Suppression of tumorigenicity 5 is a protein that in humans is encoded by the ST5 gene.[5][6] ST5 orthologs[7] have been identified in nearly all mammals for which complete genome data are available.

ST5
Identifiers
AliasesST5, DENND2B, HTS1, p126, suppression of tumorigenicity 5
External IDsOMIM: 140750 MGI: 108517 HomoloGene: 3951 GeneCards: ST5
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_005418
NM_139157
NM_213618

NM_001001326
NM_029811

RefSeq (protein)

NP_001001326
NP_084087

Location (UCSC)Chr 11: 8.69 – 8.91 MbChr 7: 109.52 – 109.7 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Function edit

This gene was identified by its ability to suppress the tumorigenicity of Hela cells in nude mice. The protein encoded by this gene contains a C-terminal region that shares similarity with the Rab 3 family of small GTP binding proteins. This protein preferentially binds to the SH3 domain of c-Abl kinase, and acts as a regulator of MAPK1/ERK2 kinase, which may contribute to its ability to reduce the tumorigenic phenotype in cells. Three alternatively spliced transcript variants of this gene encoding distinct isoforms are identified.[6]

References edit

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000166444Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000031024Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ Lichy JH, Modi WS, Seuanez HN, Howley PM (August 1992). "Identification of a human chromosome 11 gene which is differentially regulated in tumorigenic and nontumorigenic somatic cell hybrids of HeLa cells". Cell Growth & Differentiation. 3 (8): 541–8. PMID 1390339.
  6. ^ a b "Entrez Gene: ST5 suppression of tumorigenicity 5".
  7. ^ "OrthoMaM phylogenetic marker: ST5 coding sequence". Archived from the original on 2016-03-03. Retrieved 2009-12-02.

Further reading edit