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anti-Human CADPS2 Antikörper:
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Human Polyclonal CADPS2 Primary Antibody für IHC, ELISA - ABIN1001982
Sadakata, Washida, Furuichi: Alternative splicing variations in mouse CAPS2: differential expression and functional properties of splicing variants. in BMC neuroscience 2007
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Human Polyclonal CADPS2 Primary Antibody für IHC (p), WB - ABIN541345
Walent, Porter, Martin: A novel 145 kd brain cytosolic protein reconstitutes Ca(2+)-regulated secretion in permeable neuroendocrine cells. in Cell 1992
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These results indicate that LRRK2 and alpha-synuclein participate in the dysregulation of CADPS2 by altering transcription and support the hypothesis that synaptic dysfunctions, through different mechanisms, might contribute to the neuronal defects of diseases such as Parkinson's disease.
Mutation screening of 187 patients with autism spectrum disorders and 36 with intellectual disability identified a missense change of maternal origin disrupting CADPS2/D2DR interaction.
This study suggested that CADPS2DeltaExon3 affects intelligence and memory in the non-clinical population.
We speculate that haploinsufficiency of CADPS2 contributes to ASDs.
identification, cloning, and comparative characterization of a second mammalian CAPS isoform, CAPS2; concluded that at the functional level, CAPS2 is largely redundant with CAPS1
Results from Cadps2-deficient mice and human data suggest that a disturbance in CADPS2-mediated neurotrophin release contributes to autistic-like cellular and behavioral phenotypes.
CAPS proteins are involved in optimizing vesicular monoamine uptake and storage mediated by VMAT1 and VMAT2
results suggest that deregulated gene expression caused by loss of Cadps2 may cause developmental deficits and/or pathological symptoms, resulting in autistic-like phenotypes
CAPS2 plays an important role in subcellular locality (axonal vs. somato-dendritic) of enhanced BDNF and NT-3 release, which is indispensable for proper development of postnatal cerebellum.
Data suggest that adequate levels of CAPS2 are critical for normal brain development and normal behavior; allelic changes due to copy number variation may contribute to autistic behavior.
Reduced axonal localization of a Caps2 splice variant impairs axonal release of BDNF and causes autistic-like behavior in mice
results suggest that CAPS2 mediates the depolarization-dependent release of NT-3 and BDNF from granule cells, leading to regulation in cell differentiation and survival during cerebellar development
CADPS2-KO mice show autistic-like phenotypes. Moreover, the results show that some autistic patients have an aberrant splicing variant of CADPS2 mRNA, suggesting that a disturbance in CADPS2-mediated neurotrophin release contributes to autism.
CADPS2/CAPS2-knockout mice exhibit pronounced impairments in cerebellar development and functions. These results are also suggestive of an involvement of the CADPS2/CAPS2 gene, which is located within the AUTS1, in the cerebellar deficits of autism.
The results show the immunohistochemical localization of the CAPS family proteins in various mouse tissues.
The two CAPS family proteins are complementarily distributed throughout the various brain regions of mice.
This gene encodes a member of the calcium-dependent activator of secretion (CAPS) protein family, which are calcium binding proteins that regulate the exocytosis of synaptic and dense-core vesicles in neurons and neuroendocrine cells. Mutations in this gene may contribute to autism susceptibility. Multiple transcript variants encoding different isoforms have been found for this gene.
, Ca2+-dependent activator protein for secretion 2
, calcium-dependent activator protein for secretion 2
, calcium-dependent secretion activator 2
, Ca++-dependent secretion activator 2
, cerebellum postnatal development associated protein 2