Cartilage Oligomeric Matrix Protein (COMP) ELISA Kits

Horse (Equine) Cartilage Oligomeric Matrix Protein (COMP) interaction partners

1. The aims of this study were to investigate the proteomic composition of injured tendons during early and late disease stages to identify disease-specific cleavage patterns of the extracellular matrix protein cartilage oligomeric matrix protein (COMP).

2. The present results suggest that not only type III collagen but also cartilage oligomeric matrix protein is involved in the repair and remodeling processes of the digital flexor tendon.

3. Within the limitations of the study design, production of COMP during healing of skin wounds does not appear to be influenced by wound type or anatomic site, nor does it appear to be correlated with TGF-beta1 concentrations.

4. COMP concentrations in digital flexor tendon sheath synovial fluid were significantly greater than those in normal horses with noninfected tenosynovitis caused by intrathecal tendon/ligament tearing, but not by other lesions.

5. The present study indicates that dynamic in vivo compression at high load and frequency lowers matrix content of COMP in the articular cartilage of the third carpal bone.

Human Cartilage Oligomeric Matrix Protein (COMP) interaction partners

1. In this study the authors have identified a GXKGHR motif on the collagen II helix to bind to COMP, using a recombinantly expressed collagen II peptide library. This binding sequence is conserved throughout evolution and they demonstrate that TSP-4 binds to the same sequence.

2. Authors confirmed that COMP is an ECM protein which is differentially expressed between subcutaneous abdominal and gluteal AT. Despite its depot-specific expression pattern, however, AT COMP mRNA levels and plasma COMP concentration correlated positively with overall obesity but not body fat distribution.

3. Our results indicated that RvD1 impaired paracrine of CAFs-derived COMP by targeting FPR2/ROS/FOXM1 signaling to repress EMT and cancer stemness in hepatocellular carcinoma (HCC). Thus, RvD1 may be a potential agent to promote treatment outcomes in HCC.

4. presents the expression levels of ADAMTS-7 and COMP in the decidual tissues of mice and humans suffering from SA.

5. elevated plasma cartilage oligomeric matrix protein (COMP) level are associated with the progression of non-traumatic osteonecrosis of femoral head

6. COMP may have a role in acute articular cartilage adaptation to knee joint loading indicating cartilage degeneration; changes in COMP concentration after physical activity seem to be highly influenced by the COMP baseline level

7. Functional information known about COMP comes from disorders caused either by COMP mutations or, more recently, by the recognition that altered regulation of COMP contributes to disease pathology. While the mechanism(s) causing dysregulation of COMP is not known, the presence of COMP in various disease states suggest important role(s). [review]

8. Adolescent idiopathic scoliosis patients had significantly high COMP promoter methylation and low gene expression. Positive and high COMP promoter methylation was correlated with young age and high Cobb angle of main curve

9. Our findings indicated that hepatic stellate cells-derived COMP collaborated with CD36 and subsequently played an essential role in MEK/ERK and PI3K/AKT-mediated hepatocellular carcinoma (HCC) progression. COMP might act as a promising target for the diagnosis and treatment of aggressive HCC.

10. These findings suggest that Zalpha domain of human ADAR1 binding with the GAC hairpin stem in COMP can lead to a non-genetic, RNA editing-mediated substitution in COMP that may then play a crucial role in the development of pseudoachondroplasia.

11. Higher serum COMP levels in knee osteoarthritis reflect knee structural damage.

12. COMP (and C-reactive protein) serum levels were both associated with the incidence of knee osteoarthritis.

13. Data indicate cartilage oligomeric matrix protein (COMP) homozygote missense variant [c.1423G>A; p.(D475N)] in 2 severely affected pseudoachondroplasia individuals.

14. The serum COMP is a promising biomarker in rheumatoid arthritis which reflects disease activity and damage to the articular cartilage.

15. the novel mutation of COMP may result in intracellular accumulation of the mutant protein. Decreased plasma COMP and increased plasma CTX-II may potentially serve as diagnostic markers of PSACH but may not be applicable in the presymptomatic carrier.

16. COMP promoted colon cancer cell proliferation partially through the activation of PI3K/ Akt/ mTOR/ p70S6K pathway.

17. The findings suggest that upregulation of ADAMTS-7 and down regulation of COMP are associated with human AA.

18. Data show that a rare missense variant in the COMP gene (cartilage oligomeric matrix protein) and a frameshift variant in the CHADL gene (chondroadherin-like protein) strongly associate with osteoarthritis total hip replacement.

19. COMP is a novel biomarker in breast cancer, which contributes to the severity of the disease by metabolic switching and increasing invasiveness and tumor cell viability, leading to reduced survival in animal models and human patients.

