KTN1

Gene Summary

Gene:KTN1; kinectin 1 (kinesin receptor)
Aliases: CG1, KNT, MU-RMS-40.19
Location:14q22.1
Summary:This gene encodes an integral membrane protein that is a member of the kinectin protein family. The encoded protein is primarily localized to the endoplasmic reticulum membrane. This protein binds kinesin and may be involved in intracellular organelle motility. This protein also binds translation elongation factor-delta and may be involved in the assembly of the elongation factor-1 complex. Alternate splicing results in multiple transcript variants of this gene. [provided by RefSeq, Aug 2012]
Databases:OMIM, VEGA, HGNC, Ensembl, GeneCard, Gene
Protein:kinectin
HPRD
Source:NCBIAccessed: 21 August, 2015

Ontology:

What does this gene/protein do?
Show (10)

Cancer Overview

Research Indicators

Publications Per Year (1990-2015)
Graph generated 21 August 2015 using data from PubMed using criteria.

Literature Analysis

Mouse over the terms for more detail; many indicate links which you can click for dedicated pages about the topic.

  • Base Sequence
  • ZAK
  • Molecular Sequence Data
  • DNA Mutational Analysis
  • KTN1
  • Adolescents
  • Alternative Splicing
  • Cultured Cells
  • Translocation
  • Papillary Carcinoma
  • Gene Expression Profiling
  • DNA, Complementary
  • Chromosome 14
  • Thyroid Cancer
  • Young Adult
  • Proto-Oncogene Proteins c-ret
  • Radiation-Induced Cancer
  • Receptor Protein-Tyrosine Kinases
  • Ukraine
  • In Situ Hybridization
  • Protein-Tyrosine Kinases
  • Bone Cancer
  • Tumor Antigens
  • Gene Expression
  • Amino Acid Sequence
  • rho-Associated Kinases
  • Protein Kinases
  • Membrane Proteins
  • ROCK1
  • RTPCR
  • Chromosomes, Artificial, Yeast
  • Cloning, Molecular
  • Liver
  • Liver Cancer
  • Immunohistochemistry
  • Chromosome 10
  • Drosophila Proteins
  • Cell Surface Receptors
  • Radioactive Hazard Release
Tag cloud generated 21 August, 2015 using data from PubMed, MeSH and CancerIndex

Specific Cancers (4)

Data table showing topics related to specific cancers and associated disorders. Scope includes mutations and abnormal protein expression.

Note: list is not exhaustive. Number of papers are based on searches of PubMed (click on topic title for arbitrary criteria used).

Latest Publications: KTN1 (cancer-related)

Babeto E, Conceição AL, Valsechi MC, et al.
Differentially expressed genes in giant cell tumor of bone.
Virchows Arch. 2011; 458(4):467-76 [PubMed] Related Publications
Giant cells tumors of bone (GCTB) are benign in nature but cause osteolytic destruction with a number of particular characteristics. These tumors can have uncertain biological behavior often contain a significant proportion of highly multinucleated cells, and may show aggressive behavior. We have studied differential gene expression in GCTB that may give a better understanding of their physiopathology, and might be helpful in prognosis and treatment. Rapid subtractive hybridization (RaSH) was used to identify and measure novel genes that appear to be differentially expressed, including KTN1, NEB, ROCK1, and ZAK using quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry in the samples of GCTBs compared to normal bone tissue. Normal bone was used in the methodology RaSH for comparison with the GCTB in identification of differentially expressed genes. Functional annotation indicated that these genes are involved in cellular processes related to their tumor phenotype. The differential expression of KTN1, ROCK1, and ZAK was independently confirmed by qRT-PCR and immunohistochemistry. The expression of the KTN1 and ROCK1 genes were increased in samples by qRT-PCR and immunohistochemistry, and ZAK had reduced expression. Since ZAK have CpG islands in their promoter region and low expression in tumor tissue, their methylation pattern was analyzed by MSP-PCR. The genes identified KTN1, ROCK1, and ZAK may be responsible for loss of cellular homeostasis in GCTB since they are responsible for various functions related to tumorigenesis such as cell migration, cytoskeletal organization, apoptosis, and cell cycle control and thus may contribute at some stage in the process of formation and development of GCTB.

