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PRS4203

Sigma-Aldrich

Anti-Presenilin1 antibody produced in rabbit

affinity isolated antibody, buffered aqueous solution

Synonym(s):

Anti-γ-Secretase subunit presenilin-1, Anti-PS1, Anti-PSEN1, Anti-Presenilin 1

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About This Item

MDL number:
MFCD01634040
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

100

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

species reactivity

mouse, rat, human

technique(s)

immunofluorescence: suitable
immunohistochemistry: suitable
indirect ELISA: suitable
western blot: suitable

UniProt accession no.

P49768

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... PSEN1(5663)

Immunogen

a 23 amino acid peptide from near the carboxy-terminus of human presenilin1.

Linkage

The action of this antibody can be blocked using blocking peptide SBP4203.

Physical form

Solution in phosphate buffered saline containing 0.02% sodium azide

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Huang Huang et al.
Age (Dordrecht, Netherlands), 38(4), 303-322 (2016-07-22)
Transgenic APPSwe/PS1dE9 (APP/PS1) mice that overproduce amyloid beta (Aβ) are extensively used in the studies of pathogenesis and experimental therapeutics and new drug screening for Alzheimer's disease (AD). However, most of the current literature uses young or adult APP/PS1 mice.
Linmei Wang et al.
Brain pathology (Zurich, Switzerland), 29(2), 176-192 (2018-09-08)
The imbalance between production and clearance of amyloid-beta (Aβ) is a key step in the onset and development of Alzheimer's disease (AD). Therefore, reducing Aβ accumulation in the brain is a promising therapeutic strategy for AD. The recently discovered glymphatic
Min Cao et al.
CNS neuroscience & therapeutics, 24(3), 202-211 (2017-12-24)
Social isolation increases the onset of Alzheimer's disease (AD). Environmental enrichment, a complicated social and physical construct, plays beneficial effects on brain plasticity and function. This study was designed to determine whether physical enrichment can reduce the deleterious consequences of social
Tianqi Wang et al.
Aging and disease, 13(5), 1504-1522 (2022-10-04)
Non-cognitive behavioral and psychological symptoms often occur in Alzheimer's disease (AD) patients and mouse models, although the exact neuropathological mechanism remains elusive. Here, we report hyperactivity with significant inter-individual variability in 4-month-old APP/PS1 mice. Pathological analysis revealed that intraneuronal accumulation
Weixi Feng et al.
Alzheimer's research & therapy, 12(1), 125-125 (2020-10-04)
Soluble beta-amyloid (Aβ) can be cleared from the brain through various mechanisms including enzymatic degradation, glial cell phagocytosis, transport across the blood-brain barrier, and glymphatic clearance. However, the relative contribution of each clearance system and their compensatory effects in delaying

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