Aliases for ERVW-1 Gene
- Endogenous Retrovirus Group W Member 1, Envelope 2 3 5
- Endogenous Retrovirus Group W Member 1 2 3 4
- HERV-7q Envelope Protein 2 3 4
- Enverin 2 3 4
- Endogenous Retroviral Family W, Env(C7), Member 1 2 3
- HERV-W_7q21.2 Provirus Ancestral Env Polyprotein 3 4
- HERV-Tryptophan Envelope Protein 2 3
- Envelope Polyprotein GPr73 3 4
- HERV-W Env Glycoprotein 2 3
- HERV-W Envelope Protein 3 4
- Envelope Glycoprotein 2 3
- Syncytin-1 2 3
- Syncytin 2 4
- ERVWE1 3 4
External Ids for ERVW-1 Gene
Previous HGNC Symbols for ERVW-1 Gene
Previous GeneCards Identifiers for ERVW-1 Gene
Many different human endogenous retrovirus (HERV) families are expressed in normal placental tissue at high levels, suggesting that HERVs are functionally important in reproduction. This gene is part of an HERV provirus on chromosome 7 that has inactivating mutations in the gag and pol genes. This gene is the envelope glycoprotein gene which appears to have been selectively preserved. The gene's protein product is expressed in the placental syncytiotrophoblast and is involved in fusion of the cytotrophoblast cells to form the syncytial layer of the placenta. The protein has the characteristics of a typical retroviral envelope protein, including a furin cleavage site that separates the surface (SU) and transmembrane (TM) proteins which form a heterodimer. Alternatively spliced transcript variants encoding the same protein have been found for this gene. [provided by RefSeq, Mar 2010]
GeneCards Summary for ERVW-1 Gene
ERVW-1 (Endogenous Retrovirus Group W Member 1, Envelope) is a Protein Coding gene. Diseases associated with ERVW-1 include Vaccinia and T-Cell Leukemia. An important paralog of this gene is ERVFRD-1.
UniProtKB/Swiss-Prot for ERVW-1 Gene
This endogenous retroviral envelope protein has retained its original fusogenic properties and participates in trophoblast fusion and the formation of a syncytium during placenta morphogenesis. May induce fusion through binding of SLC1A4 and SLC1A5 (PubMed:10708449, PubMed:12050356, PubMed:23492904).
Endogenous envelope proteins may have kept, lost or modified their original function during evolution. Retroviral envelope proteins mediate receptor recognition and membrane fusion during early infection. The surface protein (SU) mediates receptor recognition, while the transmembrane protein (TM) acts as a class I viral fusion protein. The protein may have at least 3 conformational states: pre-fusion native state, pre-hairpin intermediate state, and post-fusion hairpin state. During viral and target cell membrane fusion, the coiled coil regions (heptad repeats) assume a trimer-of-hairpins structure, positioning the fusion peptide in close proximity to the C-terminal region of the ectodomain. The formation of this structure appears to drive apposition and subsequent fusion of membranes.