3.4.24.B4: matrix metalloproteinase-13
This is an abbreviated version!
For detailed information about matrix metalloproteinase-13, go to the full flat file.
Word Map on EC 3.4.24.B4
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3.4.24.B4
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cartilage
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chondrocytes
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osteoarthritis
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metalloproteinases
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joint
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articular
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aggrecan
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degeneration
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mmp-2
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tnf
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knee
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timp-1
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arthritis
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synovial
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interleukin-1
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proteoglycans
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degener
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cox-2
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osteoblast
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adamts-5
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ligament
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intra-articular
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collagenases
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col2a1
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thrombospondin
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pulposus
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runx2
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cruciate
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zymography
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chondrogenic
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gelatinase
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meniscus
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intervertebral
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subchondral
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disintegrin
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endochondral
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safranin
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synoviocytes
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collagenolytic
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matrix-degrading
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chondroprotective
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ossification
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temporomandibular
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mt1-mmp
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chondrogenesis
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medicine
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stromelysin-1
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diagnostics
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cartilage-specific
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condylar
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analysis
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osteophyte
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drug development
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aggrecanase
- 3.4.24.B4
- cartilage
- chondrocytes
- osteoarthritis
- metalloproteinases
- joint
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articular
- aggrecan
- degeneration
- mmp-2
- tnf
- knee
- timp-1
- arthritis
- synovial
- interleukin-1
- proteoglycans
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degener
- cox-2
- osteoblast
- adamts-5
- ligament
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intra-articular
- collagenases
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col2a1
- thrombospondin
- pulposus
- runx2
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cruciate
-
zymography
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chondrogenic
- gelatinase
- meniscus
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intervertebral
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subchondral
-
disintegrin
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endochondral
-
safranin
- synoviocytes
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collagenolytic
-
matrix-degrading
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chondroprotective
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ossification
-
temporomandibular
- mt1-mmp
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chondrogenesis
- medicine
- stromelysin-1
- diagnostics
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cartilage-specific
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condylar
- analysis
- osteophyte
- drug development
- aggrecanase
Reaction
proteolytic degradation of proteins =
Synonyms
collagenase, collagenase 3, collagenase-3, M10.013, matrix metalloproteinase 13, matrix metalloproteinase-13, MMP-13, MMP13, MMP13a, More, UMRCASE
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General Information
General Information on EC 3.4.24.B4 - matrix metalloproteinase-13
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malfunction
metabolism
physiological function
additional information
