PHOENIX SECRETOMICS

Chitinase 3-like 1


Tumor Biomarker

Fra

FAP

Endocan/ESM-1

Chitinase-3-like protein 1

Chitinase 3-like 1 (CHI3L1)

Chitinase-3-like protein 1, a 40 KDa secreted and Glycosylated extracellular matrix protein that plays
an important role in the processes of inflammation and tissue remodeling. It is expressed
in articular chondrocytes, synovial cells as well as in liver. However, CHI3L1 is not synthesized under
state of health, an induction of this protein expression is observed in the patients with rheumatoid
arthritis and cancer. It was over-expressed in the one of the most over-expressed genes in glioblastoma,
papillary thyroid carcinoma, and extracellular myxoid chondrosarcoma. It is also upregulated in a number
of solid tumors, such as cancer of the breast, colon, lung, kidney, and ovary. In cancer patients, serum
CHI3L1 concentrations are often predictive of tumor stages, response to therapy, and prognosis.

Chitinase-3-like protein 1 also is an inflammatory biomarker,  which can be upregulated after pro-inflammatory
cytokine stimulation, possesses an ability to enhance the adhesion and internalization of intracellular bacteria
into colonic epithelial cells. CHI3L1 is upregulated in inflammatory conditions, including both acute and chronic
colitis. Neutralization of CHI3L1 by anti-CHI3L1 Ab significantly suppresses DSS-induced acute colitis.

Amino Acid Sequence of Human Chitinase-3-like protein 1 : 383 aa, MW 42625 Da, Cellular component: Secreted, extracellular space;
Molecular function:May play an important role in the capacity of cells to respond to and cope with changes in their environment. May play a role in tissue remodeling and defense against pathogens. ; Swiss ID: P36222
        10         20         30         40         50         60   
MGVKASQTGF VVLVLLQCCS AYKLVCYYTS WSQYREGDGS CFPDALDRFL CTHIIYSFAN  
        70         80         90        100        110        120   
ISNDHIDTWE WNDVTLYGML NTLKNRNPNL KTLLSVGGWN FGSQRFSKIA SNTQSRRTFI  
       130        140        150        160        170        180   
KSVPPFLRTH GFDGLDLAWL YPGRRDKQHF TTLIKEMKAE FIKEAQPGKK QLLLSAALSA  
       190        200        210        220        230        240   
GKVTIDSSYD IAKISQHLDF ISIMTYDFHG AWRGTTGHHS PLFRGQEDAS PDRFSNTDYA 
       250        260        270        280        290        300   
VGYMLRLGAP ASKLVMGIPT FGRSFTLASS ETGVGAPISG PGIPGRFTKE AGTLAYYEIC 
       310        320        330        340        350        360   
DFLRGATVHR ILGQQVPYAT KGNQWVGYDD QESVKSKVQY LKDRQLAGAM VWALDLDDFQ 
       370        380   
GSFCGQDLRF PLTNAIKDAL AAT 383  
CHI3L1
(Keio J Med 56 (1) : 21-27, March 2007)
Professional Custom Sample Assay
Chitinase 3 like 1 elisa kit
CHI3L1 antibody
Western blot analysis of GP-39 (CHI3L1) expression in postnatal mouse liver tissue extract by using PS001-31-AG-03-50.
CHI3L1 antibody

Western blot analysis of GP-39 (CHI3L1) expression in rat liver tissue extract by using PS001-31-AG-04-50.

The chitinase 3-like protein human cartilage glycoprotein 39 inhibits cellular responses to the inflammatory cytokines interleukin-1 and tumour necrosis factor-alpha

