Affinage

COMP

Cartilage oligomeric matrix protein · UniProt P49747

Length
757 aa
Mass
82.9 kDa
Annotated
2026-06-09
100 papers in source corpus 22 papers cited in narrative 22 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

COMP is a disulfide-linked homopentamer, structurally related to the C-terminal half of thrombospondins, that organizes collagenous extracellular matrix in cartilage, tendon and other connective tissues (PMID:1429587). Pentameric assembly enables COMP to act as a catalyst of type I and II collagen fibrillogenesis—accelerating fibril formation and enforcing a narrow fibril diameter while dissociating from completed fibrils—a function lost by monomeric COMP (PMID:17716974); it engages fibrillar collagens through a specific GXKGHR motif on the triple helix (PMID:30464261). COMP also performs an intracellular role, assisting collagen secretion from the ER such that COMP-null cells retain collagen and show attenuated fibrotic responses, fully rescued by wild-type COMP (PMID:26746240). In the growth plate it cooperates with type IX collagen and matrilin-3 to build organized fibril bundles (PMID:15694129, PMID:18191556). Beyond matrix assembly, COMP activates the mechanosensory channel Piezo1 to drive Ca²⁺/CaMKII/eNOS-dependent nitric oxide production in vascular endothelium, with COMP⁻/⁻ mice showing elevated blood pressure (PMID:34983194), maintains vascular smooth muscle contractile identity through a mitochondrial interaction with prohibitin 2 (PMID:29867124), and signals via CD36 to activate MEK/ERK and PI3K/AKT in hepatocellular carcinoma (PMID:30231922). Dominant mutations in the calcium-binding type 3 repeats abolish Ca²⁺ binding and disrupt folding (PMID:7670471, PMID:11013461), causing chaperone-associated ER retention of mutant COMP together with collagen IX and matrilin-3 (PMID:11470401, PMID:15694129), triggering unfolded protein response, oxidative stress, and caspase-independent necroptosis of chondrocytes (PMID:22154936); these defects underlie pseudoachondroplasia, multiple epiphyseal dysplasia, and familial carpal tunnel syndrome (PMID:7670471, PMID:32686688).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 1992 High

    Establishing COMP's primary structure and quaternary organization defined it as a pentameric thrombospondin-related matrix protein and set the framework for all later functional work.

    Evidence cDNA cloning, sequence analysis, and expression in COS cells

    PMID:1429587

    Open questions at the time
    • Does not assign a biochemical or cellular function
    • Role of the unique N-terminal region undefined
  2. 1995 High

    Linking COMP to pseudoachondroplasia identified the calcium-binding type 3 repeats as functionally critical and established COMP as a disease gene.

    Evidence SSCP and sequencing of familial and isolated PSACH cases

    PMID:7670471

    Open questions at the time
    • Does not show how mutations affect protein function
    • Cellular consequence of mutations unknown
  3. 2000 High

    Showing that the D469del mutation specifically halves Ca²⁺ binding and abolishes the calcium-induced conformational change provided the biochemical basis for the disease-causing defect.

    Evidence Recombinant protein, equilibrium dialysis, and circular dichroism spectroscopy

    PMID:11013461

    Open questions at the time
    • Single mutation tested biochemically
    • Link between altered conformation and cellular retention not directly shown
  4. 2001 High

    Identifying that mutant COMP is retained in the rER alongside resident chaperones revealed an ER quality-control/chaperone-associated retention mechanism for the disease.

    Evidence Co-IP, FRET, and immunoelectron microscopy of PSACH chondrocytes

    PMID:11470401 PMID:9923655

    Open questions at the time
    • Mechanism by which retention causes cell death not yet defined
    • Chaperone associations are proximity-based, not functional dependencies
  5. 2001 Medium

    Dissecting the COMP promoter defined the transcriptional control of its tissue-specific expression in chondrocytes versus tendon/ligament cells.

    Evidence Promoter cloning, primer extension, luciferase reporters, and SP1 binding analysis

    PMID:11223338

    Open questions at the time
    • Full set of regulatory factors unresolved
    • How tissue-specific start-site usage is controlled is unknown
  6. 2007 High

    Demonstrating that pentameric but not monomeric COMP catalyzes collagen I/II fibrillogenesis established the molecular requirement of oligomerization for matrix assembly function.

    Evidence In vitro fibrillogenesis assay comparing pentameric and monomeric COMP, with EM

    PMID:17716974

    Open questions at the time
    • Structural basis of the catalytic mechanism unresolved
    • In vivo relevance not directly tested here
  7. 2007 Medium

    Showing ER-retention severity scales with clinical phenotype for type 3 repeat mutations but not C-terminal mutations indicated domain-specific pathomechanisms.

