LPHN1

Latrophilin 1
Identifiers
Symbols	LPHN1; CIRL1; CL1; LEC2
External IDs	MGI: 1929461 HomoloGene: 8951 IUPHAR: LPHN1 GeneCards: LPHN1 Gene
Gene Ontology Molecular function • signal transducer activity • receptor activity • G-protein coupled receptor activity • sugar binding • toxin binding • latrotoxin receptor activity Cellular component • plasma membrane • postsynaptic density • integral to membrane Biological process • G-protein coupled receptor signaling pathway • neuropeptide signaling pathway • brain development Sources: Amigo / QuickGO
RNA expression pattern
More reference expression data
Orthologs
Species	Human	Mouse
Entrez	22859	330814
Ensembl	ENSG00000072071	ENSMUSG00000013033
UniProt	O94910	Q80TR1
RefSeq (mRNA)	NM_001008701.2	NM_181039.2
RefSeq (protein)	NP_001008701.1	NP_851382.2
Location (UCSC)	Chr 19: 14.26 – 14.32 Mb	Chr 8: 86.42 – 86.47 Mb
PubMed search	[1]	[2]

Latrophilin-1 is a protein that in humans is encoded by the LPHN1 gene.

This gene encodes a member of the latrophilin subfamily of G-protein coupled receptors (GPCR). Latrophilins may function in both cell adhesion and signal transduction. In experiments with non-human species, endogenous proteolytic cleavage within a cysteine-rich GPS (G-protein-coupled-receptor proteolysis site) domain resulted in two subunits (a large extracellular N-terminal cell adhesion subunit and a subunit with substantial similarity to the secretin/calcitonin family of GPCRs) being non-covalently bound at the cell membrane. Latrophilin-1 has been shown to recruit the neurotoxin from black widow spider venom, alpha-latrotoxin, to the synapse plasma membrane.

See also

• Latrophilin receptor

Further reading

• Südhof TC (2001). "alpha-Latrotoxin and its receptors: neurexins and CIRL/latrophilins". Annu. Rev. Neurosci. 24: 933–62. doi:10.1146/annurev.neuro.24.1.933. PMID 11520923. 
• Ushkaryov YA, Volynski KE, Ashton AC (2004). "The multiple actions of black widow spider toxins and their selective use in neurosecretion studies". Toxicon 43 (5): 527–42. doi:10.1016/j.toxicon.2004.02.008. PMID 15066411. 
• Nagase T, Ishikawa K, Suyama M et al (1999). "Prediction of the coding sequences of unidentified human genes. XII. The complete sequences of 100 new cDNA clones from brain which code for large proteins in vitro". DNA Res. 5 (6): 355–64. doi:10.1093/dnares/5.6.355. PMID 10048485. 
• Kreienkamp HJ, Zitzer H, Gundelfinger ED et al (2000). "The calcium-independent receptor for alpha-latrotoxin from human and rodent brains interacts with members of the ProSAP/SSTRIP/Shank family of multidomain proteins". J. Biol. Chem. 275 (42): 32387–90. doi:10.1074/jbc.C000490200. PMID 10964907. 
• Strausberg RL, Feingold EA, Grouse LH et al (2003). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences". Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903. doi:10.1073/pnas.242603899. PMC 139241. PMID 12477932. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=139241. 
• Ota T, Suzuki Y, Nishikawa T et al (2004). "Complete sequencing and characterization of 21,243 full-length human cDNAs". Nat. Genet. 36 (1): 40–5. doi:10.1038/ng1285. PMID 14702039. 
• Brill LM, Salomon AR, Ficarro SB et al (2004). "Robust phosphoproteomic profiling of tyrosine phosphorylation sites from human T cells using immobilized metal affinity chromatography and tandem mass spectrometry". Anal. Chem. 76 (10): 2763–72. doi:10.1021/ac035352d. PMID 15144186. 
• 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. 
• Gerhard DS, Wagner L, Feingold EA et al (2004). "The Status, Quality, and Expansion of the NIH Full-Length cDNA Project: The Mammalian Gene Collection (MGC)". Genome Res. 14 (10B): 2121–7. doi:10.1101/gr.2596504. PMC 528928. PMID 15489334. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=528928. 

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