| 词条 | GRAFS |
| 释义 |
The GPCR superfamily is the largest gene family in the human genome containing approximately 800 genes.[1] As the vertebrate superfamily can be phylogenetically grouped into five main families the GRAFS classification system has been proposed. GRAFS stands for Glutamate, Rhodopsin, Adhesion, Frizzled/Taste2, Secretin.[2] They correspond to classical classes C (class C, glutamate), A (rhodopsin-like), B2 (Secretin receptor family, long N-terminal), F (Frizzled/Smoothened), and B1+3 (other secretin).[3] Taste2 has more recently considered to be closer to Rhodopsin-like receptors.[4] References1. ^{{cite journal|last=Lander|first=ES|author2=Linton, LM |author3=Birren |author4= International Human Genome Sequencing, Consortium |title=Initial sequencing and analysis of the human genome.|journal=Nature|date=Feb 15, 2001|volume=409|issue=6822|pages=860–921|pmid=11237011|doi=10.1038/35057062|display-authors=etal|url=https://deepblue.lib.umich.edu/bitstream/2027.42/62798/1/409860a0.pdf}} 2. ^{{cite journal|last=Fredriksson|first=R|author2=Lagerström, MC |author3=Lundin, LG |author4= Schiöth, HB |title=The G-protein-coupled receptors in the human genome form five main families. Phylogenetic analysis, paralogon groups, and fingerprints.|journal=Molecular Pharmacology|date=June 2003|volume=63|issue=6|pages=1256–72|pmid=12761335|doi=10.1124/mol.63.6.1256}} 3. ^{{cite journal |last1=Krishnan |first1=A |last2=Almén |first2=MS |last3=Fredriksson |first3=R |last4=Schiöth |first4=HB |title=The origin of GPCRs: identification of mammalian like Rhodopsin, Adhesion, Glutamate and Frizzled GPCRs in fungi. |journal=PloS One |date=2012 |volume=7 |issue=1 |pages=e29817 |doi=10.1371/journal.pone.0029817 |pmid=22238661|pmc=3251606 }} 4. ^{{cite journal |vauthors= Nordström KJ, Sällman Almén M, Edstam MM, Fredriksson R, Schiöth HB |title= Independent HHsearch, Needleman—Wunsch-based, and motif analyses reveal the overall hierarchy for most of the G protein-coupled receptor families |journal= Molecular Biology and Evolution |volume= 28 |issue= 9 |pages= 2471–80 |date= September 2011 |pmid= 21402729 |doi= 10.1093/molbev/msr061}} See also
1 : Human genetics |
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