    Evidence Expression of 12 mutations in RCS cells with immunofluorescence scoring

    PMID:17570134

    Open questions at the time
    • Single readout (immunofluorescence)
    • Mechanism for C-terminal mutations not defined
  8. 2007 Medium

    Revealing that secreted as well as retained tendon mutants induce apoptosis showed pathogenic mechanisms in tendon are heterogeneous and not solely retention-driven.

    Evidence Adenoviral expression of three mutants in tendon fibroblasts with viability and ECM assays

    PMID:17307347

    Open questions at the time
    • Apoptotic pathway not delineated
    • Single cell type, single lab
  9. 2007 Medium

    Genetic epistasis from collagen IX/COMP double knockout established that COMP cooperates with collagen IX in growth plate organization, explaining the mild single-KO phenotype.

    Evidence Double knockout mouse model with histology and morphometry

    PMID:18191556

    Open questions at the time
    • Molecular nature of the cooperation not resolved
    • Contribution of matrilin-3 not isolated
  10. 2004 Medium

    Co-retention of collagen IX and matrilin-3 with mutant COMP showed these matrix proteins assemble cooperatively and that loss from the ECM disorganizes fibril bundles.

    Evidence 3D alginate culture of PSACH chondrocytes and RCS/COS-1 cell-type comparison

    PMID:15579310 PMID:15694129

    Open questions at the time
    • Direct binding interfaces not mapped
    • Cell-type basis of the trafficking defect not mechanistically explained
  11. 2011 Medium

    Defining the downstream death pathway showed mutant COMP retention triggers UPR, ROS, DNA damage and caspase-independent necroptosis of growth plate chondrocytes in vitro and in vivo.

    Evidence Inducible RCS cell model and PSACH mouse model with pathway readouts

    PMID:22006726 PMID:22154936

    Open questions at the time
    • UPR involvement differs between models
    • Trigger linking retention to oxidative stress not fully defined
  12. 2016 High

    Loss-of-function with molecular rescue established an intracellular role for COMP in assisting collagen secretion and its requirement for fibrotic responses.

    Evidence COMP-null fibroblasts, ER retention/rescue, fibril EM, biomechanics, and in vivo fibrosis model

    PMID:26746240

    Open questions at the time
    • Mechanism of intracellular collagen chaperoning not defined
    • Whether this requires pentamerization untested
  13. 2018 Medium

    Identifying the GXKGHR motif defined the specific COMP recognition site on fibrillar collagen triple helices.

    Evidence Recombinant collagen II peptide library binding screen

    PMID:30464261

    Open questions at the time
    • In vitro binding only, limited functional validation
    • Protective role against cross-linking not directly demonstrated
  14. 2018 High

    Establishing COMP–Piezo1 coupling revealed a non-matrix signaling role in endothelial mechanotransduction and blood pressure regulation.

    Evidence Co-IP, BRET, patch-clamp, COMP⁻/⁻ mouse blood pressure with Yoda1 rescue, EPR for NO

    PMID:34983194

    Open questions at the time
    • Structural basis of the C-terminal interaction unresolved
    • Relationship to COMP's matrix function unclear
  15. 2018 Medium

    Localizing COMP to mitochondria via prohibitin 2 connected it to vascular smooth muscle bioenergetics and contractile identity.

    Evidence Subcellular fractionation, LC-MS/MS interactome, mitochondrial transplantation, carotid injury model

    PMID:29867124

    Open questions at the time
    • How a secreted matrix protein reaches mitochondria unexplained
    • Direct binding not structurally validated
  16. 2018 Medium

    Demonstrating CD36-dependent MEK/ERK and PI3K/AKT activation identified a paracrine tumor-promoting signaling axis for COMP in hepatocellular carcinoma.

    Evidence Recombinant COMP treatment, CD36 knockdown, coculture, and xenograft model

    PMID:30231922

    Open questions at the time
    • Direct COMP–CD36 binding not structurally shown
    • Generalizability beyond HCC untested
  17. 2018 Medium

    Linking miR-223 upregulation to the adipogenesis–osteogenesis imbalance connected chondrocyte ER retention to systemic bone quality defects.

    Evidence MT-COMP transgenic mouse, microCT, bone mechanics, miRNA profiling

    PMID:29309831

    Open questions at the time
    • Causal chain from miR-223 to bone phenotype not proven
    • Single model system
  18. 2020 High

    Identifying COMP mutations that cause familial carpal tunnel syndrome through impaired tenocyte secretion extended the disease spectrum and tied oligomerization failure to tendon/ligament fibrosis.

