anti-Dystrobrevin alpha (DTNA) Antibodies

Zebrafish Dystrobrevin alpha (DTNA) interaction partners

1. Ordered disorder of the astrocytic dystrophin-associated protein complex in the norm and pathology.

Mouse (Murine) Dystrobrevin alpha (DTNA) interaction partners

1. A phosphorylation site on alpha-dystrobrevin-1 is essential for functional interactions with several proteins at the neuromuscular junction.

2. Alpha-dystrobrevin is a multifunctional protein that increases dystrophin's binding to the dystrophin-glycoprotein complex.

3. Loss of alpha dystrobrevin is associated with perturbation in cell cycle progression and nuclei shape.

4. Ordered disorder of the astrocytic dystrophin-associated protein complex in the norm and pathology.

5. alpha-dystrobrevin emerges as a central organizer of dystrophin-associated protein in glial endfeet and a rare example of a glial protein with a role in maintaining BBB function

6. the interaction between alpha-catulin and alpha-dystrobrevin is evolutionarily conserved in C. elegans and mouse muscles and strongly suggests that this interaction contributes to the integrity of the dystrophin complex

7. The ErbB2 signaling maintains high efficacy of synaptic transmission by stabilizing the postsynaptic apparatus via phosphorylation of alpha-dystrobrevin1.

8. This is the first demonstration in which assembly of an astroglial protein scaffold containing syntrophin and dystrophin in perivascular astrocytes is dependent on the presence of alpha-dystrobrevin.

9. Fundamental functional differences between the alpha-dystrobrevins of mice and humans raises questions about the use of the mouse as a model animal for Duchenne muscular dystrophy.

10. identified a new dystrobrevin-associated protein, DAMAGE; interacts with the N-terminal region of alpha-dystrobrevin

11. kinetics of the dystrobrevin-Kif5A interaction showed a lower affinity of alpha compared to that of beta-dystrobrevin for binding to kinesin

12. AlphaDB, betaDB, & dystrophin are concentrated at a discrete subset of inhibitory synapses on the somata & dendrites of cerebellar Purkinje cells. Sensorimotor behaviors reflecting cerebellar function are perturbed in mice lacking any of these proteins.

13. biglycan is important for the maintenance of muscle cell integrity and plays a direct role in regulating the expression and sarcolemmal localization of the intracellular signaling proteins dystrobrevin-1 and -2, alpha- and beta1-syntrophin and nNOS

14. Complete deletion of Dtna isoforms does not reveal any new neuromuscular junction phenotype.

15. Expression of palmitoylated alpha-dystrobrevin prevented the muscular dystrophy observed in the alpha-dystrobrevin-null mice, demonstrating that the altered form of alpha-dystrobrevin was functional.

16. We propose that alpha-DB plays a role in a structure or regulation mechanism unique to MCH-expressing neurons.

17. Mice deficient for alpha-dystrobrevin (adbn(-/-)) exhibit extensive myofiber degeneration and neuromuscular junction abnormalities

18. This study suggests that alpha dystrobrevin is a significant component of the muscle intrinsic program that mediates the formation of complex AChR aggregates.

Human Dystrobrevin alpha (DTNA) interaction partners

1. Report left ventricular non-compaction associated with Barth Syndrome due to triple mutations in TAZ, DTNA, and SDHA genes in multiple members of one family.

2. we show for the first time localization of alpha-DB2 in nucleoli and Cajal bodies and provide evidence that a-DB2 is involved in the structure of nucleoli and might modulate nucleolar functions

3. our findings suggest that novel mutations in FAM136A and DTNA genes are probably causal variants in FMD.

4. Ordered disorder of the astrocytic dystrophin-associated protein complex in the norm and pathology.

5. apoptosis-induction in HL-60 cells involves not only classical markers of apoptosis but also a network alpha-DB-associated proteins at the cell membrane, the cytoplasm and nucleus, affecting key cellular transport processes and cellular structure.

6. Results suggest that alpha-dystrobrevin isoforms play a central role in cytoskeleton reorganization via their multiple interactions with actin and actin-associating proteins.

7. Data show that alpha-dystrobrevin-1 recruits alpha-catulin, which supersensitizes alpha(1D)-AR functional responses by recruiting effector molecules to the signalosome.

8. Fundamental functional differences between the alpha-dystrobrevins of mice and humans raises questions about the use of the mouse as a model animal for Duchenne muscular dystrophy.

9. During a cycle of regeneration in tibialis anterior muscle following myonecrosis, alpha-dystrobrevin reaches 50% of the protein level on day 28 by 6.6 days, regenerating more slowly than dystrophin.

10. alpha-dystrobrevin and its splice isoforms have a role in signal transduction in myeloid cells during induction of granulocytic differentiation and/or at the commitment stage of differentiation or phagocytic cells

11. Transgenic expression of either isoform of alpha-dystrobrevin prevented muscle fiber degeneration in knockout mice; however, only alphaDB1 corrected defects at neuromuscular and musculotendinous junctions.

12. patients with deficiency of beta2-syntrophin and alpha-dystrobrevin presented with severe congenital weakness and died in the first year, and patients with deficiency of alpha-DNT had congenital muscular dystrophy with complete external ophthalmoplegia.

13. findings suggest that a-dystrobrevin specifically is associated with the tight junctions during their reorganization

14. Results confirm that dystrophin is required for anchorage of the syntrophin-dystrobrevin subcomplex and suggest that expression of the syntrophin-dystrobrevin complex may be independently regulated through neuromuscular transmission.

15. Dystrobrevin mRNA including exons 11A and 12 was increased in both skeletal and cardiac muscle of DM1 patients. The aberrantly spliced alpha-dystrobrevin isoform was localized to the sarcolemma.