SEMA7A

Source: Wikipedia, the free encyclopedia.
SEMA7A
Gene ontology
Molecular function
Cellular component
Biological process
Sources:Amigo / QuickGO
Ensembl
UniProt
RefSeq (mRNA)

NM_003612
NM_001146029
NM_001146030

NM_011352

RefSeq (protein)

NP_001139501
NP_001139502
NP_003603

NP_035482

Location (UCSC)Chr 15: 74.41 – 74.43 MbChr 9: 57.85 – 57.87 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Semaphorin 7A, GPI membrane anchor (John Milton Hagen blood group) (SEMA7A) also known as CD108 (Cluster of Differentiation 108), is a human gene.[5]

SEMA7A is a membrane-bound

erythrocytes.[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]

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.[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 under in 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]

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.[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]

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.[citation needed]

Molecular biology

This protein forms dimers.[citation needed]

Notes

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

See also

References

  1. ^ a b c ENSG00000288455 GRCh38: Ensembl release 89: ENSG00000138623, ENSG00000288455Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000038264Ensembl, 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. ^ a b "Entrez Gene: SEMA7A semaphorin 7A, GPI membrane anchor (John Milton Hagen blood group)".
  6. ^ "Tissue expression of SEMA7A - Summary - The Human Protein Atlas". www.proteinatlas.org. Retrieved 2020-04-14.
  7. ^
    PMID 10885563
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Further reading

External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.


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