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Kinesin family member C3

KIFC3 belongs to the large superfamily of kinesins, molecular motors that use the energy of ATP hydrolysis to translocate cargoes along microtubules. Members share extensive homology within a globular domain containing the microtubule- and ATP-binding sites and have a coiled-coil stalk domain that mediates oligomerization. Different kinesin family members participate in specific and diverse motile processes, such as cell division, organelle transport, and nuclear movement (Hoang et al., 1998 [PubMed 9782090]).[supplied by OMIM, Mar 2009] (from NCBI)
Top mentioned proteins: KIF5B, HSET, Eg5, V1a, HAD
Papers on KIFC3
Interactome analysis reveals that FAM161A, deficient in recessive retinitis pigmentosa, is a component of the Golgi-centrosomal network.
Rivolta et al., Lausanne, Switzerland. In Hum Mol Genet, Jul 2015
Notable FAM161A interactors included AKAP9, FIP3, GOLGA3, KIFC3, KLC2, PDE4DIP, NIN and TRIP11.
Gene expression pattern of KIFC3 during spermatogenesis of the skink Eumeces chinensis.
Yang et al., Hangzhou, China. In Gene, Mar 2015
We have cloned kinesin-like gene kifc3 (termed ec-kifc3) from the total RNA of the testis of the skink Eumeces chinensis.
Minus end-directed motor KIFC3 suppresses E-cadherin degradation by recruiting USP47 to adherens junctions.
Takeichi et al., Kōbe, Japan. In Mol Biol Cell, 2015
Previous studies show that KIFC3, a minus end-directed kinesin motor, moves into AJs via microtubules that grow from clusters of CAMSAP3 (also known as Nezha), a protein that binds microtubule minus ends.
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.
Identification of the kinesin KifC3 as a new player for positioning of peroxisomes and other organelles in mammalian cells.
Dodt et al., Tübingen, Germany. In Biochim Biophys Acta, 2013
KifC3, belonging to the group of C-terminal kinesins, has been identified to interact with the human peroxin PEX1 in a yeast two-hybrid screen.
KIFC3 promotes mitotic progression and integrity of the central spindle in cytokinesis.
Müsch et al., New York City, United States. In Cell Cycle, 2013
We have identified the minus-end-directed motor, KIFC3, as an important contributor to central bridge morphology at this stage.
Intrahepatic cholestasis of pregnancy: new insights into its pathogenesis.
Gervasi et al., Padova, Italy. In J Matern Fetal Neonatal Med, 2013
Among these, three belong to genetic classes involved in pathogenic mechanisms of ICP: (1) pathophysiology of pruritus (GABRA2, cases versus controls = 2, upregulated gene); (2) lipid metabolism and bile composition (HLPT, cases versus controls = 0.6, down-regulated gene) and (3) protein trafficking and cytoskeleton arrangement (KIFC3, cases versus controls = 0.5, down-regulated gene).
Kinesin expression in the central nervous system of humans and transgenic hSOD1G93A mice with amyotrophic lateral sclerosis.
Barańczyk-Kuźma et al., Warsaw, Poland. In Neurodegener Dis, 2012
OBJECTIVE: The purpose of the study was to investigate and compare the expression of kinesins involved in anterograde (KIF5A, 5C) and retrograde (KIFC3/C2) axonal transport in SALS in humans and FALS in mice with the hSOD1G93A mutation.
Kinesin tail domains are intrinsically disordered.
Rice et al., Chicago, United States. In Proteins, 2012
In order to experimentally verify these predictions, we expressed and purified the tail domains of kinesins representing three different families (Kif5B, Kif10, and KifC3).
Specific kinesin expression profiles associated with taxane resistance in basal-like breast cancer.
Eng et al., Cleveland, United States. In Breast Cancer Res Treat, 2012
In the NCI-60 cell line dataset, overexpression of the kinesin KIFC3 is significantly correlated with resistance to both docetaxel (P < 0.001) and paclitaxel (P < 0.001), but not to platinum-based chemotherapy, including carboplatin (P = 0.49) and cisplatin (P = 0.10).
Identification of genes associated with chemosensitivity to SAHA/taxane combination treatment in taxane-resistant breast cancer cells.
Chung et al., Seoul, South Korea. In Breast Cancer Res Treat, 2011
Oligonucleotide microarray analysis identified 28 genes (MAPK13, ATP2C1, ANKRD57, MT1G, RGL4, C12orf49, EXOC6, RAB4A, TM9SF3, IFNGR1, DMD, HCG9, KIFC3, SYNGR3, NDRG4, NT5E, EOMES, SMC4, LANCL1, SCHIP1, and 8 ESTs) whose expression correlated with the combined effect of paclitaxel and SAHA.
Novel interactors and a role for supervillin in early cytokinesis.
Luna et al., Worcester, United States. In Cytoskeleton (hoboken), 2010
The interacting sequences from 12 of these proteins (BUB1, EPLIN/LIMA1, FLNA, HAX1, KIF14, KIFC3, MIF4GD/SLIP1, ODF2/Cenexin, RHAMM, STARD9/KIF16A, Tks5/SH3PXD2A, TNFAIP1) co-localize with and mis-localize EGFP-supervillin in mammalian cells, suggesting associations in vivo.
Overexpression of kinesins mediates docetaxel resistance in breast cancer cells.
Stark et al., Cleveland, United States. In Cancer Res, 2009
High expression of KIFC3 is associated with docetaxel resistance in breast cancer.
Anchorage of microtubule minus ends to adherens junctions regulates epithelial cell-cell contacts.
Takeichi et al., Kōbe, Japan. In Cell, 2008
Furthermore, we found that a minus end-directed motor, KIFC3, was concentrated at the ZA in a PLEKHA7/Nezha/MT-dependent manner; and depletion of any of these proteins resulted in disorganization of the ZA.
Kinesin superfamily proteins and their various functions and dynamics.
Takemura et al., Tokyo, Japan. In Exp Cell Res, 2004
KIFs also participate in polarized transport in epithelial cells as shown in the apical transport of annexin XIIIb-containing vesicles by KIFC3.
Role of KIFC3 motor protein in Golgi positioning and integration.
Hirokawa et al., Tokyo, Japan. In J Cell Biol, 2002
KIFC3 plays a complementary role in Golgi positioning and integration
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