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LECT1 encodes a glycosylated transmembrane protein that is cleaved to form a mature, secreted protein. Additionally we are shipping Leukocyte Cell Derived Chemotaxin 1 Antibodies (28) and Leukocyte Cell Derived Chemotaxin 1 Kits (17) and many more products for this protein.
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Chm-1 gene-modified bone marrow mesenchymal stem cells maintain the chondrogenic phenotype of tissue-engineered cartilage that can be used in cartilage tissue engineering.
The results of the present study indicated that ChMI was able to inhibit the growth of breast cancer cells; thus suggesting that ChM-I may have potential clinical applications in the treatment of breast cancer.
Data suggest ChM1 as potential tumor suppressor in gastric cancer and useful biomarker for the treatment and prognosis. Its expression was downregulated in cancer tissue, and correlated with advanced stages, lymph node metastasis, and poorer prognosis.
intact 20-25 kDa ChM-I is stored as a component of extracellular matrix in the avascular cartilage zones, but it is inactivated by a single N-terminal proteolytic cleavage in the hypertrophic zone of growth-plate cartilage
the inner meniscus contained larger amounts of ChM-I, and that the inner meniscus-derived ChM-I inhibited endothelial cell proliferation.
Degenerative intervertebral disc cells express ChM-I. Administration of bFGF (show FGF2 Proteins) down-regulates the expression of ChM-I. Expression is correlated with the degree of degeneration.
Inhibition of YY1 (show YY1 Proteins) in combination with forced expression of p300 (show EP300 Proteins) and Sp3 restored the expression of ChM-I in cells with a hypomethylated promoter region, but not in cells with hypermethylation.
Data suggest that chondromodulin-I impairs the VEGF-A (show VEGFA Proteins)-stimulated motility of endothelial cells by destabilizing lamellipodial extensions.
Methylation in the core-promoter region of the chondromodulin-I gene determines the cell-specific expression by regulating the binding of transcriptional activator Sp3
chondromodulin-I has a pivotal role in maintaining valvular normal function by preventing angiogenesis that may lead to valvular heart diseases
Cell-specific epigenetic regulation of ChM-I gene expression
These findings indicated that Chm-I was an indispensable factor for ectopic cartilage regeneration and the maintenance of cartilage homeostasis.
the inhibitory action of ChM-I on trophoblast migration and invasion, implying the potential role of the ChM-I expression in decidual cells for the regulated tissue remodeling and angiogenesis at feto-maternal interface.
chondromodulin 1 stabilizes the chondrocyte phenotype by supporting chondrogenesis but inhibiting chondrocyte hypertrophy and endochondral ossification.
Role of ChM-I in cartilage and eye development
chondromodulin I is a bone remodeling factor
Chondromodulin I suppresses T cell responses and synovial cell proliferation, implying that this cartilage matrix protein (show MATN1 Proteins) has a therapeutic potential in rheumatoid arthritis.
The expression domains of ChM-I and TeM (show TNMD Proteins) during vertebrate development incorporate the typical avascular regions of the mesenchymal tissues.
results suggest that Chm-I is involved in hypertrophic maturation of periosteal chondrocytes. Although a direct effect of Chm-I on bones is still unclear, bony callus formation was increased while external cartilaginous callus decreased in Chm1(-/-) mice
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 be involved also in the broad control of tissue vascularization during development. Alternative splicing results in multiple transcript variants encoding different isoforms.
leukocyte cell derived chemotaxin 1
, leukocyte cell-derived chemotaxin 1
, BRICHOS domain containing 3
, chondromodulin I
, multiple myeloma tumor suppressor 1
, small cartilage-derived glycoprotein
, Chondromodulin 1