Sample
serum, plasma, cell culture medium, other biological media
Intended Use
The Human YKL-39 ELISA Kit is used for the quantitative measurement of human YKL-39 in serum, plasma, cell culture medium and other biological media.
Storage
- Upon receipt store all components at 4°C.
- Don't expose reagents to excessive light.
Precision
Intra-assay (Within-Run, n=16) CV=2.4-5.7 %
Inter-assay (Run-to-Run, n=5) CV=5.0-7.4 %
Sensitivity
The limit of detection (defined as such a concentration of human YKL-39 giving absorbance higher than mean absorbance of blank* plus three standard deviations of the absorbance of blank in 24 assay) is better than 35.1 pg/mL of sample.
General Description
YKL-39, also known as chitinase 3-like 2, is secreted chitinase-like protein which contains Glyco_18 domain with no chitinase catalytic activity but with putative lectin properties. In contrast to its closest homologue YKL-40, YKL-39 is not a glycoprotein. YKL-39 is secreted by articular chondrocytes, also synoviocytes and activates signal-regulated kinases ERK1/ERK2 in human embryonic kidney cells. Increased levels of YKL-39 have been demonstrated in synovial fluids of patients with osteoarthritis (OA) or rheumatoid arthritis (RA) as well as in malignant tumors, particularly in glioblastomas. It is currently recognized as a biomarker for the activation of chondrocytes and the progress of the osteoarthritis in human. In addition, autoantibodies to YKL-39 were detected in 8-11.8% of patients with RA, and 11.1% of patients with OA, while only 1% of patients with RA had autoantibodies to YKL-40. Maturation of monocyte derived macrophages in the presence of Th2 cytokine IL-4 and TGF-beta leads to the strong activation of YKL-39 expression. Thus elevated levels of YKL-39 observed during chronic inflammations can not be attributed solely to the activity of chondrocytes. In perspective, YKL-39 is also proposed as a useful biomarker to detect macrophage-specific response in tumor, atherosclerosis and neurodegenerative diseases including Alzheimer disease, in addition to the chondrocyte-specific activation.
Citations
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