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KIF14 (kinesin family member 14)

Identity

Other namesKIAA0042
HGNC (Hugo) KIF14
LocusID (NCBI) 9928
Location 1q32.1
Location_base_pair Starts at 200520625 and ends at 200589862 bp from pter ( according to hg19-Feb_2009)  [Mapping]
Local_order Genes flanking KIF14 at 1q32.1 are (centromeric to telomeric): ZNF281 (zinc finger protein 281), KIF14, DDX59 (DEAD (Asp-Glu-Ala-Asp) box polypeptide 59).

DNA/RNA

Description Gene spans 68,5 kbp on the minus strand at 1q32.1.
Transcription One known 6586 base transcript, 30 exons. The KIF14 promoter is bound by p130/E2F4 under growth arrest conditions (Cam et al., 2004); further details of transcriptional regulation are currently lacking.
Pseudogene None annotated.

Protein

 
  Schematic representation of the KIF14 protein (not to scale). KIF14 contains two major effector domains. The first is a highly conserved 274 aa kinesin motor domain containing an ATP-binding site (aa 447-454) which is involved in microtubule-dependent ATPase activity, and a microtubule binding site (aa 455-628) involved in ATP-dependent protein transport. The second is a 67 aa forkhead-associated (FHA) domain (aa 825-891) which has similarity to the SMAD Mad Homology 2 (MH2) domain, and is involved in mediating protein-protein interactions with phosphoproteins, although no such interactions have been documented for KIF14 (Durocher et al., 2000). In addition to the highly conserved N-type neck region (N) adjacent to the motor domain, KIF14 also contains four other C-terminal regions predicted to form coiled-coil structures (1-4). Phosphorylation sites have been identified in high-throughput studies on Ser-12, Tyr-196, Thr-240, Ser-242, Ser-378, Ser-384, Ser-670, Ser-1200, Ser-1292, Ser-1631, Ser-1636 and Thr-1641 (P) (Nomura et al., 1994; Olsen et al., 2006; Vasilescu et al., 2007; Dephoure et al., 2008), and a ubiquitination site identified on Lys-275 (U) (Olsen et al., 2006; Vasilescu et al., 2007). The kinesin motor and FHA domains are flanked by a 354 aa N-terminal extension, and a 758 aa C-terminal stalk and tail region. The N-terminal extension is involved in the binding of PRC1 (protein-regulating cytokinesis 1), a protein crucial for the proper formation of the central spindle structure during cytokinesis. Citron kinase has been shown to interact with the C-terminal stalk and tail of KIF14, and this interaction is required for proper localization of KIF14 to the mitotic spindle. Supervillin, a membrane protein involved in directing cellular motility, has been shown to associate directly with the distal C-terminal tail of KIF14 and contributes to the establishment or maintenance of the cytokinetic furrow (Smith et al., 2010).
Description KIF14 is a 186 kDa, 1648 aa protein, containing kinesin motor and forkhead-associated (FHA) domains. It is a member of the N-3 family of kinesins, in which the motor domain lies close to the amino terminus (Miki et al., 2001), although the relatively long N-terminal extension in KIF14 is unique in this family. High-throughput studies have identified phosphorylations on Ser-12, Tyr-196, Thr-240, Ser-242, Ser-378, Ser-384, Ser-670, Ser-1200, Ser-1292, Ser-1631, Ser-1636 and Thr-1641 (P) (Nomura et al., 1994; Olsen et al., 2006; Vasilescu et al., 2007; Dephoure et al., 2008), and ubiquitination on Lys-275 (U) (Olsen et al., 2006; Vasilescu et al., 2007).
Expression KIF14 was cloned from an immature myeloid cell line, KG-1 (Nomura et al., 1994). By qRT-PCR, KIF14 is expressed at low levels in normal adult tissues and at higher levels in placenta and fetal tissues; highest expression is in fetal thymus and liver (Corson et al., 2005). KIF14 expression varies with the cell cycle, with highest expression at G2-M (Carleton et al., 2006).
Localisation In HeLa cells, KIF14 is localized to the cytoplasm during interphase, and becomes tightly localized to the midbody and central spindle during cytokinesis (Carleton et al., 2006; Gruneberg et al., 2006).
Function KIF14 is a mitotic kinesin motor protein with ATPase activity (Carleton et al., 2006). It interacts with protein regulator of cytokinesis 1 (PRC1) and is essential for localizing citron kinase to the mitotic spindle (Gruneberg et al., 2006). KIF14 knockdown results in failure of cytokinesis, leading to multinucleation and/or apoptosis, but no chromosome segregation defects (Carleton et al., 2006; Gruneberg et al., 2006). KIF14 also interacts with supervillin and contributes to the establishment or maintenance of the cytokinetic furrow (Smith et al., 2010). In addition, KIF14 was identified as a β-arrestin 2 interacting protein in the nucleus of mature spermatozoa (Neuhaus et al., 2006).
Homology There are KIF14 orthologs in several mammalian species. The closest Drosophila melanogaster gene, with 40% amino acid identity, is nebbish/tiovivo, encoding Klp38B (kinesin-like protein 38B). Klp38B is a mitotic kinesin that binds to chromatin and microtubules in the formation of the bipolar spindle and attachment of chromosomes to the spindle, and/or acts in cytokinesis (Molina et al., 1997; Ohkura et al., 1997).

