Coactosin-like protein (COTL1 or CLP) is a protein that in humans is encoded by the COTL1 gene.[5][6][7][8]

COTL1
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
AliasesCOTL1, CLP, coactosin like F-actin binding protein 1
External IDsOMIM: 606748; MGI: 1919292; HomoloGene: 10898; GeneCards: COTL1; OMA:COTL1 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_021149

NM_028071

RefSeq (protein)

NP_066972

NP_082347

Location (UCSC)Chr 16: 84.57 – 84.62 MbChr 8: 120.54 – 120.57 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Function

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This gene encodes one of the numerous actin-binding proteins which regulate the actin cytoskeleton. This protein binds F-actin, and also interacts with and thereby stabilizes 5-lipoxygenase (ALOX5). Although this gene has been reported to map to chromosome 17 in the Smith-Magenis syndrome region, the best alignments for this gene are to chromosome 16. The Smith-Magenis syndrome region is the site of two related pseudogenes.[8]

Interactions

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COTL1 has been shown to interact with ALOX5.[9] ALOX5 is the first committed enzyme in the metabolism of arachidonic acid to an array of biologically important cell signaling agents: a) the pro-inflammatory mediator, leukotriene B4 (LTB4); b) the airways constrictors, LTC4, LTD4, and LTE4; c) the 5-hydroxyeicosatetraenoic acid family of pro-inflammatory and pro-allergic reactions mediators, 5-HETE and 5-oxo-eicosatetraenoic acid. ALOX5 also contributes to the metabolism of arachidonic acid and other polyunsaturated fatty acids to agents which act block inflammation and allergic reactions, the specialized pro-resolving mediators of the lipoxin and resolvin subclasses. Based on in vitro studies, COTL1 serves to stabilize ALOX5, acting as a chaperone or scaffold, to avert the enzyme's inactivation and thereby to promote its metabolic activity.[10]

References

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  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000103187Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000031827Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ Provost P, Samuelsson B, Rådmark O (Apr 1999). "Interaction of 5-lipoxygenase with cellular proteins". Proc. Natl. Acad. Sci. U.S.A. 96 (5): 1881–5. Bibcode:1999PNAS...96.1881P. doi:10.1073/pnas.96.5.1881. PMC 26705. PMID 10051563.
  6. ^ Chen KS, Manian P, Koeuth T, Potocki L, Zhao Q, Chinault AC, Lee CC, Lupski JR (Nov 1997). "Homologous recombination of a flanking repeat gene cluster is a mechanism for a common contiguous gene deletion syndrome". Nat. Genet. 17 (2): 154–63. doi:10.1038/ng1097-154. PMID 9326934. S2CID 27742511.
  7. ^ Rakonjac M, Fischer L, Provost P, Werz O, Steinhilber D, Samuelsson B, Rådmark O (Sep 2006). "Coactosin-like protein supports 5-lipoxygenase enzyme activity and up-regulates leukotriene A4 production". Proc. Natl. Acad. Sci. U.S.A. 103 (35): 13150–5. Bibcode:2006PNAS..10313150R. doi:10.1073/pnas.0605150103. PMC 1559768. PMID 16924104.
  8. ^ a b "Entrez Gene: COTL1 coactosin-like 1 (Dictyostelium)".
  9. ^ Provost P, Doucet J, Hammarberg T, Gerisch G, Samuelsson B, Radmark O (May 2001). "5-Lipoxygenase interacts with coactosin-like protein". J. Biol. Chem. 276 (19): 16520–7. doi:10.1074/jbc.M011205200. PMID 11297527.
  10. ^ Anwar Y, Sabir JS, Qureshi MI, Saini KS (2014). "5-lipoxygenase: a promising drug target against inflammatory diseases-biochemical and pharmacological regulation". Current Drug Targets. 15 (4): 410–22. doi:10.2174/1389450114666131209110745. PMID 24313690.
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Further reading

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