LECT1

Protein-coding gene in humans From Wikipedia, the free encyclopedia

Chondromodulin-1 is a protein that in humans is encoded by the LECT1 gene.[5][6][7]

AliasesCNMD, BRICD3, CHM-I, CHM1, MYETS1, LECT1, leukocyte cell derived chemotaxin 1, chondromodulin
End52,739,820 bp[1]
Quick facts CNMD, Identifiers ...
CNMD
Identifiers
AliasesCNMD, BRICD3, CHM-I, CHM1, MYETS1, LECT1, leukocyte cell derived chemotaxin 1, chondromodulin
External IDsOMIM: 605147; MGI: 1341171; HomoloGene: 5095; GeneCards: CNMD; OMA:CNMD - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001011705
NM_007015

NM_010701
NM_001310655

RefSeq (protein)

NP_001011705
NP_008946

NP_001297584
NP_034831

Location (UCSC)Chr 13: 52.7 – 52.74 MbChr 14: 79.88 – 79.9 Mb
PubMed search[3][4]
Wikidata
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Function

This gene encodes a glycosylated transmembrane protein that is cleaved to form a mature, secreted protein. The N-terminus of the precursor protein shares characteristics with other surfactant proteins and is sometimes called chondrosurfactant protein, although no biological activity has yet been defined for it. The C-terminus of the precursor protein contains a 25 kDa mature protein called leukocyte cell-derived chemotaxin-1 or chondromodulin-1. The mature protein promotes chondrocyte growth and inhibits angiogenesis. This gene is expressed in the avascular zone of prehypertrophic cartilage, and its expression decreases during chondrocyte hypertrophy and vascular invasion. The mature protein likely plays a role in endochondral bone development by permitting cartilaginous anlagen to be vascularized and replaced by bone. It may also be involved in the broad control of tissue vascularization during development. Alternative splicing results in multiple transcript variants encoding different isoforms.[7]

Chondromodulin-I, an antiangiogenic factor isolated from cartilage, is abundantly expressed in cardiac valves. Gene targeting of chondromodulin-I resulted in enhanced VEGF-A expression, angiogenesis, lipid deposition and calcification in the cardiac valves of aged mice.[8]

References

Further reading

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