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anti-Rat (Rattus) Presenilin 2 Antibodies:
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Human Polyclonal Presenilin 2 Primary Antibody for WB - ABIN1944732
Li, Ma, Potter: Identification and expression analysis of a potential familial Alzheimer disease gene on chromosome 1 related to AD3. in Proceedings of the National Academy of Sciences of the United States of America 1996
Show all 4 references for ABIN1944732
Human Polyclonal Presenilin 2 Primary Antibody for EIA, WB - ABIN493378
Hansson, Popescu, Laudon, Cedazo-Minguez, Popescu, Winblad, Ankarcrona: Caspase cleaved presenilin-1 is part of active gamma-secretase complexes. in Journal of neurochemistry 2006
Show all 2 references for ABIN493378
Chicken Polyclonal Presenilin 2 Primary Antibody for IHC, WB - ABIN2781802
da Costa: Recent insights on the pro-apoptotic phenotype elicited by presenilin 2 and its caspase and presenilinase-derived fragments. in Current Alzheimer research 2005
Human Polyclonal Presenilin 2 Primary Antibody for EIA, IHC (fro) - ABIN318338
Levy-Lahad, Wasco, Poorkaj, Romano, Oshima, Pettingell, Yu, Jondro, Schmidt, Wang: Candidate gene for the chromosome 1 familial Alzheimer's disease locus. in Science (New York, N.Y.) 1995
Results showed that epigenetic mechanisms play a pivotal role in transcriptional regulation of PS1 (show PSEN1 Antibodies) and PS2 (show PDCD6 Antibodies) 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 Antibodies) to PS1 (show PSEN1 Antibodies) ratio.
The loss of PS2 (show PDCD6 Antibodies) could have a critical role in lung tumor development through the upregulation of iPLA2 (show PLA2G6 Antibodies) activity by reducing gamma-secretase.
One mechanism by which PS2 (show PDCD6 Antibodies) works to reign in proinflammatory microglial behavior and PS2 (show PDCD6 Antibodies) dysfunction or deficiency could result in unchecked proinflammatory activation. contributing to neurodegeneration.
At the transcriptional level, Psen1/2 removal induced cyclic AMP response element-binding protein (CREB)/CREB-binding protein binding.
Upregulation of PS1 (show PSEN1 Antibodies)/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 Antibodies) and PS2 (show PDCD6 Antibodies) conditional knockouts and primary cultured postnatal hippocampal neurons
data delineate a promoter responsive element targeted by parkin (show PARK2 Antibodies) that drives differential regulation of presenilin-1 (show PSEN1 Antibodies) 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 Antibodies).
Distribution and expression profile of Psen2 differs from Psen1 (show PSEN1 Antibodies) 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 Antibodies) signalling and embryo development in zebrafish than in mammals, and that the effect of reduced Psen2 can be ameliorated by Psen1 (show PSEN1 Antibodies) loss.
German early-onset Alzheimer's disease cohort reveals a substantial frequency of PSEN2 variants.
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 Antibodies)
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 Antibodies) 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
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