    Evidence Patient biopsies, mouse models, UPR assays, and co-IP for oligomerization

    PMID:32686688

    Open questions at the time
    • Tissue specificity of the phenotype not fully explained
    • Why some mutations cause CTS versus MED unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How COMP's intracellular collagen-secretion chaperone activity, its extracellular fibrillogenesis catalysis, and its distinct signaling roles (Piezo1, prohibitin 2, CD36) are coordinated within and across tissues remains unresolved.
  • No unified structural model linking matrix and signaling functions
  • Mechanism of subcellular/mitochondrial targeting unknown
  • Whether signaling roles require pentameric assembly untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 2 GO:0008092 cytoskeletal protein binding 2 GO:0044183 protein folding chaperone 1 GO:0098772 molecular function regulator activity 1
Localization
GO:0005783 endoplasmic reticulum 3 GO:0005576 extracellular region 2 GO:0031012 extracellular matrix 2 GO:0005739 mitochondrion 1
Pathway
R-HSA-1474244 Extracellular matrix organization 3 R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-1266738 Developmental Biology 2
Partners
CD36COL2A1COL9A1MATN3PHB2PIEZO1

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1992 COMP cDNA cloning revealed a 755 amino acid protein that forms a homopentamer composed of five identical disulfide-linked subunits, with structural homology to the carboxyl-terminal half of thrombospondins including calcium-binding type 3 repeat domains and type 2/EGF repeat domains; the N-terminal 84 amino acids are unique to COMP. cDNA cloning, sequence analysis, expression in COS cells The Journal of biological chemistry High 1429587
1995 Mutations in exon 17B of COMP (single base-pair changes or 3 bp deletions) cause pseudoachondroplasia; six mutations delete or alter a conserved aspartic acid residue within the calcium-binding type 3 repeats, establishing that the calcium-binding domain is functionally critical. SSCP analysis and nucleotide sequencing of familial and isolated PSACH cases Nature genetics High 7670471
1998 Mutant COMP is retained in enlarged cisternae of the rough endoplasmic reticulum (rER) of PSACH chondrocytes in vitro, and this intracellular retention is associated with chondrocyte death; retention appears linked to the differentiated chondrocyte phenotype as dedifferentiated PSACH chondrocytes in monolayer do not retain COMP intracellularly. Alginate bead 3D culture of PSACH chondrocytes, immunostaining, electron microscopy Matrix biology : journal of the International Society for Matrix Biology Medium 9923655
2000 The D469del PSACH mutation disrupts calcium binding: wild-type recombinant COMP binds 10–12 Ca²⁺ ions/molecule with cooperative, calcium-induced conformational changes (by circular dichroism), whereas D469del COMP binds approximately half as many Ca²⁺ ions and shows no large CD spectral change with Ca²⁺; the mutation specifically affects calcium binding without affecting Zn²⁺, Cu²⁺, or Ni²⁺ binding. Recombinant protein expression in E. coli, equilibrium dialysis, circular dichroism spectroscopy Cell calcium High 11013461
2001 Chaperone proteins calreticulin, PDI, Grp94, BiP, and ERp72 are co-localized with retained COMP in the enlarged rER cisternae of PSACH chondrocytes; immunoprecipitation, Western blot, and FRET analyses show CRT, PDI, and Grp94 are in close proximity to both normal and mutant COMP, and BiP is closely associated with mutant COMP, indicating these chaperones participate in processing of wild-type COMP and in retention of mutant COMP. Immunoprecipitation, Western blot, FRET, immunoelectron microscopy of PSACH chondrocytes in vivo and in alginate bead culture Matrix biology : journal of the International Society for Matrix Biology High 11470401
2004 COMP mutations in the type 3 calcium-binding repeats cause retention of COMP, type IX collagen, and matrilin-3 (but not aggrecan and type II collagen) within the rER of chondrocytes in 3D culture; the absence of COMP, type IX collagen, and matrilin-3 from the extracellular matrix leads to disorganized matrix without organized collagen fibril bundles, establishing that these proteins cooperate in matrix assembly. 3D alginate culture of PSACH chondrocytes with G427E, D469del, and D511Y mutations; immunostaining; ultrastructural analysis Matrix biology : journal of the International Society for Matrix Biology Medium 15694129