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interleukin-1beta treatment induces COX-2 and MMP-13 expressions in association with activation of ERKs, p38 MAPK, JNKs, and NF-kappaB in skin fibroblasts. Phorbol-12-myristate-13-acetate treatment also induces COX-2 and MMP-13 expressions in association with p38 MAPK activation. Glucosamine-hydrochloride differentially downregulates COX-2 andMMP-13 expression in the interleukin-1beta- or phorpbol-12-myristate-13-acetate-treated skin fibroblasts via the p38 MAPK-independent COX-2 translational inhibition and the p38 MAPK-dependent MMP-13 transcriptional suppression, respectively
metabolism
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the activation of MMP-13 expression by T3 is in a competitive balance with the regulation of osteocalcin expression, overview
metabolism
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the prodomain of MMP13 determines autoactivation of MMP13 and intracellular degradation of MMP13
metabolism
the prodomain of MMP13 determines autoactivation of MMP13 and intracellular degradation of MMP13
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functional role of MMP13 in tumor-induced osteolysis, MMP-13 regulates mammary tumor-induced osteolysis by activating MMP9 and transforming growth factor-beta signaling at the tumor-bone interface
physiological function
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inhibition of MMP-13 reduces resorptive activity of the cells indicating that MMP-13 likely plays an important role in bone giant cell tumor. Mesenchymal stromal cells and the multinucleated giant cells cell-cell cooperation involves giant cell-derived cytokine up-regulation of MMP-13 in the stromal cells, which in turn assists the giant cells in bone resorption
physiological function
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inhibition of MMP-13 reduces resorptive activity of the cells indicating that MMP-13 likely plays an important role in bone giant cell tumor. Mesenchymal stromal cells and the multinucleated giant cells cell-cell cooperation involves giant cell-derived cytokine up-regulation of MMP-13 in the stromal cells, which in turn assists the giant cells in bone resorption
physiological function
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involvement of MMP-13 and upregulation in the Cyr61-directed chondrosarcoma cells migration, the upregulation of MMP-13 is antagonized by decoy agonist AP-1-binding site, AP-1 oligonucleotide, but not by NF-kappaB oligonucleotide or scrambled oligonucleotide, as well as by RGD, PD98059 and FAK(Y397F) and ERK2 mutant
physiological function
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MMP-13 acts as an inflammatory mediator in age-related osteoarthritis
physiological function
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MMP-13 can initiate bone resorption and activate proMMP-9 in vitro, and both these MMPs are widely implicated in tissue destruction associated with chronic periodontitis, with proteolytic roles of MMP-13 during progression of chronic periodontitis, overview
physiological function
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MMP-13 efficiently degrades proteoglycans and type II collagen in articular cartilage and may therefore play a central role in articular cartilage degradation
physiological function
MMP-13 is a key enzyme implicated in the degradation of the extracellular matrix in osteoarthritis
physiological function
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MMP-13 is a key regulator involved in cancer, cellular movement, connective tissue disorders, and in cellular growth and proliferation, cellular assembly and organization, cellular movement, hierarchical cluster analysis of key regulator genes, overview
physiological function
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MMP-13 is a matrix metalloproteinase that is important for bone development and remodelling
physiological function
MMP-13 is a proteolytic enzyme that plays a key role in degradation and remodelling of host extracellular matrix proteins
physiological function
MMP-13 is involved in extracellular matrix remodeling
physiological function
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MMP-13 is involved in the degradation of extracellular matrix in many kinds of tissues. MMP-13 is an important factor leading to the disorganization of ZO-1, destruction of ZO-1 tight junction protein, and hyperpermeablility of blood-brain barrier in response to hypoxia. Hypoxia-induced MMP-13 expression in astrocytes enhances paracellular permeability of brain endothelial cells
physiological function
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MMP-13 is involved in the mechano-transduction in periodontal ligament cells, that is crucial for physiological and orthodontic tooth movement-associated periodontal remodelling
physiological function
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MMP-13 loss associated with impaired extracellular matrix remodeling disrupts chondrocyte differentiation by concerted effects on multiple regulatory factors. MMP-13 loss alone impedes the differentiation of primary chondrocyte micromasses by inhibiting the expression or activation of multiple regulatory factors including runt-related transcription factor 2, RUNX-2, vascular endothelial growth factor, VEGF, and beta-catenin, and enhances chondrocyte viability. The inhibitory effects of MMP-13 ablation on several principal regulators of chondrocyte maturation toward a hypertrophic-like state occurr in conjunction with diminished type X collagen expression
physiological function
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MMP-13 participate in the bone-remodeling mechanism involving the platelet-derived growth factor receptor
