TSRC1, a widely expressed gene containing seven thrombospondin type I repeats
- PMID: 12706885
- DOI: 10.1016/s0378-1119(03)00423-2
TSRC1, a widely expressed gene containing seven thrombospondin type I repeats
Abstract
The thrombospondin type 1 repeat domain is found in nearly 100 mammalian proteins with diverse biological functions that include cellular adhesion, angiogenesis, and patterning of the developing nervous system. We have characterized a novel thrombospondin type 1 repeat containing gene, TSRC1, encoding a predicted protein with seven thrombospondin repeats, six of which are clustered at the C-terminus. The 17 coding exons and two nontranslated exons of TSRC1 span 10 kb of genomic DNA. The human and mouse genes encode proteins of 1074 and 1036 amino acids, respectively, with 76% amino acid sequence identity. Thirty of the extra amino acids in the human protein are encoded by exon 6. Mouse Tsrc1 is expressed in all fetal and adult tissues tested. Three conserved noncoding sequence elements with potential regulatory function are located in intron 1. Mouse Tsrc1 was genetically mapped to chromosome 3 within the nonrecombinant region for the sodium channel modifier locus Scnm1. The sensitive and resistant alleles of Scnm1 did not differ in Tsrc1 protein sequence, transcript length, or transcript abundance. Human TSRC1 is located on chromosome 1q21 within an 11.7 Mb segment of conserved synteny. TSRC1 and the closely linked gene ADAM15 appear to be derived by a chromosomal inversion that interrupted an ancestral ADAMTS gene.
Similar articles
-
TAIL1: an isthmin-like gene, containing type 1 thrombospondin-repeat and AMOP domain, mapped to ARVD1 critical region.Gene. 2004 Jun 23;335:101-8. doi: 10.1016/j.gene.2004.03.008. Gene. 2004. PMID: 15194193
-
The exon/intron organization and chromosomal mapping of the mouse ADAMTS-1 gene encoding an ADAM family protein with TSP motifs.Genomics. 1997 Dec 15;46(3):466-71. doi: 10.1006/geno.1997.5064. Genomics. 1997. PMID: 9441751
-
Cloning, expression analysis, and structural characterization of seven novel human ADAMTSs, a family of metalloproteinases with disintegrin and thrombospondin-1 domains.Gene. 2002 Jan 23;283(1-2):49-62. doi: 10.1016/s0378-1119(01)00861-7. Gene. 2002. PMID: 11867212
-
The functions of thrombospondin-1 and-2.Curr Opin Cell Biol. 2000 Oct;12(5):634-40. doi: 10.1016/s0955-0674(00)00143-5. Curr Opin Cell Biol. 2000. PMID: 10978901 Review.
-
Structures of thrombospondins.Cell Mol Life Sci. 2008 Mar;65(5):672-86. doi: 10.1007/s00018-007-7484-1. Cell Mol Life Sci. 2008. PMID: 18193164 Free PMC article. Review.
Cited by
-
Genetic and functional linkage between ADAMTS superfamily proteins and fibrillin-1: a novel mechanism influencing microfibril assembly and function.Cell Mol Life Sci. 2011 Oct;68(19):3137-48. doi: 10.1007/s00018-011-0780-9. Epub 2011 Aug 20. Cell Mol Life Sci. 2011. PMID: 21858451 Free PMC article. Review.
-
A disintegrin-like and metalloprotease domain containing thrombospondin type 1 motif-like 5 (ADAMTSL5) is a novel fibrillin-1-, fibrillin-2-, and heparin-binding member of the ADAMTS superfamily containing a netrin-like module.Matrix Biol. 2012 Sep-Oct;31(7-8):398-411. doi: 10.1016/j.matbio.2012.09.003. Epub 2012 Sep 23. Matrix Biol. 2012. PMID: 23010571 Free PMC article.
-
A homozygous mutation in ADAMTSL4 causes autosomal-recessive isolated ectopia lentis.Am J Hum Genet. 2009 Feb;84(2):274-8. doi: 10.1016/j.ajhg.2009.01.007. Epub 2009 Feb 5. Am J Hum Genet. 2009. PMID: 19200529 Free PMC article.
-
Emerging roles for the ADAMTS-like family of matricellular proteins in cardiovascular disease through regulation of the extracellular microenvironment.Mol Biol Rep. 2024 Feb 7;51(1):280. doi: 10.1007/s11033-024-09255-5. Mol Biol Rep. 2024. PMID: 38324186 Free PMC article. Review.
-
Congenital anomalies of lens shape.Taiwan J Ophthalmol. 2023 Dec 20;13(4):479-488. doi: 10.4103/tjo.TJO-D-23-00076. eCollection 2023 Oct-Dec. Taiwan J Ophthalmol. 2023. PMID: 38249493 Free PMC article. Review.
Publication types
MeSH terms
Substances
Associated data
- Actions
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
Molecular Biology Databases
Miscellaneous
