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anti-Human BICD2 Anticorps:
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Human Polyclonal BICD2 Primary Antibody pour IHC, IHC (p) - ABIN4284611
Terenzio, Golding, Russell, Wicher, Rosewell, Spencer-Dene, Ish-Horowicz, Schiavo: Bicaudal-D1 regulates the intracellular sorting and signalling of neurotrophin receptors. dans The EMBO journal 2014
BICD2 facilitates infection by promoting the trafficking of viral cores to the nucleus, thereby promoting nuclear entry of the viral genome and infection
BICD2 missense mutations were identified in patients with severe muscular atrophy with arthrogryposis and asymptomatic individuals with subclinical features.
Data suggest that BICD1 (Montrer BICD1 Anticorps) and BICD2 are highly expressed in the nervous system during development and are important in neuronal homeostasis. [REVIEW]
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.
These findings give further insight into the clinical and pathoanatomical consequences of BICD2 mutations.
several analyses of vesicular transport demonstrated that Rab6A (Montrer RAB6A Anticorps) and BICD2 play crucial roles in Golgi tubule fusion with the endoplasmic reticulum (ER) in brefeldin A (BFA)-treated cells
the features of BICD2 spinal muscular atrophy, lower extremity predominant are consistent with a pathological process that preferentially affects lumbar lower motor neurons
Mutations in BICD2 cause congenital autosomal-dominant spinal muscular atrophy and massive Golgi fragmentation in affected cells.
BICD2 mutations cause non-5q linked spinal muscular atrophy in humans
Disease causing mutations resulting in amino acid substitutions in two binding regions of BICD2 increase its binding affinity for the cytoplasmic dynein (Montrer DYNC1H1 Anticorps)-dynactin (Montrer DCTN1 Anticorps) complex.
Data suggest that binding of Lis1 (Montrer PAFAH1B1 Anticorps) to DDB complex does not strongly disrupt processive motility along microtubules; motile DDB complex binds up to two Lis1 (Montrer PAFAH1B1 Anticorps) dimers; mutational analysis suggested that Lis1 (Montrer PAFAH1B1 Anticorps) binds directly to the dynein motor domains during DDB complex movement. (Lis1 (Montrer PAFAH1B1 Anticorps) = lissencephaly 1 protein (Montrer PAFAH1B1 Anticorps); DDB complex = dynein-dynactin (Montrer DCTN1 Anticorps)-BicD2 complex; BicD2 = bicaudal D homolog 2 protein)
Data indicate that Bicaudal-D2 (BICD2)-deficient mice develop disrupted laminar organization of cerebral cortex and the cerebellum, pointing to impaired radial neuronal migration.
LIS1 (Montrer PAFAH1B1 Anticorps) is required for dynein-mediated transport induced by membrane tethering of BICD2-N and LIS1 (Montrer PAFAH1B1 Anticorps) contributes to dynein accumulation at microtubule plus ends and BICD2-positive cellular structures.
BICD2-N transgene increased lifespan in 'low copy' SOD1-G93A ALS transgenic mice.
This gene is one of two human homologs of Drosophila bicaudal-D and a member of the Bicoid family. It has been implicated in dynein-mediated, minus end-directed motility along microtubules. It has also been reported to be a phosphorylation target of NIMA related kinase 8. Two alternative splice variants have been described.
, coiled-coil protein BICD2
, cytoskeleton-like bicaudal D protein homolog 2
, homolog of Drosophila bicaudal D
, protein bicaudal D homolog 2
, bicaudal D homolog 2
, bicaudal D protein
, bicaudal D homolog 2 (Drosophila)
, protein bicaudal D homolog 2-like