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05-831-I

Sigma-Aldrich

Anti-Amyloid Beta (ABeta) x-42 Antibody, clone 12F4

clone 12F4, from mouse

Synonim(y):

Amyloid beta A4 protein, ABPP, APPI, APP, Alzheimer disease amyloid protein, Cerebral vascular amyloid peptide, CVAP, PreA4, Protease nexin-II, PN-II

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About This Item

Kod UNSPSC:
12352203
eCl@ss:
32160702
NACRES:
NA.41

pochodzenie biologiczne

mouse

Poziom jakości

forma przeciwciała

purified antibody

rodzaj przeciwciała

primary antibodies

klon

12F4, monoclonal

reaktywność gatunkowa

human

metody

ELISA: suitable
immunohistochemistry: suitable

izotyp

IgG1κ

numer dostępu NCBI

numer dostępu UniProt

Warunki transportu

wet ice

docelowa modyfikacja potranslacyjna

unmodified

informacje o genach

human ... APP(351)

Opis ogólny

One of the most important and initial steps which causes loss of memory and cognition in Alzheimer’s Disease (AD) involves proteolytic cleavage of amyloid precursor protein (APP, chromosome 21) releasing short 40, 42 & 43 amino acid peptides (Amyloid Beta) 1-40, 1-42 and 1-43). Polymerization of beta-amyloid and subsequent neuronal deposit (amyloid) leads to the degeneration of neurons involved in memory and cognition.

Specyficzność

This antibody detects Amyloid Beta (ABeta) x-42, but does not cross react with Amyloid Beta (ABeta) x-40 or Amyloid Beta (Abeta) x-43.

Immunogen

KLH-conjugated linear peptide corresponding to human Amyloid Beta (ABeta) x-42.

Zastosowanie

Anti-Amyloid Beta (ABeta) x-42, clone 12F4 is an antibody targeting the Amyloid Beta (ABeta) x-42 protein, validated for use in IHC & ELISA.
Immunohistohemistry Analysis: A 1:500 dilution from a representative lot detected Amyloid Beta (ABeta) x-42 in human pons/midbrain tissue.

ELISA Analysis: A representative lot detected Amyloid Beta (ABeta) x-42, but demonstrates a loss of signal against Amyloid Beta (ABeta) x-42.

Western Blotting Analysis: A 1:1,000 dilution from a representative lot detected Amyloid Beta (ABeta) x-42, but demonstrated a loss of signal against x-40 and not x-43 in WB (Prof. J. Buxbaum, Mt. Sinai School of Medicine).

Jakość

Evaluated by Immunohistochemistry in human Alzheimer′s disease brain tissue.

Immunohistochemistry Analysis: A 1:2,000 dilution of this antibody detected Amyloid Beta (Abeta) x-42 in human Alzheimer′s disease brain tissue.

Opis wartości docelowych

4 kDa calculated

Powiązanie

Replaces: 05-831

Postać fizyczna

Format: Purified

Komentarz do analizy

Control
Human Alzheimer′s brain tissue.

Inne uwagi

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
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Kod klasy składowania

12 - Non Combustible Liquids

Klasa zagrożenia wodnego (WGK)

WGK 1

Temperatura zapłonu (°F)

Not applicable

Temperatura zapłonu (°C)

Not applicable


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Odwiedź Bibliotekę dokumentów

Yasuhisa Ano et al.
Aging, 11(10), 2949-2967 (2019-05-24)
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Mariah Beaver et al.
Epigenetics, 1-22 (2021-08-10)
Disruption of histone acetylation-mediated gene control is a critical step in Alzheimer's Disease (AD), yet chromatin analysis of antagonistic histone acetyltransferases (HATs) and histone deacetylases (HDACs) causing these alterations remains uncharacterized. We report the first Tip60 HAT versus HDAC2 chromatin
Haolin Zhang et al.
Molecular and cellular neurosciences, 109, 103570-103570 (2020-11-08)
Alzheimer's disease (AD) is an age-related neurodegenerative disorder hallmarked by amyloid-β (Aβ) plaque accumulation, neuronal cell death, and cognitive deficits that worsen during disease progression. Histone acetylation dysregulation, caused by an imbalance between reduced histone acetyltransferases (HAT) Tip60 and increased
Song Cao et al.
Journal of neuroinflammation, 18(1), 10-10 (2021-01-08)
The role of microglia in Alzheimer's disease (AD) pathogenesis is becoming increasingly important, as activation of these cell types likely contributes to both pathological and protective processes associated with all phases of the disease. During early AD pathogenesis, one of
Raul O Freitas et al.
Cells, 10(10) (2021-10-24)
Alzheimer's disease (AD) accounts for about 70% of neurodegenerative diseases and is a cause of cognitive decline and death for one-third of seniors. AD is currently underdiagnosed, and it cannot be effectively prevented. Aggregation of amyloid-β (Aβ) proteins has been

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