SEMA7A

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
Available structures PDB Ortholog search: PDBe RCSB List of PDB id codes 3NVQ
Identifiers
Aliases	SEMA7A, CD108, CDw108, H-SEMA-K1, H-Sema-L, JMH, SEMAK1, SEMAL, semaphorin 7A (John Milton Hagen blood group), PFIC11
External IDs	OMIM: 607961; MGI: 1306826; HomoloGene: 2678; GeneCards: SEMA7A; OMA:SEMA7A - orthologs
Gene location (Human) Chr. Chromosome 15 (human)[1] Band 15q24.1 Start 74,409,289 bp[1] End 74,433,958 bp[1]
Gene location (Mouse) Chr. Chromosome 9 (mouse)[2] Band 9|9 B Start 57,847,395 bp[2] End 57,870,148 bp[2]
RNA expression pattern Bgee Human Mouse (ortholog) Top expressed in spleen C1 segment primary visual cortex placenta right hemisphere of cerebellum prefrontal cortex stromal cell of endometrium superior frontal gyrus Brodmann area 9 right frontal lobe Top expressed in cumulus cell cerebellar cortex primary visual cortex superior frontal gyrus lumbar subsegment of spinal cord anterior horn of spinal cord dentate gyrus of hippocampal formation granule cell primary motor cortex lateral geniculate nucleus lobe of cerebellum More reference expression data BioGPS More reference expression data
Gene ontology Molecular function protein binding integrin binding neuropilin binding semaphorin receptor binding chemorepellent activity Cellular component membrane plasma membrane anchored component of membrane extracellular space external side of plasma membrane integral component of plasma membrane collagen-containing extracellular matrix Biological process cell differentiation positive regulation of protein phosphorylation nervous system development multicellular organism development osteoblast differentiation immune response positive regulation of ERK1 and ERK2 cascade axon extension olfactory lobe development integrin-mediated signaling pathway positive regulation of axon extension inflammatory response neuron projection development regulation of inflammatory response negative chemotaxis positive regulation of macrophage cytokine production neural crest cell migration positive regulation of cell migration negative regulation of axon extension involved in axon guidance semaphorin-plexin signaling pathway Sources:Amigo / QuickGO
Orthologs Species Human Mouse Entrez 8482 20361 Ensembl ENSG00000138623 ENSG00000288455 ENSMUSG00000038264 UniProt O75326 Q9QUR8 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 Mb Chr 9: 57.85 – 57.87 Mb PubMed search [3] [4]
Wikidata
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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]^[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

• Cluster of differentiation