physiological function
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MMP-13 plays a critical role in parathyroid hormone-induced bone resorption
physiological function
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MMP13 affects the keratinocyte migration in the skin, overview. Connective tissue growth factor, CTGF, blocks angiogenic activity of vascular epithelial growth factor, VEGF, by complex formation, and MMP13 re-activates VEGF activity through selective cleavage of CTGF in the complex
physiological function
MMP13 catalyzes the degradation of extracellular matrix components in the growth plate and at the same time cleaves and releases biologically active molecules stored in the extracellular matrix, such as the vascular endothelial growth factor A
physiological function
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MMP13 catalyzes the degradation of extracellular matrix components in the growth plate and at the same time cleaves and releases biologically active molecules stored in the extracellular matrix, such as the vascular endothelial growth factor A. In mice, ablation of Mmp9, Mmp13, or both Mmp9 and Mmp13 causes severe distortion of the metaphyseal growth plate
physiological function
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MMP13 has an essential role in highly malignant and invasive growth in skin squamous cell carcinoma. Lack of host MMP13 strongly impairs implanted tumour growth of malignant skin squamous cell carcinoma cells, leading to small, mostly avascular cysts. MMP13 is essential for maintenance of angiogenesis and for invasion
physiological function
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MMP13 plays a critical role in the redifferentiation phase of kidney development. Potential role of MMP13 in endochondral and intramembranous ossification, with a functional role in skeletal development. MMP13 plays a significant role in the cartilage collagen degradation that occurs in osteoarthritis, and a pathological role of the degradative MMP13 enzyme in rheumatoid arthritis. The catalytic activity of MMP13 may play a role in the high invasion capacity of these cancer cells. Degradation of basement membrane is thought to be an early and critical event influencing tumor invasion and metastasis. MMP13 plays a role in proteolytic activity in invasive malignant growth
physiological function
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MMPs are important regulators of tissue remodeling and repair
physiological function
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the MMP-13 knockout phenotype, which is due to an inability of chondrocytes to exit the growth plate, resolves completely by 12 weeks of age, suggesting that other (collagen degrading) proteases can at least partially functionally substitute for MMP13 in this developmental role
physiological function
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tMMP-13 is responsible for cartilage proteoglycan degradation in rat synovial joints
physiological function
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MMP-13 activity is necessary for normal skeletal development and plays a central role in cartilage degeneration associated with osteoarthritis
physiological function
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MMP13 mediates cell proliferation in melanocytes and melanoma cells. Growth stimuli are mediated via MMP13 in melanocytes and melanoma
physiological function
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MMP13 mediates cell proliferation in melanocytes and melanoma cells. Growth stimuli are mediated via MMP13 in melanocytes and melanoma
physiological function
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in a larval zebrafish model, glucose treatment induces sensory axon degeneration, which is mediated by ROS formation in the skin, and ROS-dependent MMP13 activation. Glucose-induced sensory axon degeneration is prevented upon pharmacological inhibition of ROS with N-acetylcysteine, and upon pharmacological MMP13 inhibition
physiological function
neuropathy is reversed upon injection of MMP13 inhibitor into obese mice on a high-fat/high sugar diet
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age-related accumulation of advanced glycation end products can activate chondrocytes and induce the production of proinflammatory cytokines and matrix metalloproteinases
additional information
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ALK1 and Alk5 are involved in MMP-13 activity regulation, age-related shift in ALK1/ALK5 ratio in murine cartilage. A change in balance between ALK5 and ALK1 receptors in chondrocytes causes changes in MMP-13 expression, thereby causing an osteoarthritis-like phenotype
additional information
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angiotensin II promotes a stable fibrotic phenotype by inducing severe intra-plaque hemorrhages, characterized by increased degradation of interstitial collagen I via an MMP13 or MMP8-mediated mechanism, overview
additional information
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cartilage ALK1 is highly correlated with MMP-13 expression, whereas ALK5 correlates with aggrecan and collagen type II expression. Strong correlation between ALK1 and MMP-13 expression in human cartilage
additional information
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cartilage structural damage in osteoarthritis in mice is dependent on MMP13 activity
additional information
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chloramphenicol-induced MMP-13 expression is strongly associated with metastatic capacity of solid-tumor cells
additional information
