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This study demonstrated that complexin-II differentially influence cognitive function in early and late stages of Alzheimer's disease.
Then results indicated that CPLX2 may be involved in the etiology of schizophrenia and one of its potential biological mechanisms by studying the effects of CPLX2 risk variants on working memory load-dependent neural activity in a frontoparietal network.
These results suggested that CPLX2 participated in synaptic taste transduction.
CPLX2 rs1366116*T variant represents a risk factor of schizophrenia, and , at the same time, CPLX2 rs3892909*T variant is protective against schizophrenia (study performed in Armenians).
role in synaptic vesicle exocytosis
altered immunoreactivity of this protein in prefrontal cortex in severe mental illness
in huntingtin mutation, the decline in neurotransmitter release is a direct consequence of complexin II depletion
In schizophrenia, complexin II was reduced in dorsolateral prefrontal cortex and superior temporal cortex. The impairment of synaptic transmission may contribute to the dysfunction of cortical neural circuits that characterises the disorder.
CX2 level increased between the fetal and the 6-10 years groups and then plateaued
the C2B domain of syt1, independent of complexin, is the molecular clamp that arrests synaptic vesicles prior to Ca(2+)-triggered fusion.
We describe a high degree of structural similarity between the CpxII CTD and the SNAP25-SN1 domain (C-terminal half) and show that the CTD peptide lowers the rate of SDS-resistant SNARE complex formation in vitro. Moreover, corresponding CpxII:SNAP25 chimeras do restore complexin's function and even 'superclamp' tonic secretion.
Complexin II is a central target molecule that links NADPH oxidase-derived reactive oxygen species to glutamate-mediated neuronal excitotoxicity in ischemic stroke.
CpxII attenuates fluctuations of the early fusion pore and slows its expansion.
Cplx 1 and 2 play a role in facilitating vesicle priming, and also lead to the new hypothesis that Cplxs may synchronize vesicle release by promoting coupling between secretory vesicles and calcium channels.
Cplx2 knockout mice exhibit hyperlocomotion following neonatal isolation stress.
Several months after lesion, Cplx2 null mutants showed reduced pre-pulse inhibition, deficit of spatial learning and loss of inhibition after MK-801 challenge.
Complexin 2 knockout mice show significant abnormalities in cognitive function and synaptic plasticity.
We studied the mRNA distribution of CPLXI and CPLXII in mouse brain. We show that while CPLXs are expressed in distinct cell populations they do not segregate with particular neurotransmitters or different classes of transmitter action
We found an early and progressive decrease of CPLXII expression in R6/2 mice brains. In contrast, no changes in SNARE expression were seen in R6/2 brains compared with wild type brain.
stabilization of SNARE interactions by complexin is an essential aspect of the regulated trafficking events that increase apical membrane epithelial sodium channel density either by constitutive or regulated trafficking pathways
CPXs regulate the size of the primed vesicle pools and have a positive role in Ca(2+)-triggered exocytosis in chromaffin cells
Proteins encoded by the complexin/synaphin gene family are cytosolic proteins that function in synaptic vesicle exocytosis. These proteins bind syntaxin, part of the SNAP receptor. The protein product of this gene binds to the SNAP receptor complex and disrupts it, allowing transmitter release. Two transcript variants encoding the same protein have been found for this gene.
, complexin II
, synaphin 1
, complexin 2
, LOW QUALITY PROTEIN: complexin-2