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The laminar organization of multiple neuronal types in the cerebral cortex is required for normal cognitive function. De plus, nous expédions DAB1 Anticorps (137) et DAB1 Protéines (6) et beaucoup plus de produits pour cette protéine.
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Alternatively spliced dab1 isoforms were identified.
these results establish an unstable repeat insertion in DAB1 as a cause of cerebellar degeneration.
Study shows that early neural cells transiently express Reelin (Montrer RELN Kits ELISA) at the time they leave the presumptive olfactory/vomeronasal epithelium and that Dab 1 is present in the migratory cell mass and in the presumptive ensheathing cells in the absence of reelin (Montrer RELN Kits ELISA).
this study is the first to provide genetic evidence for DAB1 as a candidate AD liability/protection gene, although the strength of the contribution of DAB1 may differ among populations
results of this study demonstrated the presence of reelin (Montrer RELN Kits ELISA), its receptors VLDLR (Montrer VLDLR Kits ELISA) and ApoER2 (Montrer LRP8 Kits ELISA) as well as Dab1 in the ENS and might indicate a novel role of the reelin (Montrer RELN Kits ELISA) system in regulating neuronal plasticity and pre-synaptic functions in the ENS.
The finding of this study suggested that variations in DAB1 involved in the Reelin signaling pathway might contribute to genetic susceptibility to autism with Chinese Han decent.
Variation in genes encoding proteins at the gateway of Reelin (Montrer RELN Kits ELISA) signaling: ligands RELN (Montrer RELN Kits ELISA) and APOE (Montrer APOE Kits ELISA), their common receptors APOER2 (Montrer LRP8 Kits ELISA) and VLDLR (Montrer VLDLR Kits ELISA), and adaptor DAB1, was examined.
show that Reelin (Montrer RELN Kits ELISA)-stimulated Notch-1 (Montrer NOTCH1 Kits ELISA) activation is dependent on Reelin (Montrer RELN Kits ELISA) signaling
alternative splicing of Dab1 is conserved in avian and mammalian species, with Dab1-L driving SFK phosphorylation in both species
we report for the first time, that DAB1 is significantly up-regulated in human frontal cortex brain samples of Alzheimer disease patients
Dab1, an essential component of the reelin (Montrer RELN Kits ELISA) pathway, is required for glia-independent somal translocation in the neocortex.
RBX2 (Montrer RNF7 Kits ELISA), a core component of the E3 ubiquitin ligase CRL5, is essential for retinal layering and function. RBX2 (Montrer RNF7 Kits ELISA) regulates the final cell position of rod bipolar cells, cone photoreceptors and Muller glia. Our data indicate that sustained RELN (Montrer RELN Kits ELISA)/DAB1 signaling, triggered by depletion of RBX2 (Montrer RNF7 Kits ELISA) or SOCS7 - a CRL5 substrate adaptor known to recruit DAB1 - causes rod bipolar cell misposition.
Mice with low or no Dab1 expression exhibited reduced calling rates, altered call-type usage, and differential vocal development trajectories.
Results showed that the Dab1 nuclear localization signal mutant can translocate into the nucleus via an unconventional temperature-dependent/ATP-dependent and cytoplasmic soluble factor-independent/RanGTP gradient-independent manner, suggesting that Dab1 has 2 (Montrer HAS2 Kits ELISA) different nuclear translocation pathways; and that the regulation of subcellular localization of Dab1 is important for the proper migration of excitatory neurons.
This study showed that spontaneous Dab1 mutations causing cerebellar pathology are impaired in motor functions during the neonatal period.
an aberrant fragment of Dab1 protein (p64 (Montrer IL2RG Kits ELISA)/60) is present in the brain of yotari mouse
When pregnant mice are exposed to EMF, Dab1 expression increases in the EMF-treated fetal cerebral cortex extracts as compared to controls and SHAM group.
It findings link reelin (Montrer RELN Kits ELISA) with Dab1 and suggest that Dab1 functions downstream of reelin (Montrer RELN Kits ELISA) action on the homeostasis of the crypt-villus unit.
The results of this study indicate a causal relation between the downregulation of Dab1 protein levels during development and the structural and behavioral deficits associated with psychiatric diseases in the adult.
The expression of Dab-1 was analyzed in the developing mouse autopod. Transcripts of Dab-1 were abundant in the autopodial tendon primordia, but transcripts were also present in the undifferentiated mesoderm located around the digits.
results suggest a major role of VEGF (Montrer VEGFA Kits ELISA) in the regulation of reelin (Montrer RELN Kits ELISA) signaling, and Dab1 as a key molecule in the cross talk between reelin (Montrer RELN Kits ELISA) and VEGF (Montrer VEGFA Kits ELISA) signaling pathways.
Alternative spliced forms of disabled homolog 1 (DAB1) have been isolated from brain and liver.
The laminar organization of multiple neuronal types in the cerebral cortex is required for normal cognitive function. In mice, the disabled-1 gene plays a central role in brain development, directing the migration of cortical neurons past previously formed neurons to reach their proper layer. This gene is similar to disabled-1, and the protein encoded by this gene is thought to be a signal transducer that interacts with protein kinase pathways to regulate neuronal positioning in the developing brain. Alternatively spliced transcript variants of this gene have been reported, but their full length nature has not been determined.
disabled homolog 1
, disabled homolog 1 (Drosophila)
, DAB1 variant protein-like
, disabled homolog 1-like