2004 DeltaD469 COMP is retained in the ER of chondrocytic RCS cells (delaying secretion) but is efficiently secreted by non-chondrocytic COS-1 cells, demonstrating a cell-type-specific trafficking defect; ER accumulation of DeltaD469 COMP in RCS cells also causes co-retention of type IX collagen but not aggrecan; secreted mutant COMP disrupts assembly of normal fibrillar matrix. Expression of DeltaD469 COMP mutant in RCS and COS-1 cells, pulse-chase, immunofluorescence, ECM assembly assay Matrix biology : journal of the International Society for Matrix Biology Medium 15579310
2007 Pentameric COMP acts as a catalyst of collagen I and II fibrillogenesis: it accelerates fibril formation, increases the amount of collagen in fibrillar form, and produces fibrils with a narrow diameter distribution (149 ± 16 nm); monomeric COMP lacking the N-terminal coiled-coil domain decelerates fibrillogenesis, demonstrating that pentameric assembly is required; COMP is not incorporated into mature fibrils and dissociates upon fibril completion. In vitro collagen fibrillogenesis assay with pentameric and monomeric COMP; turbidity measurement; electron microscopy The Journal of biological chemistry High 17716974
2007 In PSACH growth plate chondrocytes, COMP mutations (type 3 repeat) correlate with ER retention severity proportional to clinical phenotype; PSACH mutations cause more cells to retain COMP than MED mutations; C-terminal domain mutations do not show this correlation, suggesting domain-specific pathomechanisms. Expression of 12 different recombinant COMP mutations in RCS cells; immunofluorescence scoring of ER retention Journal of cellular biochemistry Medium 17570134
2000 MMP-19 and MMP-20 (enamelysin) cleave COMP, generating a major proteolytic product of 60 kDa, establishing these MMPs as enzymes capable of degrading COMP in the extracellular matrix. In vitro cleavage assay with recombinant MMP-19 and MMP-20; Western blot FEBS letters Medium 10922468
2011 Retention of D469del-COMP in chondrocytes triggers caspase-independent necroptosis: it stimulates the unfolded protein response (Chop, Gadd34), elevates Nox4 and Ero1β generating reactive oxygen species, induces DNA damage (γH2AX), and produces cleaved AIF without activated caspases; loss of growth plate chondrocytes by necroptosis was also confirmed in a PSACH mouse model. Inducible expression system in rat chondrosarcoma cells; Western blot; immunofluorescence; in vivo mouse model The American journal of pathology Medium 22154936
2011 In a knock-in mouse model expressing D469del COMP, mutant COMP is retained in chondrocyte ER causing reduced proliferation and increased apoptosis without classical unfolded protein response activation; instead, microarray identified oxidative stress, cell cycle regulation, and apoptosis gene expression changes as the primary cellular response. Knock-in mouse model; growth plate histology; TUNEL; BrdU; microarray; UPR marker analysis Human mutation Medium 22006726
2016 COMP fulfills an intracellular function in assisting collagen secretion: COMP-null fibroblasts retain collagens in the ER, collagen secretion is fully restored by reintroducing wild-type COMP; lack of COMP–collagen interaction in extracellular space also alters collagen fibril morphology and density, changing skin biomechanical properties; COMP-null mice show severely attenuated fibrotic responses. COMP knockout mouse fibroblasts; ER retention assay; collagen fibril EM; biomechanical testing; fibrosis model in vivo; rescue with wild-type COMP Journal of cell science High 26746240
2018 COMP interacts directly with the C-terminus of Piezo1 via its own C-terminus and activates endogenous Piezo1 currents, leading to intracellular Ca²⁺ influx, Ca²⁺/calmodulin-dependent protein kinase II and eNOS activation, and nitric oxide production; COMP⁻/⁻ mice display elevated blood pressure and impaired acetylcholine-induced endothelium-dependent relaxation that is rescued by Piezo1 activator Yoda1. Co-immunoprecipitation; bioluminescence resonance energy transfer (BRET); patch-clamp electrophysiology; siRNA knockdown; COMP⁻/⁻ mouse blood pressure measurement; EPR detection of NO Hypertension (Dallas, Tex. : 1979) High 34983194
