Browse our anti-BICD2 (BICD2) Antibodies

Human Bicaudal D Homolog 2 (Drosophila) (BICD2) interaction partners

1. Results provide evidence that BICD2 is a capsid-associated dynein adaptor utilized by HIV-1 for transport to the nucleus.

2. BICD2 mutations appear rather unlikely to cause a phenotype of hereditary motor and sensory neuropathy and are a very rare cause of the hereditary spastic paraplegia phenotype

3. A family with three members affected by spinal muscular dystrophy 2, caused by the first in-frame deletion of BICD2 is described.

4. our findings contribute to the better understanding of spinal muscular atrophy-2 pathology by providing evidence for a common pathomechanism of BICD2 mutations that increase microtubule stability in motor neurons leading to increased axonal branching and to impaired neuromuscular junction development.

5. BICD2 facilitates infection by promoting the trafficking of viral cores to the nucleus, thereby promoting nuclear entry of the viral genome and infection

6. BICD2 missense mutations were identified in patients with severe muscular atrophy with arthrogryposis and asymptomatic individuals with subclinical features.

7. Data suggest that BICD1 and BICD2 are highly expressed in the nervous system during development and are important in neuronal homeostasis. [REVIEW]

8. results reveal that dominant mutations in BICD2 hyperactivate DDB motility and suggest that an imbalance of minus versus plus end-directed microtubule motility in neurons may underlie spinal muscular atrophy.

9. These findings give further insight into the clinical and pathoanatomical consequences of BICD2 mutations.

10. several analyses of vesicular transport demonstrated that Rab6A and BICD2 play crucial roles in Golgi tubule fusion with the endoplasmic reticulum (ER) in brefeldin A (BFA)-treated cells

11. the features of BICD2 spinal muscular atrophy, lower extremity predominant are consistent with a pathological process that preferentially affects lumbar lower motor neurons

12. This study identified BICD3 significantly associated loci with a biologically plausible role in schizophrenia.

13. Mutations in BICD2 cause congenital autosomal-dominant spinal muscular atrophy and massive Golgi fragmentation in affected cells.

14. BICD2 mutations cause non-5q linked spinal muscular atrophy in humans

15. Disease causing mutations resulting in amino acid substitutions in two binding regions of BICD2 increase its binding affinity for the cytoplasmic dynein-dynactin complex.

16. Data suggest that ASUN promotes perinuclear enrichment of dynein at G2/M that facilitates BICD2- and CENP-F-mediated anchoring of dynein to nuclear pore complexes.

17. isolation, cloning, and characterization of human Nek8, a new mammalian NIMA-related kinase, and its candidate substrate Bicd2

Mouse (Murine) Bicaudal D Homolog 2 (Drosophila) (BICD2) interaction partners

1. Data suggest that binding of Lis1 to DDB complex does not strongly disrupt processive motility along microtubules; motile DDB complex binds up to two Lis1 dimers; mutational analysis suggested that Lis1 binds directly to the dynein motor domains during DDB complex movement. (Lis1 = lissencephaly 1 protein; DDB complex = dynein-dynactin-BicD2 complex; BicD2 = bicaudal D homolog 2 protein)

2. several analyses of vesicular transport demonstrated that Rab6A and BICD2 play crucial roles in Golgi tubule fusion with the endoplasmic reticulum (ER) in brefeldin A (BFA)-treated cells

3. Data indicate that Bicaudal-D2 (BICD2)-deficient mice develop disrupted laminar organization of cerebral cortex and the cerebellum, pointing to impaired radial neuronal migration.

4. LIS1 is required for dynein-mediated transport induced by membrane tethering of BICD2-N and LIS1 contributes to dynein accumulation at microtubule plus ends and BICD2-positive cellular structures.

5. BICD2-N transgene increased lifespan in 'low copy' SOD1-G93A ALS transgenic mice.