Leukocyte Cell Derived Chemotaxin 1 (LECT1) ELISA Kits

Rabbit Leukocyte Cell Derived Chemotaxin 1 (LECT1) interaction partners

1. 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.

Human Leukocyte Cell Derived Chemotaxin 1 (LECT1) interaction partners

1. ChMI directly suppressed the proliferation and growth of osteosarcoma cells.

2. CHM1 seems to have pleiotropic functions in Ewing sarcoma.

3. 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.

4. 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.

5. 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

6. the inner meniscus contained larger amounts of ChM-I, and that the inner meniscus-derived ChM-I inhibited endothelial cell proliferation.

7. Degenerative intervertebral disc cells express ChM-I. Administration of bFGF down-regulates the expression of ChM-I. Expression is correlated with the degree of degeneration.

8. Inhibition of YY1 in combination with forced expression of p300 and Sp3 restored the expression of ChM-I in cells with a hypomethylated promoter region, but not in cells with hypermethylation.

9. Data suggest that chondromodulin-I impairs the VEGF-A-stimulated motility of endothelial cells by destabilizing lamellipodial extensions.

10. Methylation in the core-promoter region of the chondromodulin-I gene determines the cell-specific expression by regulating the binding of transcriptional activator Sp3

11. chondromodulin-I has a pivotal role in maintaining valvular normal function by preventing angiogenesis that may lead to valvular heart diseases

12. Cell-specific epigenetic regulation of ChM-I gene expression

13. new hypoxia-inducible and SOX9-regulated genes, Gdf10 and Chm-I. In addition, Mig6 and InhbA were induced by hypoxia, predominantly via HIF-2alpha

Mouse (Murine) Leukocyte Cell Derived Chemotaxin 1 (LECT1) interaction partners

1. These findings indicated that Chm-I was an indispensable factor for ectopic cartilage regeneration and the maintenance of cartilage homeostasis.

2. 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

3. 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.

4. chondromodulin 1 stabilizes the chondrocyte phenotype by supporting chondrogenesis but inhibiting chondrocyte hypertrophy and endochondral ossification.

5. Role of ChM-I in cartilage and eye development

6. chondromodulin I is a bone remodeling factor

7. Chondromodulin I suppresses T cell responses and synovial cell proliferation, implying that this cartilage matrix protein has a therapeutic potential in rheumatoid arthritis.

8. chondromodulin-I has a pivotal role in maintaining valvular normal function by preventing angiogenesis that may lead to valvular heart diseases

9. The expression domains of ChM-I and TeM during vertebrate development incorporate the typical avascular regions of the mesenchymal tissues.

10. 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