gp38k (CHI3L1) is a novel adhesion and migration factor for vascular cells.
AuthorsNishikawa KC, Millis AJ
JournalExp Cell Res
PubMed ID12799184
'gp38k (CHI3L1) is a secreted heparin-binding glycoprotein whose expression, in vitro, is associated with vascular smooth muscle cell (VSMC) migration and invasion into the underlying gelatinous matrix. gp38k is expressed at high levels in postconfluent "nodular" VSMC cultures and at low levels in subconfluent proliferating cultures. In vivo, expression of ... More
Chitinase 3-Like-1 (CHI3L1): a putative disease marker at the interface of proteomics and glycomics.
AuthorsCoffman FD
JournalCrit Rev Clin Lab Sci
PubMed ID19003601
'Chitinase 3-Like-1 (CHI3L1) is a secreted 40 kDa glycoprotein that is upregulated in a number of human cancers and in non-neoplastic disease states characterized by chronic inflammation and tissue remodeling. Increased serum levels of CHI3L1 parallel disease severity, poorer prognosis, and shorter survival in many human neoplasias, including cancers of ... More
Transcriptional regulation of CHI3L1, a marker gene for late stages of macrophage differentiation.
The protein product of the CHI3L1 gene, human cartilage 39-kDa glycoprotein (HC-gp39), is a tissue-restricted, chitin-binding lectin and member of glycosyl hydrolase family 18. In contrast to many other monocyte/macrophage markers, its expression is absent in monocytes and strongly induced during late stages of human macrophage differentiation. To gain insights ... More
Inflammatory cytokines induce production of CHI3L1 by articular chondrocytes.
AuthorsRecklies AD, Ling H, White C, Bernier SM
JournalJ Biol Chem
PubMed ID16234240
Elevated levels of CHI3L1 (chitinase-3-like protein 1) are associated with disorders exhibiting increased connective tissue turnover, such as rheumatoid arthritis, osteoarthritis, scleroderma, and cirrhosis of the liver. This secreted protein is not synthesized in young healthy cartilage, but is produced in cartilage from old donors or patients with osteoarthritis. The ... More