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Literature summary for 3.4.24.B4 extracted from

  • Borzi, R.M.; Olivotto, E.; Pagani, S.; Vitellozzi, R.; Neri, S.; Battistelli, M.; Falcieri, E.; Facchini, A.; Flamigni, F.; Penzo, M.; Platano, D.; Santi, S.; Facchini, A.; Marcu, K.B.
    Matrix metalloproteinase 13 loss associated with impaired extracellular matrix remodeling disrupts chondrocyte differentiation by concerted effects on multiple regulatory factors (2010), Arthritis Rheum., 62, 2370-2381.
    View publication on PubMedView publication on EuropePMC

Cloned(Commentary)

Cloned (Comment) Organism
MMP-13 real-time PCR expression analysis, overview Homo sapiens

Protein Variants

Protein Variants Comment Organism
additional information knockdown of MMP-13 by stable retrotransduction of short hairpin RNA leads to impaired ECM remodeling and suppressed differentiation in conjunction with reduced levels of RUNX-2, beta-catenin, and vascular endothelial growth factor, VEGF Homo sapiens

Localization

Localization Comment Organism GeneOntology No. Textmining
extracellular matrix
-
Homo sapiens 31012
-

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
type II collagen + H2O Homo sapiens
-
?
-
?

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
cartilage
-
Homo sapiens
-
chondrocyte primary, MMP-13 real-time PCR expression analysis Homo sapiens
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
type II collagen + H2O
-
Homo sapiens ?
-
?

Synonyms

Synonyms Comment Organism
matrix metalloproteinase 13
-
Homo sapiens
MMP-13
-
Homo sapiens

General Information

General Information Comment Organism
additional information 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 Homo sapiens
physiological function 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 Homo sapiens