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anti-Human Presenilin 1 Antibodies:
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Human Monoclonal Presenilin 1 Primary Antibody for ICC, IF - ABIN261601
Stahl, Diehlmann, Südhof: Direct interaction of Alzheimer's disease-related presenilin 1 with armadillo protein p0071. in The Journal of biological chemistry 1999
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Human Polyclonal Presenilin 1 Primary Antibody for IHC, ELISA - ABIN1003039
Weihofen, Martoglio: Intramembrane-cleaving proteases: controlled liberation of proteins and bioactive peptides. in Trends in cell biology 2003
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Human Polyclonal Presenilin 1 Primary Antibody for IHC (p), WB - ABIN2476203
Sherrington, Rogaev, Liang, Rogaeva, Levesque, Ikeda, Chi, Lin, Li, Holman, Tsuda, Mar, Foncin, Bruni, Montesi, Sorbi, Rainero, Pinessi, Nee, Chumakov, Pollen, Brookes, Sanseau, Polinsky, Wasco et al.: Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease. ... in Nature 1995
Show all 4 Pubmed References
Human Monoclonal Presenilin 1 Primary Antibody for ELISA, ICC - ABIN268518
Scarpi, Cirelli, Matrone, Castronovo, Rosini, Occhiato, Romano, Bartali, Clemente, Bottegoni, Cavalli, De Chiara, Bonini, Calissano, Palamara, Garaci, Torcia, Guarna, Cozzolino: Low molecular weight, non-peptidic agonists of TrkA receptor with NGF-mimetic activity. in Cell death & disease 2012
Human Polyclonal Presenilin 1 Primary Antibody for IF (p), IHC (p) - ABIN723755
Chu, Peng, Long, Wang, Luo, Sharma, He: Distribution and expression of Pen-2 in the central nervous system of APP/PS1 double transgenic mice. in Acta biochimica et biophysica Sinica 2015
Human Polyclonal Presenilin 1 Primary Antibody for ELISA, ICC - ABIN4347240
Dursun, Gezen-Ak: Vitamin D receptor is present on the neuronal plasma membrane and is co-localized with amyloid precursor protein, ADAM10 or Nicastrin. in PLoS ONE 2017
Human Polyclonal Presenilin 1 Primary Antibody for FACS, IF - ABIN390169
Nie, Li, Yan, Wang, Zhao, Guo, Yin: Nicotine decreases beta-amyloid through regulating BACE1 transcription in SH-EP1-?4?2 nAChR-APP695 cells. in Neurochemical research 2011
Using an antisense morpholino oligonucleotide, study blocked induction of PS1IV isoform that normally occurs under hypoxia,identified gene regulatory networks that are modulated by PS1IV: observed changes in expression of genes controlling inflammation, vascular development, the UPR, protein synthesis, calcium homeostasis, catecholamine biosynthesis, TOR signaling, and cell proliferation
We identified psen1 as a regulator of the development of histaminergic neurons in zebrafish
These results suggest that Psen2 (show PSEN2 Antibodies) 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 (show PSEN2 Antibodies) can be ameliorated by Psen1 loss.
Study reports a novel PSEN1 K311R mutation in two Chinese families with late-onset Alzheimer's disease. The mutation was located within the hydrophilic loop domain of PSEN1 C-terminal cytoplasmic loop and enhanced Abeta42 production and tau phosphorylation in HEK293-APP695wt cells.
Induced pluripotent stem cells derived from somatic cells of familial Alzheimer disease patients carrying PSEN1 mutations exhibit premature neuronal differentiation with decreased proliferation and increased apoptosis.
This study shown that PSEN1 is decreased in Alzheimer's Disease platelets
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 (show PSEN2 Antibodies) and PSEN1 novel rare variants, may contribute to AD risk in this population.
that reduction in the synaptotagmin 1 (show SYT1 Antibodies) level and presenilin 1-synaptotagmin 1 (show SYT1 Antibodies) interactions in AD brain may present molecular underpinning of the pathogenic presenilin 1 conformation
Here, comprehensive analysis using FRET-based imaging reveals that activity-driven and Protein Kinase A-mediated PS1 phosphorylation at three domains (domain 1: T74, domain 2: S310 and S313, domain 3: S365, S366, and S367), with S367 being critical, is responsible for the PS1 pathogenic 'closed' conformation, and resulting increase in the Abeta42/40 ratio.
