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MATN3 encodes a member of von Willebrand factor A domain containing protein family. Zusätzlich bieten wir Ihnen Matrilin 3 Proteine (4) und Matrilin 3 Kits (1) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 56 products:
Human Polyclonal MATN3 Primary Antibody für ELISA, ICC - ABIN4332835
Ly, Essalmani, Desjardins, Seidah, Day et al.: An Unbiased Mass Spectrometry Approach Identifies Glypican-3 as an Interactor of Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) and Low Density Lipoprotein Receptor (LDLR) in Hepatocellular ... in The Journal of biological chemistry 2016
Cow (Bovine) Polyclonal MATN3 Primary Antibody für WB - ABIN2786653
Fresquet, Jackson, Loughlin, Briggs: Novel mutations in exon 2 of MATN3 affect residues within the alpha-helices of the A-domain and can result in the intracellular retention of mutant matrilin-3. in Human mutation 2008
our results revealed miR (zeige MLXIP Antikörper)-483-5p directly targeted to the cartilage matrix protein (zeige MATN1 Antikörper) matrilin 3 (Matn3) and tissue inhibitor of metalloproteinase 2 (Timp2 (zeige TIMP2 Antikörper)) to stimulate chondrocyte hypertrophy, extracellular matrix degradation, and cartilage angiogenesis, and it consequently initiated and accelerated the development of OA.
The results of the study indicate a potential role for the MATN3 rs28598872 polymorphism in the pathogenesis of Temporomandibular Joint Internal Derangement.
This report is the first to show the involvement of MATN3 in C-type natriuretic peptide/natriuretic peptide receptor-B signaling pathway during the process of transforming growth factor-beta induced chondrogenic differentiation of mesenchymal stem cells.
MATN3 plays a regulatory role in cartilage homeostasis due to its capacity to induce IL-1Ra (zeige IL1RN Antikörper), upregulate gene expression of major cartilage matrix components, and downregulate the expression of OA-associated matrix-degrading proteinases in chondrocytes.
MATN3 may have the inherent ability to inhibit premature chondrocyte hypertrophy by suppressing BMP-2 (zeige BMP2 Antikörper)/Smad1 (zeige GARS Antikörper) activity
The VWA1 (zeige VWA1 Antikörper) domain of matrilin-3 is primarily responsible for the induction of IL-6 (zeige IL6 Antikörper) release from primary human chondrocytes.
Polymorphism in the MATN3 gene might play a role in osteoarthritis in the Chinese Han population.
Haplotype-4 of MATN3 is associated with vertebral fracture risk independent of bone mineral density in Chinese postmenopausal women.
MATN3 mutations were identified in 13 multiple epiphyseal dysplasia patients and comprised predominantly of missense mutations.
Radiographic findings in patients with COMP (zeige COMP Antikörper) and MATN3 mutations showed marked abnormalities in hip and knee joints.
Data show that hand osteoarthritis (HOA)-related matrilin-3 mutation (T298M) leads to a high expression level of growth arrest DNA damage-inducible gene 153 (GADD153 (zeige DDIT3 Antikörper))
MATN3 may have the inherent ability to inhibit premature chondrocyte hypertrophy by suppressing BMP-2 (zeige BMP2 Antikörper)/Smad1 (zeige SMAD1 Antikörper) activity
study will facilitate better awareness of the differential diagnoses that might be associated with the PSACH (zeige COMP Antikörper)/MED spectrum and subsequent care of PSACH (zeige COMP Antikörper)/MED patients
Lack of COMP (zeige COMP Antikörper) and matrilin 3 leads to increased deposition of TIMP-3 (zeige TIMP3 Antikörper), which causes partial inactivation of matrix metalloproteinases in bone, including MMP-13 (zeige MMP13 Antikörper).
Secretion of matrilin 3 V194D mutant protein is not dependent on hetero-oligomerization with matrilin 1 (zeige MATN1 Antikörper).
matrilin-3 mutation associated with osteoarthritis does not affect collagen affinity but promotes the formation of wider cartilage collagen (zeige COL2A1 Antikörper) fibrils
potential of matrilin-3 to modulate gene expression profile of primary chondrocytes; tested matrilin3-dependent induction of pro-inflammatory cytokines, inducible nitric oxide synthetase & cyclooxygenase-2 (zeige PTGS2 Antikörper), MMP1 (zeige MMP1 Antikörper), -3 & -13, & matrilin-3 itself
Expression of matrilin-3 during maturation of mouse skeletal tissues
To assess the function of matrilin-3 during skeletal development, we have generated Matn-3 null mice; phenotypes of multiple epiphyseal dysplasia disorders are not caused by the absence of matrilin-3 in cartilage ECM (zeige MMRN1 Antikörper).
This gene encodes a member of von Willebrand factor A domain containing protein family. This family of proteins is thought to be involved in the formation of filamentous networks in the extracellular matrices of various tissues. This protein contains two von Willebrand factor A domains\; it is present in the cartilage extracellular matrix and has a role in the development and homeostasis of cartilage and bone. Mutations in this gene result in multiple epiphyseal dysplasia.