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These results indicate that LRRK2 (show LRRK2 ELISA Kits) 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 (show DRD2 ELISA Kits) interaction.
We speculate that haploinsufficiency of CADPS2 contributes to ASDs.
identification, cloning, and comparative characterization of a second mammalian CAPS (show CAPS ELISA Kits) isoform, CAPS2 (show CAPS2 ELISA Kits); concluded that at the functional level, CAPS2 (show CAPS2 ELISA Kits) is largely redundant with CAPS1 (show CAPS ELISA Kits)
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 (show SSTR5 ELISA Kits)-dendritic) of enhanced BDNF (show BDNF ELISA Kits) and NT-3 (show NTF3 ELISA Kits) 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 (show BDNF ELISA Kits) and causes autistic-like behavior in mice
identification, cloning, and comparative characterization of a second mammalian CAPS (show CAPS ELISA Kits) isoform, CAPS2; concluded that at the functional level, CAPS2 is largely redundant with CAPS1 (show CAPS ELISA Kits)
results suggest that CAPS2 mediates the depolarization-dependent release of NT-3 (show NTF3 ELISA Kits) and BDNF (show BDNF ELISA Kits) 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 (show BDNF ELISA Kits) 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 (show CAPS ELISA Kits) family proteins in various mouse tissues.
The two CAPS (show CAPS ELISA Kits) 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
, Ca++-dependent secretion activator 2
, Ca2+-dependent activator protein
, Ca2+-dependent secretion activator
, Ca<2+-dependent activator protein for secretion
, calcium-dependent activator protein for secretion 1
, calcium-dependent secretion activator 1
, calcium-dependent activator protein for secretion 2
, calcium-dependent secretion activator 2
, cerebellum postnatal development associated protein 2