LECT1

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

CNMD
Identifiers
Aliases	CNMD, BRICD3, CHM-I, CHM1, MYETS1, LECT1, leukocyte cell derived chemotaxin 1, chondromodulin
External IDs	OMIM: 605147; MGI: 1341171; HomoloGene: 5095; GeneCards: CNMD; OMA:CNMD - orthologs
Gene location (Human) Chr. Chromosome 13 (human)[1] Band 13q14.3 Start 52,703,264 bp[1] End 52,739,820 bp[1]
Gene location (Mouse) Chr. Chromosome 14 (mouse)[2] Band 14|14 D3 Start 79,875,130 bp[2] End 79,899,610 bp[2]
RNA expression pattern Bgee Human Mouse (ortholog) Top expressed in tibia cartilage tissue testicle ventricular zone gonad ganglionic eminence nucleus accumbens caudate nucleus retinal pigment epithelium putamen Top expressed in vestibular membrane of cochlear duct vestibular sensory epithelium saccule cochlea human fetus lumbar spinal ganglion trachea intercostal muscle calvaria utricle More reference expression data BioGPS More reference expression data
Orthologs Species Human Mouse Entrez 11061 16840 Ensembl ENSG00000136110 ENSMUSG00000022025 UniProt O75829 Q9Z1F6 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 Mb Chr 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]