Expression of the chitinase 3-like protein HC-gp39 (human cartilage glycoprotein 39) is associated with conditions of increased matrix turnover and tissue remodelling. High levels of this protein have been found in sera and synovial fluids of patients with inflammatory and degenerative arthritis. In order to assess the role of HC-gp39 in matrix degradation induced by inflammatory cytokines, we have examined its effect on the responses of connective tissue cells to TNF-alpha (tumour necrosis factor-alpha) and IL-1 (interleukin-1) with respect to activation of signalling pathways and production of MMPs (matrix metalloproteases) and chemokines. Stimulation of human skin fibroblasts or articular chondrocytes with IL-1 or TNF-alpha in the presence of HC-gp39 resulted in a marked reduction of both p38 mitogen-activated protein kinase and stress-activated protein kinase/Jun N-terminal kinase phosphorylation, whereas nuclear translocation of nuclear factor kappaB proceeded unimpeded. HC-gp39 suppressed the cytokine-induced secretion of MMP1, MMP3 and MMP13, as well as secretion of the chemokine IL-8. The suppressive effects of HC-gp39 were dependent on phosphoinositide 3-kinase activity, and treatment of cells with HC-gp39 resulted in AKT-mediated serine/threonine phosphorylation of apoptosis signal-regulating kinase 1. This process could therefore be responsible for the down-regulation of cytokine signalling by HC-gp39. These results suggest a physiological role for HC-gp39 in limiting the catabolic effects of inflammatory cytokines.

Hua Ling and Anneliese D Recklies. Biochem J. 2004 June 15; 380(Pt 3): 651–659.
 
Role of mammalian chitinases in inflammatory conditions

Abstract. It has been hypothesized that dysregulated host/microbial interactions play a pivotal role in the pathogenesis of inflammatory bowel disease. However, the exact mecha­nisms underlying the induction and perpetuation of the intestinal disorder are unclear. Re­cently, we unexpectedly discovered significantly upregulated gene expression of chitinase 3-like-1 in inflamed colon of the dextran sulfate sodium-induced colitis model by employing the DNA-microarray analysis. Chitinase 3-like-1 has a chitin binding ability, but lacks the enzymatic activity of lysing microbial cell wall. Chitinase 3-like-1 protein is mainly ex­pressed in colonic epithelial cells and macrophages in the inflamed colon of dextran sulfate sodium-induced colitis. Chitinase 3-like-1, which can be upregulated after pro-inflammatory cytokine stimulation, possesses an ability to enhance the adhesion and internalization of intracellular bacteria into colonic epithelial cells. Most importantly, in vivo neutralization of chitinase 3-like-1 significantly suppressed the development of dextran sulfate sodium-induced colitis by dramatically decreasing the bacterial adhesion and invasion into colonic epithelial cells. Furthermore, anti-chitinase 3-like-1 antibody-treated mice exhibited a sig­nificantly lower load of Salmonella typhimurium in peripheral organs as compared to control rabbit IgG-treated mice. Recently, it has been reported that acidic mammalian chitinase is expressed in the setting of T helper-2-associated inflammation and subsequently induces airway hyperresponsiveness in allergic asthma patients. In addition, pan-chitinase inhibi­tor significantly ameliorates T helper-2-mediated inflammation and airway hypersensitivity. These studies provide to be a novel insight into the physiological role of mammalian chitin­ases in host/microbial interactions, and inhibition of chitinase activity would be considered a novel therapeutic strategy of allergic and inflammatory disorders. (Keio J Med 56 (1) : 21-27, March 2007)

 

Custom Service
Sample vol. Dilution Range Sample type
Catalog No.
Quantity
Price ($)
Human Chitinase-3-like protein 1 Assay
50 ul
50 x
62.5 -2000 pg/ml
Serum or EDTA plasma, cell culture supernates
PS001-31-SH
40
40
Mouse Chitinase-3-like protein 1 Assay
50 ul
50 x
62.5 -2000 pg/ml
Serum or EDTA plasma, cell culture supernates
PS001-31-SM
40
40

 

Antibody Name Application Species Host Catalog No
Quantity
Price ($)
Chitinase-3-like protein 1 Antibody WB, E human goat PS001-31-AG-01-50
50 ug
350
Chitinase-3-like protein 1 Monoclonal Antibody WB, IHC, E human rat PS001-31-MAG-01-50
50 ug
240
Chitinase-3-like protein 1 Antibody WB h, r, m goat PS001-31-AG-04-50
50 ug
160
Chitinase-3-like protein 1 Antibody WB mouse goat PS001-31-AG-02-50
50 ug
350
Chitinase-3-like protein 1 Monoclonal Antibody WB, E mouse rat PS001-31-MAG-02-50
50 ug
240
Chitinase-3-like protein 1 C-Terminal Antibody WB, E mouse goat PS001-31-AG-03-50
50 ug
160
             

 

 

 

 

 

 

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