Alternative titles; symbolsTHETA ANTIGENCD90 ANTIGEN; CD90HGNC Approved Gene Symbol: THY1Cytogenetic location: 11q23.3 Genomic coordinates (GRCh38): 11:119,4...
Alternative titles; symbols
HGNC Approved Gene Symbol: THY1
Cytogenetic location: 11q23.3 Genomic coordinates (GRCh38): 11:119,415,475-119,424,984 (from NCBI)
Thy-1 is the designation for a major cell surface glycoprotein characteristic to T cells, as first defined in the mouse and rat (Raff, 1971; Letarte-Muirhead et al., 1975). The Thy-1 glycoproteins are constituents of thymocytes and neurons and probably are involved in cell-cell interactions. The putative human homolog of Thy-1 of the mouse is called K117. The human homolog of the rodent antigen was studied by Ades et al. (1980). Using a monoclonal antibody, McKenzie and Fabre (1981) studied the tissue distribution of the antigen. By use of a gene clone in somatic cell hybrids, Seki et al. (1985) assigned the THY1 gene to chromosome 11. Van den Elsen et al. (1985) predicted that the human Thy-1 homolog maps to chromosome 11 because that is where they found T3D (186790) to map and in the mouse T3D and Thy-1 map to chromosome 9 along with certain other loci that are on human 11q. A multigene family is a group of homologous genes with similar function. A supergene family is a set of multigene families and single genes related by sequence (implying common ancestry) but not necessarily related in function. Hood et al. (1985) refer to the immunoglobulin supergene family which includes Thy-1, poly-Ig receptor, heavy, kappa and lambda immunoglobulins, Lyt-2 (T8), alpha and beta chains of T-cell antigen receptor and the closely homologous gamma chain, class I MHC antigen, beta-2-microglobulin, and the alpha and beta chains of class II MHC antigens. Thy-1 is structurally the simplest of these, consisting of a single immunoglobulin homology unit that is either intermediate between V and C or somewhat more similar to a V homology unit (Williams and Gagnon, 1982). The Thy-1 glycoprotein is also exceptional in that it is on the cell surface as a free homology unit and apparently does not associate either with itself or with other polypeptides. Its role in immune response is unclear. It is expressed on fibroblasts and brain cells in addition to some T cells. The significant role of Thy-1 in developing nervous tissue (Morris, 1985) may be of relevance to disorders such as ataxia-telangiectasia (208900) that combine neurologic and immunologic defects. By somatic cell and in situ hybridization, van Rijs et al. (1985) localized the gene to 11q23-11q24. Rettig et al. (1985) assigned the gene to 11q13-qter, by Southern analysis of DNA from hybrid cells containing rearranged chromosomes 11. HGM7 gave the regional assignment as 11q22.3. Tunnacliffe and McGuire (1990) constructed a physical map of 11q23 by pulsed field gel electrophoresis and showed that THY1 lies in 11q23.3 as the most telomeric of a group of 6 genes: cen--CD3E--CD3D--CD3G--PBGD--CBL2--THY1--qter.
Chromosome 11 seems to carry an inordinately large number of genes for cell surface antigens (Rettig et al., 1985); according to the 1985 workshop on Human Gene Mapping (Grzeschik and Kazazian, 1985), at least 21 cellular antigens recognized by monoclonal antibodies and other serologic means map to 11. Mansour et al. (1987) gave a useful history of our understanding of the Thy-1 glycoprotein and a review of its evolution. Using RFLPs, Gatti et al. (1987) mapped the THY1 gene against APOA1 (107680). THY1 appeared to be distal to APOA1; there was 1% recombination between the 2 loci in males and 2% in females. Gatti et al. (1988) demonstrated RFLPs in the THY1 gene that are potentially useful as markers in linkage studies. Greenspan and O'Brien (1989) showed in the mouse that a factor secreted by nonneuronal accessory cells of dorsal root ganglion cultures stimulates neurite outgrowth in neonatal sympathetic ganglion neurons. They presented evidence that this is identical to Thy-1. It is this function in separate tissues that might explain pleiotropic manifestations of some syndromes such as ataxia-telangiectasia (208900) or cartilage-hair hypoplasia (250250).
Cao et al. (2001) found that introduction of chromosome 11 completely suppressed tumorigenicity of the highly malignant and tumorigenic ovarian cancer cell line SKOV-3 but introduction of chromosome 17 could only partially suppress tumorigenicity. Microcell-mediated chromosome transfer was applied to introduce a normal copy of chromosome 11 into SKOV-3 cells; a panel of 5 hybrid clones were generated. Two of the clones were completely nontumorigenic in severe combined immunodeficiency (SCID) mice for up to 150 and 200 days; 2 other clones had a latency period of 123 and 109 days, respectively. In vitro cell doubling time was found to be highly variable and did not correlate with tumorigenicity, implying that suppression of in vivo tumorigenicity and in vitro cell proliferation are under separate genetic control. A number of studies had demonstrated a high frequency of loss of heterozygosity (LOH) of chromosome 11, both 11p and 11q, in ovarian cancer. To identify the gene or genes associated with tumor suppression in the ovarian cell line SKOV-3, Abeysinghe et al. (2003) performed cDNA subtractive hybridization using a suppression subtractive hybridization method. Using this approach, they identified the differential expression of the cell surface glycoprotein THY1, the gene for which maps to 11q23.3. The expression of THY1 was found to be exclusive in the 2 nontumorigenic clones as determined by Northern blot analysis at the mRNA level and by immunocytochemistry and quantitative flow cytometry at the protein expression level. Several genes related to cell growth and differentiation were found to be upregulated in the nontumorigenic clones, including THBS1 (188060), SPARC (182120), and fibronectin (135600).