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Human Polyclonal Presenilin 2 Primary Antibody pour WB - ABIN1944732
Li, Ma, Potter: Identification and expression analysis of a potential familial Alzheimer disease gene on chromosome 1 related to AD3. dans Proceedings of the National Academy of Sciences of the United States of America 1996
Show all 4 Pubmed References
Human Polyclonal Presenilin 2 Primary Antibody pour IHC (f), IHC (p) - ABIN966891
Levy-Lahad, Wijsman, Nemens, Anderson, Goddard, Weber, Bird, Schellenberg: A familial Alzheimer's disease locus on chromosome 1. dans Science (New York, N.Y.) 1995
Show all 3 Pubmed References
PS1- and PS2-dependent substrate processing in murine cells lacking presenilins (PSs) or stably re-expressing human PS1 or PS2 in an endogenous PS-null (PSdKO) background, were studied.
Study uncovers a role of PS in presynaptic mechanisms, through APP cleavage and regulation of Syt7, that highlights aberrant synaptic vesicle processing as a possible new pathway in Alzheimer's disease.
The altered expressions of hippocampal microRNAs were associated to the imbalance between neurotoxic and neuroprotective functions and seemed to affect neurodegeneration in PSEN1/PSEN2 double knockout mice more severely than in wild-type mice.
These observations illustrate a novel PS2-dependent means of modulating LPS-mediated immune responses and identify a functional distinction between PS1 and PS2 in innate immunity.
Although hyperactivity and hypersynchronicity were respectively detected in mice expressing the PS2-N141I or the APP Swedish mutant alone, the increase in cross-frequency coupling specifically characterized the 6-month-old PS2APP mice, just before the surge of the cognitive decline
Presenilin 2 (PS2), mutations in which underlie familial Alzheimer's disease (FAD), promotes endoplasmic reticulum-mitochondria coupling only in the presence of mitofusin 2 (Mfn2).
Study shows that the binding of HSF-1, Cdx1, Ets-1 and Sp1 to Presenilin 1 promoter and that of Nkx2.2, HFH-2, Cdx1 and NF-kappaB to Presenilin 2 promoter regulate their differential expression during brain development.
ARF4 is required for Presenilin basal body localization, Notch signaling, and subsequent epidermal differentiation.
Results suggest that mutation of PS2 can lead to NF-kappaB mediate amyloidogensis, and this effect can be amplified by the absence of estrogen.
Results showed that epigenetic mechanisms play a pivotal role in transcriptional regulation of PS1 and PS2 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 to PS1 ratio.
The loss of PS2 could have a critical role in lung tumor development through the upregulation of iPLA2 activity by reducing gamma-secretase.
One mechanism by which PS2 works to reign in proinflammatory microglial behavior and PS2 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/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 and PS2 conditional knockouts and primary cultured postnatal hippocampal neurons
data delineate a promoter responsive element targeted by parkin that drives differential regulation of presenilin-1 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.
Distribution and expression profile of Psen2 differs from Psen1 in the cerebral cortex during development.
PS2 mutation significantly accelerates the onset of cognitive impairment in associative trace eyeblink memory.
PSEN2 is required for melanocytic skin pigmentation in adult zebrafish.
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 signalling and embryo development in zebrafish than in mammals, and that the effect of reduced Psen2 can be ameliorated by Psen1 loss.
Young healthy adults carrying APOE epsilon4 and APP/presenilin-1/2 displayed different hippocampus functional connectivity patterns
Determined whether a pathogenic mutation in the PSEN2 gene in a Korean patient was associated with early onset Alzheimer's disease. Findings revealed that the p.His169Asn might be an important residue in PSEN2, which may alter the functions of PSEN2, suggesting its potential involvement with AD phenotype.
Dominant negative effect of the loss-of-function gamma-secretase mutants on the wild-type enzyme through heterooligomerization has been demonstrated.
The present data suggest that PS2 mutations suppress lung tumor development by inhibiting the iPLA2 activity of PRDX6 via a gamma-secretase cleavage mechanism and may explain the inverse relationship between lung cancer and Alzheimer's disease incidence.
The results show that in cognitively normal young adults carrying Presenelin 2 mutations had different spontaneous brain activity patterns without cerebral structural differences.
Whole-exome sequencing of 238 African American subjects identified 6 rare missense variants within the early-onset Alzheimer's disease (AD) genes, which were observed in AD cases but never among controls. These variants were analyzed in an independent cohort of 300 African American subjects, which indicated that a PSEN2 and PSEN1 novel rare variants, may contribute to AD risk in this population.
The search for the genetic factors contributing to Alzheimer disease (AD) has evolved tremendously throughout the years. It started from the discovery of fully penetrant mutations in Amyloid precursor protein, Presenilin 1, and Presenilin 2 as a cause of autosomal dominant AD
Data show that presenilin 1 (PS1)/anterior-pharynx-defective protein 1 (Aph1b), presenilin 2 (PS2)/Aph1aL, PS2/Aph1aS and PS2/anterior pharynx defective 1 homolog B (Aph1b) gamma-secretase produced amyloid beta peptide (Abeta) with a higher Abeta42+Abeta43-to-Abeta40 (Abeta42(43)/Abeta40) ratio than the other gamma-secretases.
This review reveled that Mutations in APP and PS-1 and PS-2 genes that are associated with early-onset, autosomal, dominantly inherited AD.
Most of the early-onset Alzheimer's disease -associated mutations have been detected in PSEN1, and several novel PSEN1 mutations were recently identified in patients from various parts of the world, including Asia. Until 2014, no PSEN2 mutations were found in Asian patients; however, emerging studies from Korea and the People's Republic of China discovered probably pathogenic PSEN2 mutations. [review]
Familial Alzheimer's disease Patients with PSEN2 mutations have a delayed AOO with longest disease duration and presented more frequently with disorientation. [review]
Study identified a unique motif in PSEN2 that directs gamma-secretase to late endosomes/lysosomes via a phosphorylation-dependent interaction with the AP-1 adaptor complex. PSEN2 selectively cleaves late endosomal/lysosomal localized substrates and generates the prominent pool of intracellular Abeta that contains longer Abeta; familial Alzheimer's disease-associated mutations in PSEN2 increased the levels of longer Ab...
Data show that presenilin 1 (PS1)-containing gamma-secretase complexes were targeted to the plasma membrane, whereas presenilin 2 (PS2)-containing ones were addressed to the trans-Golgi network, to recycling endosomes.
German early-onset Alzheimer's disease cohort reveals a substantial frequency of PSEN2 variants.
Its mutation is pathogenic to early onset familial AD associated with atypical symptom presentation.
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.
Both human PS2V and zebrafish PS1IV can stimulate gamma-secretase activity despite extreme structural divergence.
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