Semaphorin 7A, GPI membrane anchor (John Milton Hagen blood group) (SEMA7A) also known asCD108 (Cluster ofDifferentiation 108), is a humangene.[5]
SEMA7A is a membrane-boundsemaphorin that associates with cell surfaces via a glycosylphosphatidylinositol (GPI) linkage. SEMA7A is also known as the John-Milton-Hagen (JMH) blood group antigen, an 80-kD glycoprotein expressed on activatedlymphocytes anderythrocytes.[supplied by OMIM][5] SEMA7A is expressed in various adult tissues such as adipose, colon, esophagus, heart, brain, spleen, testis, lung, ovary, and uterus.[6]
SEMA7A promotes axonal growth and is involved inmesoderm derived somite formation. Murine embryonic Sema7A expression is highest on day 7, which is indicative of its role on the differentiation of germ layer structure.[7] Embryonic Sema7A expression is noticeable at all developmental stages as well as in the newborn and adult thymus, indicative of a development T-cell role.[7] In wild type neurons, addition of Sema7A underin vitro conditions promotes elongation and branching in a dose dependent manner.[8] Unlike the majority of semaphorins, SEMA7A enhances axonal growth and is imperative for proper embryonic axonal tract formation.[9] Limited expression of SEMA7A is found in the hindbrain as opposed to an abundance of SEMA7A expression found in both the cranial and trunk neural crest cells, which indicates an involvement in migration and differentiation.[10] Sema7A -/- mice show defects in olfactory tract development.[11]
In normal breast tissue, mRNA expression of SEMA7A is low or not expressed, but activation to re-express SEMA7A occurs in these adult tissues to cause pleiotropic effects which increase tumorigenesis.[12][13] Tumor cell growth, EMT, lung metastasis and angiogenesis have been linked to increased Sema7a expression in murine models.[14][15][16] Increased SEMA7A expression correlates with poor prognosis in breast cancer patients.[13] Tumors increase SEMA7A expression in an involuting environment, but knockout of SEMA7a in mouse models undergoing involution decreases lymphangiogenesis.[17]
This protein is known to have eight variants in the extracellular region: seven lie within the Sema domain and one within the PSI domain.[citation needed]
Lange C, Liehr T, Goen M, Gebhart E, Fleckenstein B, Ensser A (August 1998). "New eukaryotic semaphorins with close homology to semaphorins of DNA viruses".Genomics.51 (3):340–350.doi:10.1006/geno.1998.5256.PMID9721204.
Angelisová P, Drbal K, Cerný J, Hilgert I, Horejsí V (June 1999). "Characterization of the human leukocyte GPI-anchored glycoprotein CDw108 and its relation to other similar molecules".Immunobiology.200 (2):234–245.doi:10.1016/s0171-2985(99)80073-4.PMID10416131.
Maurin JC, Delorme G, Machuca-Gayet I, Couble ML, Magloire H, Jurdic P, et al. (May 2005). "Odontoblast expression of semaphorin 7A during innervation of human dentin".Matrix Biology.24 (3):232–238.doi:10.1016/j.matbio.2005.03.005.PMID15907379.