2018 COMP localizes within mitochondria of vascular smooth muscle cells and interacts with prohibitin 2; disruption of the COMP–prohibitin 2 interaction impairs mitochondrial oxidative phosphorylation and causes VSMC dedifferentiation (loss of contractile phenotype) in vitro and enhanced neointima formation after rat carotid artery injury in vivo. Subcellular fractionation; fluorescence assay; liquid chromatography-tandem MS interactome; mitochondrial transplantation; microarray; carotid artery injury model Cell death & disease Medium 29867124
2018 Mutant COMP retention in chondrocytes upregulates miR-223, disturbing the adipogenesis–osteogenesis balance, reducing bone mineral density, bone quality, mechanical strength, and subchondral bone thickness in the MT-COMP pseudoachondroplasia mouse model. MT-COMP transgenic mouse model; microCT; bone mechanical testing; miRNA profiling; multiple analytic approaches Matrix biology : journal of the International Society for Matrix Biology Medium 29309831
2018 HSC-derived COMP signals through the CD36 receptor on HCC cells to phosphorylate ERK and AKT, upregulating EMT markers (Slug, Twist), MMP-2, and MMP-9, promoting HCC proliferation and metastasis in vitro and in vivo; knockdown of COMP in LX2 hepatic stellate cells reduces MEK/ERK and PI3K/AKT activation in HCC cells. Recombinant COMP protein treatment; CD36 siRNA knockdown; Western blot; transwell coculture; mouse xenograft model Journal of experimental & clinical cancer research : CR Medium 30231922
2018 COMP binds specifically to a GXKGHR motif on the collagen II triple helix found exclusively in fibrillar collagens; this binding site was identified using a recombinant collagen II peptide library and overlaps with recognition sites of other collagen-binding partners (PEDF, heparin) and spans lysine residues involved in collagen cross-links, suggesting COMP may protect collagen helices from premature cross-linking. Recombinant collagen II peptide library binding screen; binding assays with COMP and TSP-4 Scientific reports Medium 30464261
2020 Two mutations in COMP cause familial carpal tunnel syndrome by impairing COMP secretion in tenocytes (the CTS-specific mutation also causes ER stress, unfolded protein response, cell death, inflammation, and progressive fibrosis in tendons/ligaments); the CTS-specific mutation fails to oligomerize properly and is trapped in the ER, whereas the mutation associated with both CTS and MED also perturbs secretion in chondrocytes. Patient biopsy histology; mouse models; ER stress markers; UPR assays; co-IP for oligomerization; immunofluorescence Nature communications High 32686688
2007 Expression of PSACH-associated mutant COMP in tendon fibroblasts increases apoptotic cell death irrespective of secretory pattern: D475N and D469Δ are retained in ER while H587R is secreted like wild-type, yet all three mutants disrupt collagen I matrix assembly and induce apoptosis, indicating heterogeneous pathogenic mechanisms in tendon. Adenoviral gene transfer into tendon fibroblast cultures; immunostaining; cell viability assays; ECM analysis Matrix biology : journal of the International Society for Matrix Biology Medium 17307347
2001 Transcription of the COMP gene is driven by a TATA-less/CAAT-less promoter with multiple transcription start sites; the 370 bp proximal region has the strongest promoter activity; the SP1 transcription factor plays a role in regulating COMP expression; tissue-specific usage of transcription start sites differs between chondrocytes and tendon/ligament cells. Promoter cloning; primer extension; reporter gene (luciferase) assays in chondrocyte, tendon, and ligament cells; SP1 binding analysis Matrix biology : journal of the International Society for Matrix Biology Medium 11223338
2007 Combined ablation of collagen IX and COMP in mice produces shortened, widened long bones with severe growth plate abnormalities (large hypocellular areas, loss of columnar chondrocyte organization) not seen in COMP-single-KO mice; COMP-null mice alone have no overt skeletal phenotype but show altered matrilin-3 deposition, indicating COMP cooperates with collagen IX in growth plate organization. Double knockout mouse model (collagen IX and COMP); histology; bone morphometry; immunostaining Matrix biology : journal of the International Society for Matrix Biology Medium 18191556

