EMR3: Difference between revisions
Content deleted Content added
| Line 4: | Line 4: | ||
== Function == |
== Function == |
||
The gene product is a member of the [[adhesion-GPCRs|adhesion-GPCR]] family of receptors. Family members are characterized by an extended extracellular region with a variable number of protein domains coupled to a TM7 domain via a domain known as the GPCR-Autoproteolysis INducing ([[GAIN domain|GAIN]]) domain. In the case of EMR3, the N-terminal protein domains consists of 2 epidermal growth factor (EGF)-like domains <ref>{{cite book|last=Yona|first=Stacey|title=Adhesion-GPCRs|year=2011|publisher=Springer|isbn=978-1-4419-7912-4|pages=1-200}}</ref> <ref>{{cite journal|last=Yona|first=S|coauthors=Lin, HH; Siu, WO; Gordon, S; Stacey, M|title=Adhesion-GPCRs: emerging roles for novel receptors.|journal=Trends in biochemical sciences|date=2008 Oct|volume=33|issue=10|pages=491-500|pmid=18789697}}</ref> EMR3 is expressed predominantly by cells of the immune system. This gene is closely linked to the gene encoding egf-like molecule containing mucin-like hormone receptor 2 [[EMR2]] on chromosome 19. The protein may play a role in [[myeloid]]-myeloid interactions during immune and inflammatory responses.<ref name="entrez">{{cite web | title = Entrez Gene: EMR3 egf-like module containing, mucin-like, hormone receptor-like 3| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=84658| accessdate = }}</ref> |
The gene product is a member of the [[adhesion-GPCRs|adhesion-GPCR]] family of receptors. Family members are characterized by an extended extracellular region with a variable number of protein domains coupled to a TM7 domain via a domain known as the GPCR-Autoproteolysis INducing ([[GAIN domain|GAIN]]) domain. In the case of EMR3, the N-terminal protein domains consists of 2 epidermal growth factor [[EGF-like domain|(EGF)-like]] domains. <ref>{{cite book|last=Yona|first=Stacey|title=Adhesion-GPCRs|year=2011|publisher=Springer|isbn=978-1-4419-7912-4|pages=1-200}}</ref> <ref>{{cite journal|last=Yona|first=S|coauthors=Lin, HH; Siu, WO; Gordon, S; Stacey, M|title=Adhesion-GPCRs: emerging roles for novel receptors.|journal=Trends in biochemical sciences|date=2008 Oct|volume=33|issue=10|pages=491-500|pmid=18789697}}</ref> EMR3 is expressed predominantly by cells of the immune system. This gene is closely linked to the gene encoding egf-like molecule containing mucin-like hormone receptor 2 [[EMR2]] on chromosome 19. The protein may play a role in [[myeloid]]-myeloid interactions during immune and inflammatory responses.<ref name="entrez">{{cite web | title = Entrez Gene: EMR3 egf-like module containing, mucin-like, hormone receptor-like 3| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=84658| accessdate = }}</ref> |
||
==See also== |
==See also== |
||
Revision as of 10:40, 17 October 2012
Template:PBB EGF-like module-containing mucin-like hormone receptor-like 3 is a protein that in humans is encoded by the EMR3 gene.[1]
Function
The gene product is a member of the adhesion-GPCR family of receptors. Family members are characterized by an extended extracellular region with a variable number of protein domains coupled to a TM7 domain via a domain known as the GPCR-Autoproteolysis INducing (GAIN) domain. In the case of EMR3, the N-terminal protein domains consists of 2 epidermal growth factor (EGF)-like domains. [2] [3] EMR3 is expressed predominantly by cells of the immune system. This gene is closely linked to the gene encoding egf-like molecule containing mucin-like hormone receptor 2 EMR2 on chromosome 19. The protein may play a role in myeloid-myeloid interactions during immune and inflammatory responses.[4]
See also
References
- ^ Stacey M, Lin HH, Hilyard KL, Gordon S, McKnight AJ (2001). "Human epidermal growth factor (EGF) module-containing mucin-like hormone receptor 3 is a new member of the EGF-TM7 family that recognizes a ligand on human macrophages and activated neutrophils". J Biol Chem. 276 (22): 18863–70. doi:10.1074/jbc.M101147200. PMID 11279179.
{{cite journal}}: Unknown parameter|month=ignored (help)CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link) - ^ Yona, Stacey (2011). Adhesion-GPCRs. Springer. pp. 1–200. ISBN 978-1-4419-7912-4.
- ^ Yona, S (2008 Oct). "Adhesion-GPCRs: emerging roles for novel receptors". Trends in biochemical sciences. 33 (10): 491–500. PMID 18789697.
{{cite journal}}: Check date values in:|date=(help); Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ "Entrez Gene: EMR3 egf-like module containing, mucin-like, hormone receptor-like 3".
Further reading
- Bjarnadóttir TK, Fredriksson R, Höglund PJ; et al. (2005). "The human and mouse repertoire of the adhesion family of G-protein-coupled receptors". Genomics. 84 (1): 23–33. doi:10.1016/j.ygeno.2003.12.004. PMID 15203201.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: multiple names: authors list (link) - Olsen JV, Blagoev B, Gnad F; et al. (2006). "Global, in vivo, and site-specific phosphorylation dynamics in signaling networks". Cell. 127 (3): 635–48. doi:10.1016/j.cell.2006.09.026. PMID 17081983.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: multiple names: authors list (link) - Matmati M, Pouwels W, van Bruggen R; et al. (2007). "The human EGF-TM7 receptor EMR3 is a marker for mature granulocytes". J. Leukoc. Biol. 81 (2): 440–8. doi:10.1189/jlb.0406276. PMID 17108056.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: multiple names: authors list (link) - Kane AJ, Sughrue ME, Rutkowski MJ, Phillips JJ, Parsa AT (2010). "EMR3: A Potential Mediator of Invasive Phenotypic Variation in Glioblastoma and Novel Therapeutic Target". Neuroreport. 21 (16): 1018–22. doi:10.1097/WNR.0b013e32833f19f2. PMC 3064464. PMID 20827226.
{{cite journal}}: Unknown parameter|month=ignored (help)CS1 maint: multiple names: authors list (link)
 | This transmembrane receptor-related article is a stub. You can help Wikipedia by expanding it. |
This article incorporates text from the United States National Library of Medicine, which is in the public domain.