Wang HC, Su YR, Han KJ, et al.
Multiple variants and a differential splicing pattern of kinectin in human hepatocellular carcinoma.
Biochem Cell Biol. 2004; 82(2):321-7 [PubMed] Related Publications
To extend the search for hepatocellular carcinoma (HCC) associated antigens with immunogenicity for clinical applications, we constructed a cDNA expression library using resected human HCC tissue sample and screened it by serological analysis of recombinant cDNA expression library (SEREX) with autologous and allogeneic sera. A total of 24 distinct antigens were isolated and kinectin was the antigen most frequently identified. We found that kinectin was alternatively spliced at four sites and obtained all eight theoretical forms of variant, six by SEREX and two by RT-PCR, from the different splicing combinations of the last three sites. In addition, the splicing patterns of four sites were analyzed. Variant containing D2 was overexpressed in cancerous tissues and this alteration may be tumor associated. The four splicing sites, the variants generated by alternative splicing, and the humoral immune response in HCC patients, may help to analyze the role of kinectin in human HCC cell biology.

Zhou XG, Sandvej K, Li PJ, et al.
Epstein--Barr virus gene polymorphisms in Chinese Hodgkin's disease cases and healthy donors: identification of three distinct virus variants.
J Gen Virol. 2001; 82(Pt 5):1157-67 [PubMed] Related Publications
Epstein--Barr virus (EBV) is associated with several malignancies. Specific EBV gene variants, e.g. the BamHI f configuration, a C-terminal region 30 bp deletion in the latent membrane protein-1 (LMP1) gene (del-LMP) and the loss of an XhoI site in LMP1 (XhoI-loss), are found in Chinese cases of nasopharyngeal carcinoma (NPC), suggesting that EBV sequence variation may be involved in oncogenesis. In order to understand better the epidemiology of these EBV variants, they were studied in virus isolates from EBV-positive Chinese cases of Hodgkin's disease (HD; n=71) and donor throat washings from healthy CHINESE: Sequencing was performed of 15 representative EBV isolates, including the first analysis of the LMP1 promoter in Asian wild-type EBV isolates. The following observations were made. (i) Three EBV LMP1 variants were identified, designated Chinese groups (CG) 1--3. In both EBV-associated HD and in healthy Chinese, CG1-like viruses showing del-LMP1 and XhoI-loss were predominant. (ii) CG1viruses were distinct from European and African variants, suggesting that this profile is useful for epidemiological studies. (iii) Specific patterns of mutations were present in the LMP1 promoter in both CG1 and CG2. (iv) The BamHI f variant was not found in Chinese HD, in contrast to Chinese NPC and European HD. This study confirms that EBV isolates in Chinese HD and other tumours differ from those reported in Western cases. However, this reflects the predominant virus strain present in the healthy Chinese population, suggesting that these are geographically restricted polymorphisms rather than tumour-specific strains.

Salassidis K, Bruch J, Zitzelsberger H, et al.
Translocation t(10;14)(q11.2:q22.1) fusing the kinetin to the RET gene creates a novel rearranged form (PTC8) of the RET proto-oncogene in radiation-induced childhood papillary thyroid carcinoma.
Cancer Res. 2000; 60(11):2786-9 [PubMed] Related Publications
Evaluation of 20 cases of radiation-induced childhood papillary thyroid carcinoma using fluorescence in situ hybridization demonstrated the presence of clonal translocations affecting the RET locus. Semiquantitative reverse transcription-PCR indicated overexpression of the RET tyrosine kinase (TK) domain in four cases. In two cases, the RET rearrangements PTC6 and PTC7 were identified and assigned to balanced translocations t(7;10)(q32;q11.2) and t(1;10)(p13;q11.2), respectively. In one case with a balanced translocation t(10;14)(q11.2;q22.1), 5' rapid amplification of cDNA ends revealed a novel type of RET oncogenic activation (PTC8), arising from a fusion of the 5' part of the kinectin (KTN1) gene to the TK domain of the RET gene. The presence of coiled-coil domains in the resulting ktn1/ret fusion protein suggests ligand-independent dimerization and thus constitutive activation of the ret TK domain.

Disclaimer: This site is for educational purposes only; it can not be used in diagnosis or treatment.

Cite this page: Cotterill SJ. KTN1, Cancer Genetics Web: http://www.cancer-genetics.org/KTN1.htm Accessed:

Creative Commons License
This page in Cancer Genetics Web by Simon Cotterill is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License.
Note: content of abstracts copyright of respective publishers - seek permission where appropriate.

 [Home]    Page last revised: 21 August, 2015     Cancer Genetics Web, Established 1999