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1995 Mutations in exon 17B of cartilage oligomeric matrix protein (COMP) cause pseudoachondroplasia. Nature genetics 312 7670471
1992 COMP (cartilage oligomeric matrix protein) is structurally related to the thrombospondins. The Journal of biological chemistry 283 1429587
2007 COMP acts as a catalyst in collagen fibrillogenesis. The Journal of biological chemistry 240 17716974
2004 COMP-Ang1: a designed angiopoietin-1 variant with nonleaky angiogenic activity. Proceedings of the National Academy of Sciences of the United States of America 220 15060279
1994 Release of cartilage oligomeric matrix protein (COMP) into joint fluid after knee injury and in osteoarthritis. Annals of the rheumatic diseases 197 8311563
2009 Cartilage Oligomeric Matrix Protein (COMP): A Biomarker of Arthritis. Biomarker insights 145 19652761
2001 Cartilage oligomeric matrix protein (COMP) and collagen IX are sensitive markers for the differentiation state of articular primary chondrocytes. The Biochemical journal 138 11485547
1991 DegS-DegU and ComP-ComA modulator-effector pairs control expression of the Bacillus subtilis pleiotropic regulatory gene degQ. Journal of bacteriology 135 1901055
2018 HSCs-derived COMP drives hepatocellular carcinoma progression by activating MEK/ERK and PI3K/AKT signaling pathways. Journal of experimental & clinical cancer research : CR 120 30231922
2005 Long-term and sustained COMP-Ang1 induces long-lasting vascular enlargement and enhanced blood flow. Circulation research 111 15961719
1998 COMP (cartilage oligomeric matrix protein) is synthesized in ligament, tendon, meniscus, and articular cartilage. Connective tissue research 109 11063004
2000 Matrix metalloproteinases 19 and 20 cleave aggrecan and cartilage oligomeric matrix protein (COMP). FEBS letters 107 10922468
1998 Characterization of cartilage oligomeric matrix protein (COMP) in human normal and pseudoachondroplasia musculoskeletal tissues. Matrix biology : journal of the International Society for Matrix Biology 98 9749943
2009 Changes in serum cartilage oligomeric matrix protein (COMP), plasma CPK and plasma hs-CRP in relation to running distance in a marathon (42.195 km) and an ultra-marathon (200 km) race. European journal of applied physiology 95 19125286
2004 COMP mutations, chondrocyte function and cartilage matrix. Matrix biology : journal of the International Society for Matrix Biology 90 15694129
2008 The role of cartilage oligomeric matrix protein (COMP) in skeletal disease. Current drug targets 84 18855621
1998 Retention of cartilage oligomeric matrix protein (COMP) and cell death in redifferentiated pseudoachondroplasia chondrocytes. Matrix biology : journal of the International Society for Matrix Biology 84 9923655
2001 Calreticulin, PDI, Grp94 and BiP chaperone proteins are associated with retained COMP in pseudoachondroplasia chondrocytes. Matrix biology : journal of the International Society for Matrix Biology 83 11470401
2009 COMP-angiopoietin-1 decreases lipopolysaccharide-induced acute kidney injury. Kidney international 80 19812542
2016 COMP-assisted collagen secretion--a novel intracellular function required for fibrosis. Journal of cell science 78 26746240
2011 Deformational behaviour of knee cartilage and changes in serum cartilage oligomeric matrix protein (COMP) after running and drop landing. Osteoarthritis and cartilage 78 21616158
2006 COMP-angiopoietin-1 ameliorates renal fibrosis in a unilateral ureteral obstruction model. Journal of the American Society of Nephrology : JASN 76 16885409
1998 Cartilage oligomeric matrix protein (COMP)-induced arthritis in rats. Clinical and experimental immunology 75 9844060
2011 COMP-Ang1 stimulates HIF-1α-mediated SDF-1 overexpression and recovers ischemic injury through BM-derived progenitor cell recruitment. Blood 72 21200018
1999 Trinucleotide expansion mutations in the cartilage oligomeric matrix protein (COMP) gene. Human molecular genetics 72 9887340
2004 Chondrocyte cell death and intracellular distribution of COMP and type IX collagen in the pseudoachondroplasia growth plate. Journal of orthopaedic research : official publication of the Orthopaedic Research Society 69 15183431
2000 Expression of cartilage oligomeric matrix protein (COMP) by embryonic and adult osteoblasts. Journal of orthopaedic research : official publication of the Orthopaedic Research Society 69 11117291
1998 Novel and recurrent COMP (cartilage oligomeric matrix protein) mutations in pseudoachondroplasia and multiple epiphyseal dysplasia. Human genetics 65 9921895
1998 Identification of twelve mutations in cartilage oligomeric matrix protein (COMP) in patients with pseudoachondroplasia. American journal of medical genetics 60 9880218
1999 Mutational analysis and membrane topology of ComP, a quorum-sensing histidine kinase of Bacillus subtilis controlling competence development. Journal of bacteriology 58 10419951
2004 Serum cartilage oligomeric matrix protein (COMP) in rheumatoid arthritis and knee osteoarthritis. Clinical rheumatology 55 15940561
2015 Intravitreal AAV2.COMP-Ang1 Prevents Neurovascular Degeneration in a Murine Model of Diabetic Retinopathy. Diabetes 54 26340930
2002 Novel types of COMP mutations and genotype-phenotype association in pseudoachondroplasia and multiple epiphyseal dysplasia. Human genetics 54 12483304
2005 COMP mutation screening as an aid for the clinical diagnosis and counselling of patients with a suspected diagnosis of pseudoachondroplasia or multiple epiphyseal dysplasia. European journal of human genetics : EJHG 51 15756302
