United States. In Mol Cancer Res, 2014
Estrogen strongly induces expression of 19 kinesin genes such as Kif4A/4B, Kif5A/5B, Kif10, Kif11, Kif15, Kif18A/18B, Kif20A/20B, Kif21, Kif23, Kif24, Kif25, and KifC1, whereas suppresses the expression of seven others, including Kif1A, Kif1C, Kif7, and KifC3.
KIF1C mutations in two families with hereditary spastic paraparesis and cerebellar dysfunction.
Edvardson et al., Jerusalem, Israel. In J Med Genet, 2014
Here we report a novel genetic defect in KIF1C of patients with spastic paraparesis and cerebellar dysfunction in two consanguineous families of Palestinian and Moroccan ancestry.
Directional persistence of migrating cells requires Kif1C-mediated stabilization of trailing adhesions.
Straube et al., Warwick, United Kingdom. In Dev Cell, 2013
Here, we show that the microtubule motor Kif1C contributes to persistent cell migration primarily through stabilization of an extended cell rear.
Identification of Orch3, a locus controlling dominant resistance to autoimmune orchitis, as kinesin family member 1C.
Teuscher et al., Burlington, United States. In Plos Genet, 2011
Here, by utilizing a forward genetic approach, we identified kinesin family member 1C (Kif1c) as a positional candidate for Orch3 and, using a transgenic approach, demonstrated that Kif1c is Orch3.
Pericentrosomal targeting of Rab6 secretory vesicles by Bicaudal-D-related protein 1 (BICDR-1) regulates neuritogenesis.
Hoogenraad et al., Rotterdam, Netherlands. In Embo J, 2010
BICDR-1 interacts with kinesin motor Kif1C, the dynein/dynactin retrograde motor complex, regulates the pericentrosomal localization of Rab6-positive secretory vesicles and is required for neural development in zebrafish.
Exclusion of Kif1c as a candidate gene for anthrax toxin susceptibility.
Tanaka et al., Tokyo, Japan. In Microb Pathog, 2010
Kif1c was excluded as a candidate anthrax susceptibility gene
Antimitotic effect of the retinoid 4-oxo-fenretinide through inhibition of tubulin polymerization: a novel mechanism of retinoid growth-inhibitory activity.
Formelli et al., Milano, Italy. In Mol Cancer Ther, 2009
Data show that 4-oxo-4-HPR inhibited tubulin polymerization and modulated gene expression of spindle aberration associated genes Kif 1C, Kif 2A, Eg5, Tara, tankyrase-1, centractin, and TOGp.
Mutational evolution in a lobular breast tumour profiled at single nucleotide resolution.
Aparicio et al., Vancouver, Canada. In Nature, 2009
Five of the 32 mutations (in ABCB11, HAUS3, SLC24A4, SNX4 and PALB2) were prevalent in the DNA of the primary tumour removed at diagnosis 9 years earlier, six (in KIF1C, USP28, MYH8, MORC1, KIAA1468 and RNASEH2A) were present at lower frequencies (1-13%), 19 were not detected in the primary tumour, and two were undetermined.
Kif5B and Kifc1 interact and are required for motility and fission of early endocytic vesicles in mouse liver.
Wolkoff et al., United States. In Mol Biol Cell, 2007
More than 90% of early endocytic vesicles associated with Kifc1 also contained Kif5B, and inhibition of Kifc1 with antibody resulted in enhancement of plus-end-directed motility.
The kinesin KIF1C and microtubule plus ends regulate podosome dynamics in macrophages.
Linder et al., München, Germany. In Mol Biol Cell, 2006
Hairpin RNA-based depletion of KIF1C resulted in decreased podosome dynamics and ultimately in podosome deficiency.
Nalp1b controls mouse macrophage susceptibility to anthrax lethal toxin.
Dietrich et al., Boston, United States. In Nat Genet, 2006
This trait difference has been mapped to a locus on chromosome 11 named Ltxs1 (refs.
Quickening the pace of anthrax research: three advances point towards possible therapies.
Leppla et al., In Trends Microbiol, 2002
Finally, the susceptibility of certain inbred mice to anthrax lethal toxin was associated with mutations in the kinesin-like protein Kif1C, a discovery that could help to explain how anthrax toxin kills animals.
Anthrax: a motor protein determines anthrax susceptibility.
Hanna, Ann Arbor, United States. In Curr Biol, 2001
A new study has found that polymorphisms in the host gene kif1C, which encodes a kinesin-like motor protein, determine whether mouse macrophages are resistant or sensitive to anthrax lethal toxin.
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