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anti-Rat (Rattus) Presenilin 2 Antikörper:
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Human Polyclonal Presenilin 2 Primary Antibody für 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
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Human Polyclonal Presenilin 2 Primary Antibody für IHC (f), IHC (p) - ABIN966891
Levy-Lahad, Wijsman, Nemens, Anderson, Goddard, Weber, Bird, Schellenberg: A familial Alzheimer's disease locus on chromosome 1. in Science (New York, N.Y.) 1995
Show all 3 Pubmed References
Although hyperactivity and hypersynchronicity were respectively detected in mice expressing the PS2 (zeige PDCD6 Antikörper)-N141I or the APP (zeige APP Antikörper) 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 (zeige FANCD2 Antikörper)), promotes endoplasmic reticulum-mitochondria coupling only in the presence of mitofusin 2 (Mfn2 (zeige MFN2 Antikörper)).
Study shows that the binding of HSF-1 (zeige HSF1 Antikörper), Cdx1 (zeige CDX1 Antikörper), Ets-1 (zeige ETS1 Antikörper) and Sp1 (zeige SP1 Antikörper) to Presenilin 1 (zeige PSEN1 Antikörper) promoter and that of Nkx2.2 (zeige Nkx2-2 Antikörper), HFH-2 (zeige FOXD3 Antikörper), Cdx1 (zeige CDX1 Antikörper) and NF-kappaB (zeige NFKB1 Antikörper) to Presenilin 2 promoter regulate their differential expression during brain development.
ARF4 (zeige ARF4 Antikörper) is required for Presenilin basal body localization, Notch (zeige NOTCH1 Antikörper) signaling, and subsequent epidermal differentiation.
Results suggest that mutation of PS2 (zeige PDCD6 Antikörper) can lead to NF-kappaB (zeige NFKB1 Antikörper) 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 (zeige PSEN1 Antikörper) and PS2 (zeige PDCD6 Antikörper) 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 (zeige PDCD6 Antikörper) to PS1 (zeige PSEN1 Antikörper) ratio.
The loss of PS2 (zeige PDCD6 Antikörper) could have a critical role in lung tumor development through the upregulation of iPLA2 (zeige PLA2G6 Antikörper) activity by reducing gamma-secretase.
One mechanism by which PS2 (zeige PDCD6 Antikörper) works to reign in proinflammatory microglial behavior and PS2 (zeige PDCD6 Antikörper) 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.
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 (zeige NOTCH1 Antikörper) signalling and embryo development in zebrafish than in mammals, and that the effect of reduced Psen2 can be ameliorated by Psen1 (zeige PSEN1 Antikörper) loss.
Presenilin 2 (PS2), mutations in which underlie familial Alzheimer's disease (FAD (zeige BRCA2 Antikörper)), promotes endoplasmic reticulum-mitochondria coupling only in the presence of mitofusin 2 (Mfn2 (zeige MFN2 Antikörper)).
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 (zeige APP Antikörper), Presenilin 1 (zeige PSEN1 Antikörper), and Presenilin 2 as a cause of autosomal dominant AD
Data show that presenilin 1 (PS1 (zeige PSEN1 Antikörper))/anterior-pharynx-defective protein 1 (Aph1b (zeige aph1b Antikörper)), presenilin 2 (PS2)/Aph1aL, PS2/Aph1aS and PS2/anterior pharynx defective 1 homolog B (Aph1b (zeige aph1b Antikörper)) gamma-secretase produced amyloid beta peptide (Abeta (zeige APP Antikörper)) with a higher Abeta42+Abeta43-to-Abeta40 (Abeta42(43)/Abeta40) ratio than the other gamma-secretases.
This review reveled that Mutations in APP (zeige APP Antikörper) and PS-1 (zeige PSEN1 Antikörper) 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 (zeige PSEN1 Antikörper), and several novel PSEN1 (zeige PSEN1 Antikörper) 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 (zeige FOSB Antikörper) adaptor complex. PSEN2 selectively cleaves late endosomal/lysosomal localized substrates and generates the prominent pool of intracellular Abeta (zeige APP Antikörper) that contains longer Abeta (zeige APP Antikörper); familial Alzheimer's disease-associated mutations in PSEN2 increased the levels of longer Ab...
Data show that presenilin 1 (PS1 (zeige PSEN1 Antikörper))-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.
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.
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