2013 Functional analysis of the interdependence between DNA uptake sequence and its cognate ComP receptor during natural transformation in Neisseria species. PLoS genetics 50 24385921
1998 Production of cartilage oligomeric matrix protein (COMP) by cultured human dermal and synovial fibroblasts. Osteoarthritis and cartilage 50 10343777
1993 Genetic linkage of mild pseudoachondroplasia (PSACH) to markers in the pericentromeric region of chromosome 19. Genomics 49 8307576
2007 Ablation of collagen IX and COMP disrupts epiphyseal cartilage architecture. Matrix biology : journal of the International Society for Matrix Biology 44 18191556
2004 Role of TSP-5/COMP in pseudoachondroplasia. The international journal of biochemistry & cell biology 44 15094116
2021 COMP and TSP-4: Functional Roles in Articular Cartilage and Relevance in Osteoarthritis. International journal of molecular sciences 42 33668140
2011 A novel form of chondrocyte stress is triggered by a COMP mutation causing pseudoachondroplasia. Human mutation 41 22006726
2011 D469del-COMP retention in chondrocytes stimulates caspase-independent necroptosis. The American journal of pathology 41 22154936
2022 COMP (Cartilage Oligomeric Matrix Protein), a Novel PIEZO1 Regulator That Controls Blood Pressure. Hypertension (Dallas, Tex. : 1979) 40 34983194
2000 Molecular cloning, sequencing, and tissue and developmental expression of mouse cartilage oligomeric matrix protein (COMP). Journal of orthopaedic research : official publication of the Orthopaedic Research Society 39 11052496
2014 Pseudoachondroplasia/COMP - translating from the bench to the bedside. Matrix biology : journal of the International Society for Matrix Biology 38 24892720
2012 COMP-angiopoietin-1 recovers molecular biomarkers of neuropathy and improves vascularisation in sciatic nerve of ob/ob mice. PloS one 38 22412941
2014 Novel cartilage oligomeric matrix protein (COMP) neoepitopes identified in synovial fluids from patients with joint diseases using affinity chromatography and mass spectrometry. The Journal of biological chemistry 35 24917676
2004 MED, COMP, multilayered and NEIN: an overview of multiple epiphyseal dysplasia. Pediatric radiology 35 15503005
2000 Delta 469 mutation in the type 3 repeat calcium binding domain of cartilage oligomeric matrix protein (COMP) disrupts calcium binding. Cell calcium 35 11013461
2017 VISTA.COMP - an engineered checkpoint receptor agonist that potently suppresses T cell-mediated immune responses. JCI insight 34 28931757
2008 Angiopoietin-1 variant, COMP-Ang1 attenuates hydrogen peroxide-induced acute lung injury. Experimental & molecular medicine 33 18587270
2008 Model systems for studying skeletal dysplasias caused by TSP-5/COMP mutations. Cellular and molecular life sciences : CMLS 32 18193163
2001 Measurement of cartilage oligomeric matrix protein (COMP) in normal and diseased equine synovial fluids. Osteoarthritis and cartilage 32 11237659
1998 Analysis of cartilage oligomeric matrix protein (COMP) in synovial fibroblasts and synovial fluids. British journal of rheumatology 32 9714346
2020 Aggrecan and COMP Improve Periosteal Chondrogenesis by Delaying Chondrocyte Hypertrophic Maturation. Frontiers in bioengineering and biotechnology 31 32984292
2000 Cartilage oligomeric matrix protein (COMP) levels in digital sheath synovial fluid and serum with tendon injury. Equine veterinary journal 31 10661386
2019 Cartilage oligomeric matrix protein (COMP) promotes cell proliferation in early-onset colon cancer tumorigenesis. Surgical endoscopy 30 31617091
2009 Genetic mouse models for the functional analysis of the perifibrillar components collagen IX, COMP and matrilin-3: Implications for growth cartilage differentiation and endochondral ossification. Histology and histopathology 29 19554514
2003 Identification of cartilage oligomeric matrix protein (COMP) gene mutations in patients with pseudoachondroplasia and multiple epiphyseal dysplasia. Journal of human genetics 29 12768438
2018 COMP-prohibitin 2 interaction maintains mitochondrial homeostasis and controls smooth muscle cell identity. Cell death & disease 28 29867124
2017 Quantitative evaluation of the relationship between COMP promoter methylation and the susceptibility and curve progression of adolescent idiopathic scoliosis. European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society 28 28951969
2010 Protective role of COMP-Ang1 in ischemic rat brain. Journal of neuroscience research 28 19885826
2009 A designed angiopoietin-2 variant, pentameric COMP-Ang2, strongly activates Tie2 receptor and stimulates angiogenesis. Biochimica et biophysica acta 28 19339208
2018 Mutant cartilage oligomeric matrix protein (COMP) compromises bone integrity, joint function and the balance between adipogenesis and osteogenesis. Matrix biology : journal of the International Society for Matrix Biology 27 29309831
2001 Concentration of collagen, aggrecan and cartilage oligomeric matrix protein (COMP) in synovial fluid from equine middle carpal joints. Equine veterinary journal 27 11469774
2004 Characterization of a pseudoachondroplasia-associated mutation (His587-->Arg) in the C-terminal, collagen-binding domain of cartilage oligomeric matrix protein (COMP). The Biochemical journal 26 14580238
2004 Cell-type specific trafficking of expressed mutant COMP in a cell culture model for PSACH. Matrix biology : journal of the International Society for Matrix Biology 26 15579310
