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ERV3

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Protein-coding gene in the species Homo sapiens
ERV3-1
Identifiers
AliasesERV3-1, ERV-R, ERV3, ERVR, HERV-R, HERVR, envR, endogenous retrovirus group 3 member 1, endogenous retrovirus group 3 member 1, envelope
External IDsOMIM: 131170; HomoloGene: 128310; GeneCards: ERV3-1; OMA:ERV3-1 - orthologs
RNA expression pattern
Bgee
HumanMouse (ortholog)
Top expressed in
  • left adrenal gland

  • monocyte

  • gallbladder

  • ganglionic eminence

  • islet of Langerhans

  • right lung

  • minor salivary glands

  • Achilles tendon

  • appendix

  • right uterine tube
    n/a
More reference expression data
BioGPS
More reference expression data
Gene ontology
Molecular function
Cellular component
Biological process
Sources:Amigo / QuickGO
Orthologs
SpeciesHumanMouse
Entrez

2086

n/a

Ensembl

n/a

n/a

UniProt

Q14264

n/a

RefSeq (mRNA)

NM_001007253
NM_001396062

n/a

RefSeq (protein)

NP_001007254

n/a

Location (UCSC)n/an/a
PubMed searchn/a
Wikidata
View/Edit Human

HERV-R_7q21.2 provirus ancestral envelope (Env) polyprotein is a protein that in humans is encoded by the ERV3 gene.

Function

The human genome includes many retroelements including the human endogenous retroviruses (HERVs), which compose about 7-8% of the human genome. ERV3, one of the most studied HERVs, is thought to have integrated 30 to 40 million years ago and is present in higher primates with the exception of gorillas. Taken together, the observation of genome conservation, the detection of transcript expression, and the presence of conserved ORFs is circumstantial evidence for a functional role. Similar endogenous retroviral Env genes like syncytin-1 have important roles in placental formation and embryonic development by enabling cell-cell fusion. Despite its origin as an Env gene, ERV3 has a premature stop codon that precludes any cell-cell fusion functionality. However, it does have an immunosuppressive function that helps the fetus evade a damaging maternal immune response, which may explain its high expression in the placenta.

There is speculation that ERV3 originally did have cell-cell fusion functionality in the placenta, but that it was eventually supplanted by other Env genes like syncytin, leading to a loss of this function.

Another functional role is suggested by the observation that downregulation of ERV3 is reported in choriocarcinoma.

References

  1. "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  2. Kato N, Shimotohno K, VanLeeuwen D, Cohen M (August 1990). "Human proviral mRNAs down regulated in choriocarcinoma encode a zinc finger protein related to Krüppel". Molecular and Cellular Biology. 10 (8): 4401–5. doi:10.1128/mcb.10.8.4401. PMC 361000. PMID 2115127.
  3. O'Connell C, O'Brien S, Nash WG, Cohen M (October 1984). "ERV3, a full-length human endogenous provirus: chromosomal localization and evolutionary relationships". Virology. 138 (2): 225–35. doi:10.1016/0042-6822(84)90347-7. PMID 6495650.
  4. ^ "Entrez Gene: ERV3 endogenous retroviral sequence 3 (includes zinc finger protein H-plk/HPF9)".
  5. Jern P, Coffin JM (December 2008). "Effects of retroviruses on host genome function". Annual Review of Genetics. 42 (1): 709–32. doi:10.1146/annurev.genet.42.110807.091501. PMID 18694346. S2CID 9254616.
  6. Vargas A, Moreau J, Landry S, LeBellego F, Toufaily C, Rassart E, et al. (September 2009). "Syncytin-2 plays an important role in the fusion of human trophoblast cells". Journal of Molecular Biology. 392 (2): 301–18. doi:10.1016/j.jmb.2009.07.025. PMID 19616006.
  7. Mallet F, Bouton O, Prudhomme S, Cheynet V, Oriol G, Bonnaud B, et al. (February 2004). "The endogenous retroviral locus ERVWE1 is a bona fide gene involved in hominoid placental physiology". Proceedings of the National Academy of Sciences of the United States of America. 101 (6): 1731–6. Bibcode:2004PNAS..101.1731M. doi:10.1073/pnas.0305763101. PMC 341840. PMID 14757826.
  8. de Parseval N, Heidmann T (April 1998). "Physiological knockout of the envelope gene of the single-copy ERV-3 human endogenous retrovirus in a fraction of the Caucasian population". Journal of Virology. 72 (4): 3442–5. doi:10.1128/JVI.72.4.3442-3445.1998. PMC 109847. PMID 9525678.
  9. Mangeney M, Renard M, Schlecht-Louf G, Bouallaga I, Heidmann O, Letzelter C, et al. (December 2007). "Placental syncytins: Genetic disjunction between the fusogenic and immunosuppressive activity of retroviral envelope proteins". Proceedings of the National Academy of Sciences of the United States of America. 104 (51): 20534–9. Bibcode:2007PNAS..10420534M. doi:10.1073/pnas.0707873105. PMC 2154466. PMID 18077339.
  10. Chuong EB (October 2013). "Retroviruses facilitate the rapid evolution of the mammalian placenta". BioEssays. 35 (10): 853–61. doi:10.1002/bies.201300059. PMC 4332834. PMID 23873343.

Further reading

External links

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

Transcription factors and intracellular receptors
(1) Basic domains
(1.1) Basic leucine zipper (bZIP)
(1.2) Basic helix-loop-helix (bHLH)
Group A
Group B
Group C
bHLH-PAS
Group D
Group E
Group F
bHLH-COE
(1.3) bHLH-ZIP
(1.4) NF-1
(1.5) RF-X
(1.6) Basic helix-span-helix (bHSH)
(2) Zinc finger DNA-binding domains
(2.1) Nuclear receptor (Cys4)
subfamily 1
subfamily 2
subfamily 3
subfamily 4
subfamily 5
subfamily 6
subfamily 0
(2.2) Other Cys4
(2.3) Cys2His2
(2.4) Cys6
(2.5) Alternating composition
(2.6) WRKY
(3) Helix-turn-helix domains
(3.1) Homeodomain
Antennapedia
ANTP class
protoHOX
Hox-like
metaHOX
NK-like
other
(3.2) Paired box
(3.3) Fork head / winged helix
(3.4) Heat shock factors
(3.5) Tryptophan clusters
(3.6) TEA domain
  • transcriptional enhancer factor
(4) β-Scaffold factors with minor groove contacts
(4.1) Rel homology region
(4.2) STAT
(4.3) p53-like
(4.4) MADS box
(4.6) TATA-binding proteins
(4.7) High-mobility group
(4.9) Grainyhead
(4.10) Cold-shock domain
(4.11) Runt
(0) Other transcription factors
(0.2) HMGI(Y)
(0.3) Pocket domain
(0.5) AP-2/EREBP-related factors
(0.6) Miscellaneous
see also transcription factor/coregulator deficiencies
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