Mutations

Germinal None yet identified.
Somatic Missense somatic mutations were detected in two metastatic melanomas. Each mutations was heterozygous and observed in a single tumor. They were c.1490 C>T, P351S and c.1539 C>T, P367L (Wei et al., 2011).
Heterozygous somatic mutations were detected in five breast ductal carcinoma tumors. Each mutation was observed in a single tumor and included three missense mutations (c.3676T>A, p.S1226T; c.4363G>C, p.E1455Q and c.1A>G, p.M1V), one synonymous mutation (c.4539T>A, p.A1513A), and one nonsense mutation (c.4402G>T, p.E1468*) (Wood et al., 2007).
Missense heterozygous somatic mutations were detected in two ovarian carcinomas and each mutation was observed in a single tumor: c.2096G>A, p.R699H and c.4654C>T, p.P1552S (Cancer Genome Atlas Research Network, 2011).

Implicated in

Entity Retinoblastoma
Prognosis KIF14 mRNA and protein expression is greatly increased in retinoblastoma tumors versus normal adult and fetal retina (Corson et al., 2005). mRNA expression is higher in older patients' tumors than younger (Madhavan et al., 2007), and shows a modest association with unilateral disease (Madhavan et al., 2009). KIF14 mRNA level increases with the progression from normal retina to benign retinoma to retinoblastoma (Dimaras et al., 2008).
Cytogenetics KIF14 lies in a "hotspot" of genomic gain at 1q31.3-1q32.1 (Corson et al., 2005). Low-level genomic gain (3-5 copies) of the gene is observed in 50% of tumors (Bowles et al., 2007). High-level amplification has been observed in one tumor (along with, but independent of, MYCN amplification) (Bowles et al., 2007). KIF14 copy number increases during the progression from normal retina to benign retinoma to retinoblastoma (Dimaras et al., 2008).
Oncogenesis In support of KIF14's importance in retinoblastoma, the mouse ortholog Kif14 is expressed in retinal tumors in the retinal SV40 Large T Antigen (TAg-RB) model of retinoblastoma at levels higher than at any point in mouse retinal development (Pajovic et al., 2011).
  
Entity Breast carcinoma
Prognosis mRNA expression increases with grade, and is higher in ductal than lobular carcinoma, and in estrogen receptor (ER) negative over ER positive tumors. Expression correlates with proliferation, and overexpression is prognostic for poor overall and disease-free survival (Corson and Gallie, 2006).
Cytogenetics KIF14 lies in a "hotspot" of genomic gain at 1q31.3-1q32.1. Low-level genomic gain of the gene is observed in 50% of breast cancer cell lines (Bowles et al., 2007).
  
Entity Non-small-cell lung carcinoma (NSCLC)
Prognosis mRNA expression decreases with differentiation, and is higher in squamous cell than adenocarcinoma. Overexpression is independently prognostic for poor disease-free survival, and prognostic for poor overall survival (Corson et al., 2007).
Oncogenesis Knockdown of KIF14 decreases proliferation of H1299 NSCLC cells, and decreases their ability to form colonies in soft agar (Corson et al., 2007).
  
Entity Ovarian carcinoma
Prognosis KIF14 is overexpressed in the majority of ovarian cancers tested (91%). KIF14 mRNA expression is independently prognostic for poor overall survival and prognostic for poor progression-free survival in serous ovarian cancers (Thériault et al., 2012).
Cytogenetics Low-level gain (3 to 5 copies) of KIF14 is observed in 30% of serous ovarian cancers, and corresponds to high mRNA overexpression (Thériault et al., 2012). KIF14 was the only gene within the documented 1q "hot spot" region of gain (1q31.3-1q32.1) (Corson et al., 2005) to be overexpressed in ovarian carcinomas compared to normal tubal epithelium and ovarian surface epithelium (Thériault et al., 2012).
Oncogenesis Overexpression of KIF14 enhances proliferation, and in vitro tumorigenic potential in ovarian cancer cell lines. Knockdown significantly reduces in vitro proliferation and tumorigenicity, and induces an apoptotic response (Thériault et al., 2012).
  
