anti-Matrilin 3 (MATN3) Anticorps

Human Matrilin 3 (MATN3) interaction partners

1. Our data highlights the importance of detection and careful characterization of intragenic duplication CNVs, presenting them as a novel and very rare genetic mechanism in IFT81-related Jeune syndrome and MATN3-related MED.

2. miR-448 contributed to the progression of osteoarthritis by directly targeting matrilin-3.

3. Study confirmed that MATN3 protein was highly expressed in GAC patients, and MATN3 overexpression could be used as an independent predictor of poor prognosis in GAC patients.

4. our results revealed miR-483-5p directly targeted to the cartilage matrix protein matrilin 3 (Matn3) and tissue inhibitor of metalloproteinase 2 (Timp2) to stimulate chondrocyte hypertrophy, extracellular matrix degradation, and cartilage angiogenesis, and it consequently initiated and accelerated the development of OA.

5. The results of the study indicate a potential role for the MATN3 rs28598872 polymorphism in the pathogenesis of Temporomandibular Joint Internal Derangement.

6. 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.

7. MATN3 plays a regulatory role in cartilage homeostasis due to its capacity to induce IL-1Ra, upregulate gene expression of major cartilage matrix components, and downregulate the expression of OA-associated matrix-degrading proteinases in chondrocytes.

8. MATN3 may have the inherent ability to inhibit premature chondrocyte hypertrophy by suppressing BMP-2/Smad1 activity

9. The VWA1 domain of matrilin-3 is primarily responsible for the induction of IL-6 release from primary human chondrocytes.

10. Polymorphism in the MATN3 gene might play a role in osteoarthritis in the Chinese Han population.

11. Haplotype-4 of MATN3 is associated with vertebral fracture risk independent of bone mineral density in Chinese postmenopausal women.

12. MATN3 mutations were identified in 13 multiple epiphyseal dysplasia patients and comprised predominantly of missense mutations.

13. Radiographic findings in patients with COMP and MATN3 mutations showed marked abnormalities in hip and knee joints.

14. a matrilin-3 mutation associated with osteoarthritis does not affect collagen affinity but promotes the formation of wider cartilage collagen fibrils

15. increased expression of MATN3 in osteoarthritis might contribute to the degeneration of articular cartilage.

16. 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, MMP1, -3 & -13, & matrilin-3 itself

17. Mutation in MATN3 had significant association for patients with osteoarthritis.

18. Four novel missense mutations and one recurrent missense mutation were identified in MATN3 in seven families with multiple epiphyseal dysplasia.

19. MATN3 mutations is associated with multiple epiphyseal dysplasia

20. Contrary to the previous assumption that the MATN3 mutation in multiple epiphyseal dysplasia is confined to the beta-sheet regions, one novel mutation is located outside the beta-sheet region, within an alpha-helix region

Mouse (Murine) Matrilin 3 (MATN3) interaction partners

1. 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)

2. MATN3 plays a regulatory role in cartilage homeostasis due to its capacity to induce IL-1Ra, upregulate gene expression of major cartilage matrix components, and downregulate the expression of OA-associated matrix-degrading proteinases in chondrocytes.

3. MATN3 may have the inherent ability to inhibit premature chondrocyte hypertrophy by suppressing BMP-2/Smad1 activity

4. 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

5. 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.

6. Secretion of matrilin 3 V194D mutant protein is not dependent on hetero-oligomerization with matrilin 1.

7. matrilin-3 mutation associated with osteoarthritis does not affect collagen affinity but promotes the formation of wider cartilage collagen fibrils

8. 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, MMP1, -3 & -13, & matrilin-3 itself

9. Expression of matrilin-3 during maturation of mouse skeletal tissues

10. 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.

11. Matrilin-3 can be considered as an interface component, capable of interconnecting macromolecular networks

12. The lack of Matn3 does not lead to postnatal chondrodysplasia but accounts for higher incidence of osteoarthritis.

13. Matrilin-1 and matrilin-3 modulate collagen fibrillogenesis in cartilage and show that biochemical compensation might exist between matrilins, evidenced by Matn3 deficiency.

14. a matn3 mutation causes decreased chondrocyte proliferation and dysregulated apoptosis leading to epiphyseal dysplasia

Cow (Bovine) Matrilin 3 (MATN3) interaction partners

1. Data suggest that matrilins 1 and 3 dose-dependently mediate weak cell attachment without promoting focal adhesion formation.