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Results showed that epigenetic mechanisms play a pivotal role in transcriptional regulation of PS1 (show PSEN1 ELISA Kits) and PS2 (show PDCD6 ELISA Kits) during cerebral cortical development
This study presents novel evidence for the differential expression of PS proteins in a nongenetic model for aging, resulting in an overall increase of the PS2 (show PDCD6 ELISA Kits) to PS1 (show PSEN1 ELISA Kits) ratio.
The loss of PS2 (show PDCD6 ELISA Kits) could have a critical role in lung tumor development through the upregulation of iPLA2 (show PLA2G6 ELISA Kits) activity by reducing gamma-secretase.
One mechanism by which PS2 (show PDCD6 ELISA Kits) works to reign in proinflammatory microglial behavior and PS2 (show PDCD6 ELISA Kits) dysfunction or deficiency could result in unchecked proinflammatory activation. contributing to neurodegeneration.
At the transcriptional level, Psen1 (show PSEN1 ELISA Kits)/2 removal induced cyclic AMP response element-binding protein (CREB)/CREB (show CREB ELISA Kits)-binding protein (show CREBBP ELISA Kits) binding.
Upregulation of PS1 (show PSEN1 ELISA Kits)/gamma-secretase activity may be a risk factor for late onset sporadic Alzheimer's disease.
mechanism by which PS regulates synaptic function and calcium homeostasis using acute hippocampal slices from PS1 (show PSEN1 ELISA Kits) and PS2 (show PDCD6 ELISA Kits) conditional knockouts and primary cultured postnatal hippocampal neurons
data delineate a promoter responsive element targeted by parkin (show PARK2 ELISA Kits) that drives differential regulation of presenilin-1 (show PSEN1 ELISA Kits) and presenilin-2 transcription with functional consequences for gamma-secretase activity and cell death.
Interactome analyses of mature gamma-secretase complexes reveal distinct molecular environments of presenilin (PS) paralogs and preferential binding of signal peptide peptidase to PS2 (show PDCD6 ELISA Kits).
Distribution and expression profile of Psen2 differs from Psen1 (show PSEN1 ELISA Kits) in the cerebral cortex during development.
Zebrafish pre2 is maternally and ubiquitously expressed during early embryo development, whereas Pre2 protein expression is initiated between 6 and 12 hours post fertilisation (hpf), suggesting strict regulation of pre2 translation.
These results suggest that Psen2 plays a more prominent role in Notch (show NOTCH1 ELISA Kits) signalling and embryo development in zebrafish than in mammals, and that the effect of reduced Psen2 can be ameliorated by Psen1 (show PSEN1 ELISA Kits) loss.
This study identified variants in PSEN2 across a range of phenotypes (Alzheimer's Disease , Alzheimer's Disease and cerebrovascular disease,frontotemporal dementia and progressive supranuclear palsy.
Its mutations of PSEN2 account for pathogenicity of early-onset familial Alzheimer's disease.
PSEN2 mutations appeared not only in Alzheimer's Disease patients but also in patients with other disorders, including frontotemporal dementia, dementia with Lewy bodies, breast cancer, dilated cardiomyopathy, and Parkinson's disease with dementia
Mutations in PSEN2 are relatively rare cause of the autosomal-dominant cases of Early onset familial Alzheimer Disease.
The results of this study showed that PSEN2 was significantly downregulated in the auditory cortex of Alzheimer's disease patients when compared to controls.
PSEN2 mutations are common in the Chinese Han population with a history of AD and FTD (show FTL ELISA Kits)
A review, representing the first attempt to systematically organize the available evidence concerning the phenotypic characteristics of familial Alzheimer's disease due to PSEN2 mutations
Mutation of on PS1 (show PSEN1 ELISA Kits) and PS2 AXXXAXXXG motifs strongly impacts gamma-secretase activity.
study describes a previously unrecognized sequence change (c.376G>A) in PSEN2 in an early onset Alzheimer's disease patient and her likewise affected mother
The loss of PS2 could have a critical role in lung tumor development through the upregulation of iPLA2 (show PLA2G6 ELISA Kits) activity by reducing gamma-secretase.
Alzheimer's disease (AD) patients with an inherited form of the disease carry mutations in the presenilin proteins (PSEN1 or PSEN2) or the amyloid precursor protein (APP). These disease-linked mutations result in increased production of the longer form of amyloid-beta (main component of amyloid deposits found in AD brains). Presenilins are postulated to regulate APP processing through their effects on gamma-secretase, an enzyme that cleaves APP. Also, it is thought that the presenilins are involved in the cleavage of the Notch receptor such that, they either directly regulate gamma-secretase activity, or themselves act are protease enzymes. Two alternatively spliced transcript variants encoding different isoforms of PSEN2 have been identified.
presenilin 2 (Alzheimer disease 4)
, presenilin beta