LECT1

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

CNMD
Identifiers
AliasesCNMD, BRICD3, CHM-I, CHM1, MYETS1, LECT1, leukocyte cell derived chemotaxin 1, chondromodulin
External IDsOMIM: 605147 MGI: 1341171 HomoloGene: 5095 GeneCards: CNMD
Gene location (Human)
Chr.Chromosome 13 (human)[1]
Band13q14.3Start52,703,264 bp[1]
End52,739,820 bp[1]
RNA expression pattern
More reference expression data
Orthologs
SpeciesHumanMouse
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 MbChr 14: 79.64 – 79.66 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

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

  1. GRCh38: Ensembl release 89: ENSG00000136110 - Ensembl, May 2017
  2. GRCm38: Ensembl release 89: ENSMUSG00000022025 - Ensembl, 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. Shukunami C, Hiraki Y (August 1998). "Expression of cartilage-specific functional matrix chondromodulin-I mRNA in rabbit growth plate chondrocytes and its responsiveness to growth stimuli in vitro". Biochemical and Biophysical Research Communications. 249 (3): 885–90. doi:10.1006/bbrc.1998.9233. PMID 9731231.
  6. Hiraki Y, Mitsui K, Endo N, Takahashi K, Hayami T, Inoue H, Shukunami C, Tokunaga K, Kono T, Yamada M, Takahashi HE, Kondo J (March 1999). "Molecular cloning of human chondromodulin-I, a cartilage-derived growth modulating factor, and its expression in Chinese hamster ovary cells". European Journal of Biochemistry / FEBS. 260 (3): 869–78. doi:10.1046/j.1432-1327.1999.00227.x. PMID 10103018.
  7. "Entrez Gene: LECT1 leukocyte cell derived chemotaxin 1".
  8. Yoshioka M, Yuasa S, Matsumura K, Kimura K, Shiomi T, Kimura N, Shukunami C, Okada Y, Mukai M, Shin H, Yozu R, Sata M, Ogawa S, Hiraki Y, Fukuda K (October 2006). "Chondromodulin-I maintains cardiac valvular function by preventing angiogenesis". Nature Medicine. 12 (10): 1151–9. doi:10.1038/nm1476. PMID 16980969.

Further reading

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