Filamin Binding LIM Protein 1 Proteins (FBLIM1)

Human Filamin Binding LIM Protein 1 (FBLIM1) interaction partners

1. data implicate FBLIM1 in the pathogenesis of sterile bone inflammation and our findings suggest CRMO is a disorder of chronic inflammation and imbalanced bone remodeling

2. the present study emphasizes for the first time to our knowledge the role of Migfilin in osteoarthritis(OA) and highlights the importance of cell-ECM adhesion proteins in OA pathogenesis.

3. Migfilin expression is reduced in breast cancer.

4. alpha-parvin, beta-parvin and migfilin were expressed in tumor cells in 53%, 2%, 28% and 53% of effusions and 57%, 20%, 83% and 25% of solid lesions, respectively.

5. Migfilin positively modulates the expression and activity of epidermal growth factor receptor, and Migfilin-mediated migration and invasion depend on epidermal growth factor receptor-induced PLC-gamma and STAT3-signaling pathways.

6. Migfilin promoted beta-catenin degradation by reinforcing the association between beta-catenin and GSK-3beta.

7. Migfilin can activate beta1, beta2 and beta3 integrins and promote integrin mediated responses while migfilin depletion impairs the spreading and migration of endothelial cells

8. The association between filamin B and FBLP-1 may play a hitherto unknown role in cytoskeletal function, cell adhesion, and cell motility.

9. A review of migfilin's role as a key regulator both at cell adhesion sites and nuclei. It's possible role in the pathogenesis of several human diseases is also discussed.

10. Migfilin has a role in interacting with vasodilator-stimulated phosphoprotein (VASP) and regulates VASP localization to cell-matrix adhesions and migration

11. Results suggest a role for cytoplasmic migfilin in the progression of leiomyosarcomas (LMS) and identify cytoplasmic migfilin as a potentially important biological marker for human LMS progression.

12. Loss-of-function mutations in KIND1 result in marked variability in kindlin-1 immunolabeling in Kindler syndrome skin, which is mirrored by similar changes in kindlin-2 and migfilin immunoreactivity.

13. analysis of the migfilin-filamin interaction and competition with integrin beta 7 tails

14. Migfilin thus acts as a molecular switch to disconnect filamin from integrin for regulating integrin activation and dynamics of extracellular matrix-actin linkage.

15. Migfilin interacts with Src and contributes to cell-matrix adhesion-mediated survival signaling

Mouse (Murine) Filamin Binding LIM Protein 1 (FBLIM1) interaction partners

1. Suggest migfilin regulates cardiac hypertrophy in transverse aortic constriction.

2. C-terminal LIM domains of migfilin dictate its focal adhesion localization, and these domains mediate an interaction with kindlin in vitro and in cells, demonstrating that kindlin is important for normal migfilin dynamics.

3. results identify FBLP-1 as a key regulator of bone homeostasis and suggest that FBLP-1 functions in this process through modulating both the intrinsic properties of OB/BMSCs (i.e., BMSC-extracellular matrix adhesion and migration

4. This study demonistrated that a molecular mechanism whereby FlnA loss impaired G2 to M phase entry, leading to cell cycle prolongation, compromised neural progenitor proliferation, and reduced brain size.

5. The findings indicate that the roles of migfilin are functionally redundant during mouse development and tissue homeostasis.

6. results suggest that a novel LIM protein Cal induces cardiomyocyte differentiation through its dynamic intracellular shuttling and association with CSX/NKX2-5

7. analysis of the migfilin-filamin interaction and competition with integrin beta 7 tails