2012 Serum COMP-C3b complexes in rheumatic diseases and relation to anti-TNF-α treatment. Arthritis research & therapy 25 22264230
2008 COMP mutations: domain-dependent relationship between abnormal chondrocyte trafficking and clinical PSACH and MED phenotypes. Journal of cellular biochemistry 25 17570134
2015 COMP-1 promotes competitive advantage of nematode sperm. eLife 24 25789512
2002 Serum level of cartilage oligomeric matrix protein (COMP) in equine osteoarthritis. Equine veterinary journal 24 12358001
2019 Identifying the role of ASPN and COMP genes in knee osteoarthritis development. Journal of orthopaedic surgery and research 23 31665048
2017 Cartilage oligomeric matrix protein (COMP) in rheumatoid arthritis and its correlation with sonographic knee cartilage thickness and disease activity. Clinical rheumatology 23 28889184
2005 Enhanced concentration of COMP (cartilage oligomeric matrix protein) in osteochondral fractures from racing Thoroughbreds. Journal of orthopaedic research : official publication of the Orthopaedic Research Society 23 15607888
2021 Long non-coding RNA SNHG25 promotes epithelial ovarian cancer progression by up-regulating COMP. Journal of Cancer 22 33613753
2020 Mutations in COMP cause familial carpal tunnel syndrome. Nature communications 22 32686688
2005 Analysis of cartilage oligomeric matrix protein (COMP) degradation and synthesis in equine joint disease. Equine veterinary journal 22 15651731
2014 Thyroid hormones increase collagen I and cartilage oligomeric matrix protein (COMP) expression in vitro human tenocytes. Muscles, ligaments and tendons journal 21 25489544
2009 COMP-angiopoietin-1 enhances skeletal muscle blood flow and insulin sensitivity in mice. American journal of physiology. Endocrinology and metabolism 21 19491299
2018 COMP and TSP-4 interact specifically with the novel GXKGHR motif only found in fibrillar collagens. Scientific reports 20 30464261
2014 COMP-angiopoietin 1 increases proliferation, differentiation, and migration of stem-like cells through Tie-2-mediated activation of p38 MAPK and PI3K/Akt signal transduction pathways. Biochemical and biophysical research communications 20 25446117
2008 Protective effect of COMP-angiopoietin-1 on cyclosporine-induced renal injury in mice. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 20 18463324
2015 Donor Heart Treatment With COMP-Ang1 Limits Ischemia-Reperfusion Injury and Rejection of Cardiac Allografts. American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons 19 25932532
2015 The Angiopoietin-1 Variant COMP-Ang1 Enhances BMP2-Induced Bone Regeneration with Recruiting Pericytes in Critical Sized Calvarial Defects. PloS one 18 26465321
2014 Cartilage oligomeric matrix protein (COMP) in murine brachiocephalic and carotid atherosclerotic lesions. Atherosclerosis 18 25133350
2010 COMP-angiopoietin-1 accelerates bone formation during distraction osteogenesis. Bone 18 20149905
2015 Designed angiopoietin-1 variant, COMP-angiopoietin-1, rescues erectile function through healthy cavernous angiogenesis in a hypercholesterolemic mouse. Scientific reports 16 25783805
2004 Circulating COMP is decreased in pseudoachondroplasia and multiple epiphyseal dysplasia patients carrying COMP mutations. American journal of medical genetics. Part A 16 15266613
2001 Analysis of the promoter region of human cartilage oligomeric matrix protein (COMP). Matrix biology : journal of the International Society for Matrix Biology 16 11223338
2017 Antisense Reduction of Mutant COMP Reduces Growth Plate Chondrocyte Pathology. Molecular therapy : the journal of the American Society of Gene Therapy 15 28162960
2016 COMP-Ang1 prevents periodontitic damages and enhances mandible bone growth in an experimental animal model. Bone 15 27612438
2006 Urine cartilage oligomeric matrix protein (COMP) measurement is useful in discriminating the osteoarthritic Thoroughbreds. Osteoarthritis and cartilage 15 16895759
2017 Correlation of serum cartilage oligomeric matrix protein (COMP) and interleukin-16 (IL-16) levels with disease severity in primary knee osteoarthritis: A pilot study in a Malaysian population. PloS one 14 28910372
2014 COMP-angiopoietin1 potentiates the effects of bone morphogenic protein-2 on ischemic necrosis of the femoral head in rats. PloS one 14 25329960
2005 In vivo human Cartilage oligomeric matrix protein (COMP) promoter activity. Matrix biology : journal of the International Society for Matrix Biology 14 16214313
2022 Intracameral Injection of AAV-DJ.COMP-ANG1 Reduces the IOP of Mice by Reshaping the Trabecular Outflow Pathway. Investigative ophthalmology & visual science 13 36520455
2021 COMP-Ang1: Therapeutic potential of an engineered Angiopoietin-1 variant. Vascular pharmacology 13 34583025
2013 COMP-Ang1 promotes chondrogenic and osteogenic differentiation of multipotent mesenchymal stem cells through the Ang1/Tie2 signaling pathway. Journal of orthopaedic research : official publication of the Orthopaedic Research Society 13 23893855
2008 Analysis of cartilage oligomeric matrix protein (COMP) in synovial fluid, serum and urine from 51 racehorses with carpal bone fracture. The Journal of veterinary medical science 13 18840965
2007 Expression of PSACH-associated mutant COMP in tendon fibroblasts leads to increased apoptotic cell death irrespective of the secretory characteristics of mutant COMP. Matrix biology : journal of the International Society for Matrix Biology 13 17307347

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