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4YLI

CL-K1 trimer

Summary for 4YLI
Entry DOI10.2210/pdb4yli/pdb
DescriptorCollectin-11, CALCIUM ION, CHLORIDE ION, ... (5 entities in total)
Functional Keywordsc-type carbohydrate-recognition domain, collectin, c-type lectin, sugar binding protein
Biological sourceHomo sapiens (Human)
Cellular locationSecreted : Q9BWP8
Total number of polymer chains6
Total formula weight105834.61
Authors
Wallis, R.,Girija, U.V.,Gingras, A.R.,Moody, P.C.E.,Marshall, J.E. (deposition date: 2015-03-05, release date: 2015-04-08, Last modification date: 2024-11-06)
Primary citationGirija, U.V.,Furze, C.M.,Gingras, A.R.,Yoshizaki, T.,Ohtani, K.,Marshall, J.E.,Wallis, A.K.,Schwaeble, W.J.,El-Mezgueldi, M.,Mitchell, D.A.,Moody, P.C.,Wakamiya, N.,Wallis, R.
Molecular basis of sugar recognition by collectin-K1 and the effects of mutations associated with 3MC syndrome.
Bmc Biol., 13:27-27, 2015
Cited by
PubMed Abstract: Collectin-K1 (CL-K1, or CL-11) is a multifunctional Ca(2+)-dependent lectin with roles in innate immunity, apoptosis and embryogenesis. It binds to carbohydrates on pathogens to activate the lectin pathway of complement and together with its associated serine protease MASP-3 serves as a guidance cue for neural crest development. High serum levels are associated with disseminated intravascular coagulation, where spontaneous clotting can lead to multiple organ failure. Autosomal mutations in the CL-K1 or MASP-3 genes cause a developmental disorder called 3MC (Carnevale, Mingarelli, Malpuech and Michels) syndrome, characterised by facial, genital, renal and limb abnormalities. One of these mutations (Gly(204)Ser in the CL-K1 gene) is associated with undetectable levels of protein in the serum of affected individuals.
PubMed: 25912189
DOI: 10.1186/s12915-015-0136-2
PDB entries with the same primary citation
Experimental method
X-RAY DIFFRACTION (2.45 Å)
Structure validation

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