Entity Hepatocellular carcinoma (HCC)
Prognosis KIF14 is overexpressed in HCC.
Cytogenetics Low-level gain of the KIF14 locus is seen in 58% tumors (Bowles et al., 2007). A KIF14-containing region spanning 1q32.1-1q44 was the second most common alteration in a series of HCC, and KIF14 mRNA and protein expression were increased in tumors with gain of this region (Kim et al., 2008).
  
Entity Pancreatic carcinoma
Prognosis KIF14 was identified by expression microarray (and confirmed by RT-PCR and immunoblot) as downregulated in neuroinvasive versus non-invasive pancreatic carcinoma cell lines. However, KIF14 was upregulated in chronic pancreatitis and pancreatic cancer versus normal pancreas (Abiatari et al., 2009).
Oncogenesis Knockdown of KIF14 increased invasiveness of T3M4 cells and also increased resistance to anoikis of these cells (Abiatari et al., 2009).
  
Entity Papillary renal cell tumors
Prognosis Gain of a region of 1q including KIF14 is associated with fatal progression, and KIF14 is one of two genes overexpressed in tumors with this gain to a higher level than in tumors without 1q gain (Szponar et al., 2009).
  
Entity Glioblastoma multiforme
Cytogenetics Two translocation breakpoints in a series of 32 tumors mapped to 1q32. KIF14 was identified as an overexpressed gene in a region of somatic gain around this breakpoint (Leone et al., 2012).
  
Entity Laryngeal carcinoma
Oncogenesis KIF14 is one of three microarray-identified genes validated as a marker of laryngeal carcinoma (Markowski et al., 2009).
  

To be noted

Numerous microarray studies indexed in Oncomine document overexpression of KIF14 in other cancers, including brain tumors, seminoma, prostate and tongue cancers.

Other Solid tumors implicated (Data extracted from papers in the Atlas)