One family harbored a novel mutation in PSEN1:p.Phe283Leu. MRI (show C7ORF49 Antibodies) demonstrated severe parietal, perirolandic, and temporal atrophy, with relative sparing of frontal and ipsilateral hippocampal regions. Autopsy confirmed pure AD pathology.
Study examined the presence of causative and low frequency coding variants in the Alzheimer disease (AD), Frontotemporal lobar degeneration, Amyotrophic lateral sclerosis and Parkinson disease Mendelian genes, in over 450 families with clinical history of AD and over 11,710 sporadic cases and cognitive normal participants from North America.Only PSEN1 and PINK1 (show PINK1 Antibodies) showed consistent association with AD cases.
Cultured hippocampal neurons expressing mutant PS1 had attenuated CCE that was associated with destabilized dendritic spines, which were rescued by either gamma-secretase inhibition or overexpression of STIM1 (show STIM1 Antibodies).
PSEN1 mutations responsible for early-onset Alzheimer's disease with extrapyramidal phenotype.
The cognitive function of APP (show APP Antibodies)/PS1 mice was impaired at 10months of age; moreover, the hypermetabolic state identified in various brain regions at 5months of age was also significantly decreased.
Using knockout cell lines in combination with siRNA and immunoprecipitation approaches, our data clearly demonstrated that the Pen-2 (show PSENEN Antibodies) and PS1 are sufficient to form a functionally active gamma-secretase that is capable of catalyzing the processing of Notch (show NOTCH1 Antibodies). This finding strongly suggests that Pen-2 (show PSENEN Antibodies) is the most crucial component in gamma-secretase complex in addition to presenilin that functions as the catalytic subunit.
PS1 plays a crucial role in the cerebrovascular system and the vascular reactivity is decreased through altered Ca(2 (show CA2 Antibodies)+) signals in PS1dE9 mutant mice.
Loss of PS1 is associated with cognitive impairment.
Conditionally targeted deletion of PSEN1 leads to diastolic heart dysfunction and ultrastructural cardiomyocyte abnormalities.
findings indicate that impaired processing or localization of apoER2 (show LRP8 Antibodies) may contribute to the pathogenic effects of familial Alzheimer's disease mutations in PS1
Tspan3 (show TSPAN3 Antibodies) is a central endocytic membrane component regulating the expression of ADAM10 (show ADAM10 Antibodies), presenilin and the amyloid precursor protein (show APP Antibodies).
Study shows that the binding of HSF-1 (show HSF1 Antibodies), Cdx1 (show CDX1 Antibodies), Ets-1 (show ETS1 Antibodies) and Sp1 (show SP1 Antibodies) to Presenilin 1 promoter and that of Nkx2.2 (show Nkx2-2 Antibodies), HFH-2 (show FOXD3 Antibodies), Cdx1 (show CDX1 Antibodies) and NF-kappaB (show NFKB1 Antibodies) to Presenilin 2 (show PSEN2 Antibodies) promoter regulate their differential expression during brain development.
maternal dietary betaine supplementation during gestation inhibits hepatic cell proliferation in neonatal piglets, at least partly, through epigenetic regulation of hepatic CCND2 (show CCND2 Antibodies) and PSEN1 genes via a STAT3 (show STAT3 Antibodies)-dependent pathway
gamma-Secretase and presenilin mediate cleavage and phosphorylation of vascular endothelial growth factor receptor-1 (show FLT1 Antibodies)
Alzheimer's disease (AD) patients with an inherited form of the disease carry mutations in the presenilin proteins (PSEN1\; PSEN2) or in 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 are protease enzymes. Several alternatively spliced transcript variants encoding different isoforms have been identified for this gene, the full-length nature of only some have been determined.
, presenilin 1 (Alzheimer disease 3)
, presenilin-1 isoform I-463
, presenilin-1 isoform I-467
, presenilin 1
, presenilin alpha