Lect1 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] [from: Wikipedia contributors. (2017, October 27). LECT1. In Wikipedia, The Free Encyclopedia. Retrieved 17:42, June 3, 2019, from https://en.wikipedia.org/w/index.php?title=LECT1&oldid=807301938]

Lect1 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] [from: Wikipedia contributors. (2017, October 27). LECT1. In Wikipedia, The Free Encyclopedia. Retrieved 17:42, June 3, 2019, from https://en.wikipedia.org/w/index.php?title=LECT1&oldid=807301938]