Solid Tumors AmeloblastomID5945

External links

Nomenclature
HGNC (Hugo)KIF14   19181
Cards
AtlasKIF14ID44138ch1q32
Entrez_Gene (NCBI)KIF14  9928  kinesin family member 14
GeneCards (Weizmann)KIF14
Ensembl (Hinxton)ENSG00000118193 [Gene_View]  chr1:200520625-200589862 [Contig_View]  KIF14 [Vega]
ICGC DataPortalENSG00000118193
AceView (NCBI)KIF14
Genatlas (Paris)KIF14
WikiGenes9928
SOURCE (Princeton)NM_014875
Genomic and cartography
GoldenPath (UCSC)KIF14  -  1q32.1   chr1:200520625-200589862 -  1q32.1   [Description]    (hg19-Feb_2009)
EnsemblKIF14 - 1q32.1 [CytoView]
Mapping of homologs : NCBIKIF14 [Mapview]
OMIM611279   
Gene and transcription
Genbank (Entrez)BC098582 BC113742 BC144068 D26361 HQ258545
RefSeq transcript (Entrez)NM_014875
RefSeq genomic (Entrez)AC_000133 NC_000001 NC_018912 NT_004487 NW_001838533 NW_004929293
Consensus coding sequences : CCDS (NCBI)KIF14
Cluster EST : UnigeneHs.3104 [ NCBI ]
CGAP (NCI)Hs.3104
Alternative Splicing : Fast-db (Paris)GSHG0002834
Alternative Splicing GalleryENSG00000118193
Gene ExpressionKIF14 [ NCBI-GEO ]     KIF14 [ SEEK ]   KIF14 [ MEM ]
Protein : pattern, domain, 3D structure
UniProt/SwissProtQ15058 (Uniprot)
NextProtQ15058  [Medical]
With graphics : InterProQ15058
Splice isoforms : SwissVarQ15058 (Swissvar)
Domaine pattern : Prosite (Expaxy)KINESIN_MOTOR_1 (PS00411)    KINESIN_MOTOR_2 (PS50067)   
Domains : Interpro (EBI)FHA_dom    Kinesin-like_fam    Kinesin_motor_CS    Kinesin_motor_dom    P-loop_NTPase    SMAD_FHA_domain   
Related proteins : CluSTrQ15058
Domain families : Pfam (Sanger)FHA (PF00498)    Kinesin (PF00225)   
Domain families : Pfam (NCBI)pfam00498    pfam00225   
Domain families : Smart (EMBL)FHA (SM00240)  KISc (SM00129)  
DMDM Disease mutations9928
Blocks (Seattle)Q15058
Human Protein AtlasENSG00000118193
Peptide AtlasQ15058
HPRD06605
IPIIPI00299554   
Protein Interaction databases
DIP (DOE-UCLA)Q15058
IntAct (EBI)Q15058
FunCoupENSG00000118193
BioGRIDKIF14
IntegromeDBKIF14
STRING (EMBL)KIF14
Ontologies - Pathways
QuickGOQ15058
Ontology : AmiGOmicrotubule motor activity  protein binding  ATP binding  nucleus  cytoplasm  spindle  kinesin complex  microtubule  microtubule-based movement  microtubule binding  metabolic process  membrane  regulation of cell adhesion  PDZ domain binding  regulation of cell migration  regulation of Rap protein signal transduction  negative regulation of integrin activation  substrate adhesion-dependent cell spreading  establishment of protein localization  
Ontology : EGO-EBImicrotubule motor activity  protein binding  ATP binding  nucleus  cytoplasm  spindle  kinesin complex  microtubule  microtubule-based movement  microtubule binding  metabolic process  membrane  regulation of cell adhesion  PDZ domain binding  regulation of cell migration  regulation of Rap protein signal transduction  negative regulation of integrin activation  substrate adhesion-dependent cell spreading  establishment of protein localization  
Protein Interaction DatabaseKIF14
Wikipedia pathwaysKIF14
Gene fusion - rearrangments
Polymorphisms : SNP, mutations, diseases
SNP Single Nucleotide Polymorphism (NCBI)KIF14
SNP (GeneSNP Utah)KIF14
SNP : HGBaseKIF14
Genetic variants : HAPMAPKIF14
1000_GenomesKIF14 
ICGC programENSG00000118193 
CONAN: Copy Number AnalysisKIF14 
Somatic Mutations in Cancer : COSMICKIF14 
LOVD (Leiden Open Variation Database)Whole genome datasets
LOVD (Leiden Open Variation Database)LOVD - Leiden Open Variation Database
LOVD (Leiden Open Variation Database)LOVD 3.0 shared installation
DECIPHER (Syndromes)1:200520625-200589862
Mutations and Diseases : HGMDKIF14
OMIM611279   
MedgenKIF14
GENETestsKIF14
Disease Genetic AssociationKIF14
Huge Navigator KIF14 [HugePedia]  KIF14 [HugeCancerGEM]
Genomic VariantsKIF14  KIF14 [DGVbeta]
Exome VariantKIF14
dbVarKIF14
ClinVarKIF14
snp3D : Map Gene to Disease9928
General knowledge
Homologs : HomoloGeneKIF14
Homology/Alignments : Family Browser (UCSC)KIF14
Phylogenetic Trees/Animal Genes : TreeFamKIF14
Chemical/Protein Interactions : CTD9928
Chemical/Pharm GKB GenePA38820
Clinical trialKIF14
Cancer Resource (Charite)ENSG00000118193
Other databases
Other databaseKEGG
Other databaseHUGE
Probes
Litterature
PubMed34 Pubmed reference(s) in Entrez
CoreMineKIF14
GoPubMedKIF14
iHOPKIF14

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Profiling genomic copy number changes in retinoblastoma beyond loss of RB1.
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Last year publicationsautomatic search in PubMed

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Contributor(s)

Written12-2007Brigitte L Thériault, Timothy W Corson
Division of Applied Molecular Oncology, Ontario Cancer Institute/Princess Margaret Hospital, University Health Network, Toronto, ON, Canada (BLT); Department of Molecular, Cellular and Developmental Biology, Yale (TWC)
Updated04-2012Brigitte L Thériault, Timothy W Corson
Division of Applied Molecular Oncology, Ontario Cancer Institute/Princess Margaret Hospital, University Health Network, Toronto, ON, Canada (BLT); Eugene & Marilyn Glick Eye Institute, Department of Ophthalmology, and Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, USA (TWC)

Citation

This paper should be referenced as such :
Thériault, BL ; Corson, TW
KIF14 (kinesin family member 14)
Atlas Genet Cytogenet Oncol Haematol. 2012;16(10):695-699.
Free online version   Free pdf version   [Bibliographic record ]
History of this paper:
Thériault, BL ; Corson, TW. KIF14 (kinesin family member 14). Atlas Genet Cytogenet Oncol Haematol. 2012;16(10):695-699.
http://documents.irevues.inist.fr/bitstream/handle/2042/48141/1/04-2012-KIF14ID44138ch1q32.pdf
URL : http://AtlasGeneticsOncology.org/Genes/KIF14ID44138ch1q32.html

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indexed on : Sat Nov 8 16:56:42 CET 2014

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