SEMA7A explained

Semaphorin 7A, GPI membrane anchor (John Milton Hagen blood group) (SEMA7A) also known as CD108 (Cluster of Differentiation 108), is a human gene.[1]

SEMA7A is a membrane-bound semaphorin 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 activated lymphocytes and erythrocytes.[supplied by OMIM][1] SEMA7A is expressed in various adult tissues such as adipose, colon, esophagus, heart, brain, spleen, testis, lung, ovary, and uterus.[2]

Development

SEMA7A promotes axonal growth and is involved in mesoderm 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.[3] 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.[3] In wild type neurons, addition of Sema7A under in vitro conditions promotes elongation and branching in a dose dependent manner.[4] Unlike the majority of semaphorins, SEMA7A enhances axonal growth and is imperative for proper embryonic axonal tract formation.[5] 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.[6] Sema7A -/- mice show defects in olfactory tract development.[7]

Tumorigenesis

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.[8] [9] Tumor cell growth, EMT, lung metastasis and angiogenesis have been linked to increased Sema7a expression in murine models.[10] [11] [12] Increased SEMA7A expression correlates with poor prognosis in breast cancer patients.[9] Tumors increase SEMA7A expression in an involuting environment, but knockout of SEMA7a in mouse models undergoing involution decreases lymphangiogenesis.[13]

Genetics

This protein is known to have eight variants in the extracellular region: seven lie within the Sema domain and one within the PSI domain.

Molecular biology

This protein forms dimers.

Notes

This protein acts as a receptor for the malaria parasite Plasmodium falciparum.

See also

Further reading

External links

Notes and References

  1. Web site: Entrez Gene: SEMA7A semaphorin 7A, GPI membrane anchor (John Milton Hagen blood group).
  2. Web site: Tissue expression of SEMA7A - Summary - The Human Protein Atlas. www.proteinatlas.org. 2020-04-14.
  3. Mine. T.. Harada. K.. Matsumoto. T.. Yamana. H.. Shirouzu. K.. Itoh. K.. Yamada. A.. May 2000. CDw108 expression during T-cell development. Tissue Antigens. en. 55. 5. 429–436. 10.1034/j.1399-0039.2000.550505.x. 10885563. 0001-2815.
  4. Integrin-mediated dendrite branch maintenance requires Abelson (Abl) family kinases.. Journal of Neuroscience. 2005. 25. 6105–6118. 10.1523/JNEUROSCI.1432-05.2005. Moresco. E. M. Y.. 26. 15987940. 6725048.
  5. Scott. Glynis A.. McClelland. Lindy A.. Fricke. Alex F.. January 2008. Semaphorin 7a Promotes Spreading and Dendricity in Human Melanocytes through β1-Integrins. Journal of Investigative Dermatology. en. 128. 1. 151–161. 10.1038/sj.jid.5700974. 17671519. free.
  6. Bao. Zheng-Zheng. Jin. Zhe. August 2006. Sema3D and Sema7A have distinct expression patterns in chick embryonic development. Developmental Dynamics. en. 235. 8. 2282–2289. 10.1002/dvdy.20882. 1058-8388. 1564195. 16804892.
  7. Jeroen Pasterkamp. R.. Peschon. Jacques J.. Spriggs. Melanie K.. Kolodkin. Alex L.. July 2003. Semaphorin 7A promotes axon outgrowth through integrins and MAPKs. Nature. en. 424. 6947. 398–405. 10.1038/nature01790. 12879062. 2003Natur.424..398J. 12690989. 0028-0836.
  8. Moserle. Lidia. Casanovas. Oriol. March 2012. Exploiting pleiotropic activities of semaphorins as multi-target therapies for cancer. EMBO Molecular Medicine. en. 4. 3. 168–170. 10.1002/emmm.201200206. 1757-4676. 3376851. 22323445.
  9. Black. S A. Nelson. A C. Gurule. N J. Futscher. B W. Lyons. T R. September 2016. Semaphorin 7a exerts pleiotropic effects to promote breast tumor progression. Oncogene. en. 35. 39. 5170–5178. 10.1038/onc.2016.49. 0950-9232. 5720143. 27065336.
  10. Garcia-Areas. Ramon. Libreros. Stephania. Amat. Samantha. Keating. Patricia. Carrio. Roberto. Robinson. Phillip. Blieden. Clifford. Iragavarapu-Charyulu. Vijaya. 2014. Semaphorin7A promotes tumor growth and exerts a pro-angiogenic effect in macrophages of mammary tumor-bearing mice. Frontiers in Physiology. 5. 17. 10.3389/fphys.2014.00017. 1664-042X. 3914020. 24550834. free.
  11. Allegra. Maryline. Zaragkoulias. Andreas. Vorgia. Elena. Ioannou. Marina. Litos. Gabriele. Beug. Hartmut. Mavrothalassitis. George. October 2012. Chernoff. Jonathan. Semaphorin-7a reverses the ERF-induced inhibition of EMT in Ras-dependent mouse mammary epithelial cells. Molecular Biology of the Cell. en. 23. 19. 3873–3881. 10.1091/mbc.e12-04-0276. 1059-1524. 3459863. 22875994.
  12. Ringnér. Markus. Fredlund. Erik. Häkkinen. Jari. Borg. Åke. Staaf. Johan. 2011-03-21. Creighton. Chad. GOBO: Gene Expression-Based Outcome for Breast Cancer Online. PLOS ONE. en. 6. 3. e17911. 10.1371/journal.pone.0017911. 1932-6203. 3061871. 21445301. 2011PLoSO...617911R. free.
  13. Elder. Alan M. Tamburini. Beth AJ. Crump. Lyndsey S. Black. Sarah A. Wessells. Veronica M. Schedin. Pepper J. Borges. Virginia F.. Lyons. Traci R.. 2018-09-25. Semaphorin 7A promotes macrophage-mediated lymphatic remodeling during postpartum mammary gland involution and in breast cancer. Cancer Research. 78. 22. en. 6473–6485. 10.1158/0008-5472.CAN-18-1642. 0008-5472. 6239927. 30254150.