05-831-I
Anti-Amyloid Beta (ABeta) x-42 Antibody, clone 12F4
clone 12F4, from mouse
Synonym(s):
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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All Photos(4)
About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
mouse
Quality Level
antibody form
purified antibody
antibody product type
primary antibodies
clone
12F4, monoclonal
species reactivity
human
technique(s)
ELISA: suitable
immunohistochemistry: suitable
isotype
IgG1κ
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Gene Information
human ... APP(351)
General description
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.
Specificity
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.
Application
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).
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).
Quality
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.
Immunohistochemistry Analysis: A 1:2,000 dilution of this antibody detected Amyloid Beta (Abeta) x-42 in human Alzheimer′s disease brain tissue.
Target description
4 kDa calculated
Linkage
Replaces: 05-831
Physical form
Format: Purified
Analysis Note
Control
Human Alzheimer′s brain tissue.
Human Alzheimer′s brain tissue.
Other Notes
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
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Storage Class Code
12 - Non Combustible Liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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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
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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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Molecular and cellular neurosciences, 109, 103570-103570 (2020-11-08)
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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
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