20. The average sCOMP level was highest among the controls and lowest among the infected children. In the juvenile idiopathic arthritis patients, the level of sCOMP was not associated with the level of CRP or with clinical signs of disease activity.

Mouse (Murine) Cartilage Oligomeric Matrix Protein (COMP) interaction partners

1. While identifying the cellular pathologic mechanisms underlying the murine mutant (MT)-COMP model of pseudoachondroplasia, increased midline-1 (MID1) expression and mammalian target of rapamycin complex 1 (mTORC1) signaling was found.

2. COMP N-terminus directly interacted with the EGF11-12 domain of Notch1 and activated Notch1 signaling, as evidenced by co-immunoprecipitation and mammalian two-hybrid assay. In conclusion, COMP served as a potential ligand of Notch1, thereby driving embryonic stem cell (ESC)-vascular smooth muscle cells (VSMCs) differentiation.

3. presents the expression levels of ADAMTS-7 and COMP in the decidual tissues of mice and humans suffering from SA.

4. Of the six biomarkers, only COMP and DPP4 showed high and SPP1 moderate correlation with the spinal muscular atrophy phenotype. PLS3 overexpression neither influenced the SMN level nor the six biomarkers, supporting the hypothesis that PLS3 acts as an independent protective modifier.

5. Study describes a novel mechanism by which the deleterious consequences of mutant COMP retention results in upregulation of miR-223 disturbing the adipogenesis - osteogenesis balance. This results in reduction in bone mineral density, bone quality, mechanical strength and subchondral bone thickness which align with the pseudoachondroplasia phenotype.

6. COMP could normally have a protective role against PASMC phenotype switching

7. these findings revealed the essential role of COMP in retarding the development of vascular aging and vascular smooth muscle cell senescence.

8. COMP deficiency drove macrophages toward the atherogenic phenotype and thereby aggravated atherosclerotic calcification.

9. COMP forms a complex with collagens intracellularly that is a prerequisite for collagen secretion.

10. The accumulation and thereby the functionality of thrombospondin in extracellular matrix is controlled by concentration-dependent, intermolecular "matrix trapping" mechanism.

11. COMP-Ang1 can enhance BMP2-induced cranial bone regeneration with increased pericyte recruitment. Combined delivery of the proteins might be a therapeutic strategy to repair cranial bone damage.

12. COMP deficiency shortened tail-bleeding and clotting time and accelerated ferric-chloride-induced thrombosis. COMP specifically inhibited thrombin-induced platelet aggregation, activation, and retraction and the thrombin-mediated cleavage of fibrinogen.

13. COMP immunoreactivity was observed in about half of the investigated plaques from the ApoE null mice, mainly located along the intima-medial border. Plaques in the brachiocephalic artery from ApoE mice lacking COMP were increased in size with 54%.

14. study will facilitate better awareness of the differential diagnoses that might be associated with the PSACH/MED spectrum and subsequent care of PSACH/MED patients

15. The lack of arthritis, together with high levels of COMP-specific antibodies, in COMP-deficient mice indicates that susceptibility to arthritis is COMP specific and that endogenous expression of COMP in wild-type mice tolerizes B cells in vivo.

16. results imply that COMP is not a key upstream mediator of the anabolic effects of ML on the skeleton.

17. Lack of COMP and matrilin 3 leads to increased deposition of TIMP-3, which causes partial inactivation of matrix metalloproteinases in bone, including MMP-13.

18. A novel form of chondrocyte stress triggered by the expression of a human-like mutation in COMP is central to the pathogenesis of pseudoachondroplasia.

19. reducing steady state levels of COMP mRNA alleviates intracellular retention of other extracellular matrix proteins associated with the pseudoachondroplasia cellular pathology

20. Data show that cartilage oligomeric matrix protein (COMP) promotes cell attachment via independent mechanisms involving cell surface CD47 and alphaVbeta3 integrin and that cell attachment to COMP induces formation of fascin-stabilized actin microspikes.

Cow (Bovine) Cartilage Oligomeric Matrix Protein (COMP) interaction partners

1. COMP synthesis is differentially regulated by TGFbeta1 in the surface and middle zones of bovine articular cartilage.

2. role for proteinases other than MMPs in the degradation of COMP in cartilage

3. COMP mutant expression in tendon fibroblasts leads to increased apoptotic cell death irrespective of the secretory characteristics of mutant COMP

4. COMP mRNA expression level was markedly increased by ball oscillation.

5. COMP acts as a catalyst in collagen fibrillogenesis.