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These observations illustrate a novel PS2 (show PDCD6 Proteins)-dependent means of modulating LPS (show TLR4 Proteins)-mediated immune responses and identify a functional distinction between PS1 (show PSEN1 Proteins) and PS2 (show PDCD6 Proteins) in innate immunity.
Although hyperactivity and hypersynchronicity were respectively detected in mice expressing the PS2 (show PDCD6 Proteins)-N141I or the APP (show APP Proteins) 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 (show MFN2 Proteins)).
Study shows that the binding of HSF-1 (show HSF1 Proteins), Cdx1 (show CDX1 Proteins), Ets-1 (show ETS1 Proteins) and Sp1 (show SP1 Proteins) to Presenilin 1 (show PSEN1 Proteins) promoter and that of Nkx2.2 (show Nkx2-2 Proteins), HFH-2 (show FOXD3 Proteins), Cdx1 (show CDX1 Proteins) and NF-kappaB (show NFKB1 Proteins) to Presenilin 2 promoter regulate their differential expression during brain development.
ARF4 (show ARF4 Proteins) is required for Presenilin basal body localization, Notch (show NOTCH1 Proteins) signaling, and subsequent epidermal differentiation.
Results suggest that mutation of PS2 (show PDCD6 Proteins) can lead to NF-kappaB (show NFKB1 Proteins) 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 (show PSEN1 Proteins) and PS2 (show PDCD6 Proteins) 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 Proteins) to PS1 (show PSEN1 Proteins) ratio.
The loss of PS2 (show PDCD6 Proteins) could have a critical role in lung tumor development through the upregulation of iPLA2 (show PLA2G6 Proteins) activity by reducing gamma-secretase.
One mechanism by which PS2 (show PDCD6 Proteins) works to reign in proinflammatory microglial behavior and PS2 (show PDCD6 Proteins) dysfunction or deficiency could result in unchecked proinflammatory activation. contributing to neurodegeneration.
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 Proteins) signalling and embryo development in zebrafish than in mammals, and that the effect of reduced Psen2 can be ameliorated by Psen1 (show PSEN1 Proteins) loss.
The present data suggest that PS2 mutations suppress lung tumor development by inhibiting the iPLA2 (show PLA2G6 Proteins) activity of PRDX6 (show PRDX6 Proteins) via a gamma-secretase cleavage mechanism and may explain the inverse relationship between lung cancer and Alzheimer's disease incidence.
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 (show PSEN1 Proteins) novel rare variants, may contribute to AD risk in this population.
Presenilin 2 (PS2), mutations in which underlie familial Alzheimer's disease (FAD (show BRCA2 Proteins)), promotes endoplasmic reticulum-mitochondria coupling only in the presence of mitofusin 2 (Mfn2 (show MFN2 Proteins)).
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 (show APP Proteins), Presenilin 1 (show PSEN1 Proteins), and Presenilin 2 as a cause of autosomal dominant AD
Data show that presenilin 1 (PS1 (show PSEN1 Proteins))/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 (show APP Proteins)) with a higher Abeta42+Abeta43-to-Abeta40 (Abeta42(43)/Abeta40) ratio than the other gamma-secretases.
This review reveled that Mutations in APP (show APP Proteins) and PS-1 (show PSEN1 Proteins) 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 (show PSEN1 Proteins), and several novel PSEN1 (show PSEN1 Proteins) 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 (show FOSB Proteins) adaptor complex. PSEN2 selectively cleaves late endosomal/lysosomal localized substrates and generates the prominent pool of intracellular Abeta (show APP Proteins) that contains longer Abeta (show APP Proteins); familial Alzheimer's disease-associated mutations in PSEN2 increased the levels of longer Ab...
Data show that presenilin 1 (PS1 (show PSEN1 Proteins))-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.
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