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clinical outcomes of periodontal treatment and gingival crevicular fluid MMP-13 levels in MMP-13 genotype subjects, overview
additional information
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down-regulation of MMP13, Birc2, or Birc3 results in reduced tumor growth when transplanted into immunodeficient recipient mice, high MMP13 expression enhances osteosarcoma cell survival
additional information
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down-regulation of MMP13, Birc2, or Birc3 results in reduced tumor growth, while high MMP13 expression enhances osteosarcoma cell survival
additional information
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high MMP13 expression is correlated with poor prognosis and reduced median overall survival in patients with head and neck cancer. High MMP13 levels in patients with salivary gland cancer are also associated with poor survival. And high levels of tumor-derived MMP13 correlate with poor prognosis in invasive breast cancer and reduced overall survival
additional information
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in addition to phosphorylation of Elk-1, dynamic posttranslational modification of Elk-1 by small ubiquitin-related modifier, SUMO, serves as an important mechanism through which MMP-13 gene expression is regulated
additional information
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interleukin-1beta-induced activation of signal transduction pathways associated with the expression of MMP-13 downregulates the expression of miR-27b micro-RNA. Thus, miR-27b may play a role in regulating the expression of MMP-13 in human chondrocytes, with negative regulation of miR-27b expression by activation of NF-kappaB
additional information
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kinetics of MMP13 mRNA expression and tumor-induced osteolysis
additional information
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lack of transcription-translation coupling on MMP-13 expression in experimental periodontal disease
additional information
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matrix metalloproteinase-13 expression associates to cisplatin resistance in head and neck cancer cell lines
additional information
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miRNAs miR-140 and miR-27a act as regulators of the MMP-13 and IGFBP-5 genes, expression regulation in normal and osteoarthritic chondrocytes, detailed overview
additional information
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MMP-13 expression is increased in rheumatoid arthritis and osteoarthritis
additional information
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MMP-13 levels in vitro and extracellular matrix remodeling in vitro and in vivo are linked to changes in SOX9 subcellular localization, loss of MMP-13 or IKKalpha leads to the nuclear localization of SOX9. IKKalpha ablation in articular chondrocytes stabilizes their extracellular matrix by posttranscriptionally suppressing MMP-13 activity, thereby blocking their differentiation and maintaining them in an early periarticular-like state
additional information
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MMP-13 overexpression in stromal tissue of non-nevoid basal cell carcinoma syndrome-associated keratocyst odontogenic tumours explains the higher aggressiveness of these cysts
additional information
MMP13 involvement in age-related macular degeneration
additional information
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Obedience in the expression of MMP-13 as extracellular matrix remodelling executioner from the activation state of mechano-transducing molecules. The transcription factor c-fos is a constituent of the AP1-complex addressing the MMP-13 promotor. Role of activated MAP-kinases pp38 and pp42/44 in strain-induced expression of the active form of MMP-13, activated, phosphorylated p42/44 and p38 are responsible for the expression of MMP-13, overview
additional information
osteoarthritis, involving MMP-13, is a degenerative joint disease characterized by the erosion of articular cartilage leading to pain and reduced mobility
additional information
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potential role of MMP13 in choroidal angiogenesis in a murine model of laser-induced ocular neovascularisation. Deficiency of Mmp13 impaires choroidal neovascularization formation which is fully restored by wild-type bone marrow engraftment and partially rescued by several injections of wild-type mesenchymal stem cells. Mmp13 deficiency not only affects vessel recruitment, but also impairs their maturation through pericyte coverage
additional information
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protective effects of tetracycline compounds are more pronounced in synoviocytes than cartilage, and following minocycline compared to doxycycline, molecular mechanism of action, overview
additional information
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the ING2-HDAC1-mSin3A complex members regulates expression of MMP13. Upregulation of ING2 is associated with colon cancer and MMP13-dependent cellular invasion
additional information
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potential role of MMP13 in choroidal angiogenesis in a murine model of laser-induced ocular neovascularisation. Deficiency of Mmp13 impaires choroidal neovascularization formation which is fully restored by wild-type bone marrow engraftment and partially rescued by several injections of wild-type mesenchymal stem cells. Mmp13 deficiency not only affects vessel recruitment, but also impairs their maturation through pericyte coverage
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