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Merck
CN

MAB348-AF647

Anti-APP A4, a.a. 66-81 of APP {NT} Antibody, clone 22C11, Alexa Fluor™ 647 Conjugate

clone 22C11, from mouse, ALEXA FLUOR™ 647

别名:

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

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关于此项目

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

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产品名称

Anti-APP A4, a.a. 66-81 of APP {NT} Antibody, clone 22C11, Alexa Fluor™ 647 Conjugate, clone 22C11, from mouse, ALEXA FLUOR™ 647

biological source

mouse

conjugate

ALEXA FLUOR™ 647

antibody form

purified antibody

antibody product type

primary antibodies

clone

22C11, monoclonal

species reactivity

canine, porcine, rat, fish, human, monkey, mouse

technique(s)

immunocytochemistry: suitable

isotype

IgG1

NCBI accession no.

NM_000484.2
NM_201413.1
NM_201414

UniProt accession no.

P05067

shipped in

wet ice

target post-translational modification

unmodified

Quality Level

100

Gene Information

human ... APP(351)

Analysis Note

Evaluated by Immunocytochemistry in SH-SY5Y cells.

Immunocytochemistry Analysis: A 1:100 dilution of this antibody detected APP A4 in SH-SY5Y cells.

Application

Anti-APP A4, a.a. 66-81 of APP {NT} Antibody, clone 22C11, Alexa Fluor™ 647 Conjugate is an antibody against APP A4 for use in Immunocytochemistry.

General description

Amyloid beta A4 protein (UniProt P05067; also known as ABPP, Alzheimer disease amyloid protein, Amyloid precursor protein, APP, APPI, Cerebral vascular amyloid peptide, CVAP, PN-II, PreA4, Protease nexin-II) is encoded by the APP (also known as A4, AD1) gene (Gene ID 351) in human. Amyloid precursor protein (APP) is initially produced with a signal peptide sequence (a.a. 1-17), the removal of which yields the mature protein with a large extracellular portion (a.a. 18-699), followed by a transmembrane segment (a.a. 700-723) and a cytoplasmic (a.a. 724-770) tail. APP can be further processed by the α-, β-, and γ-secretases in two alternative processing pathways. In the non-amyloidogenic pathway, APP is first cleaved by the plasma membrane-localized α-secretase to generate an N-terminal extracellular sAPPα fragment (a.a. 18-687) and a membrane-bound C-terminal fragment C83 (CTFα), which can be further cleaved by γ-secretase to produce a non-toxic small peptide p3 and a cytoplasmic APP intracellular domain (AICD). In the amyloidogenic pathway, APP undergoes β-cleavage in BACE-1 (β-site APP-cleaving enzyme)-enriched endosomes to generate an N-terminal extracellular sAPPβ fragment (a.a. 18-671) and a membrane-bound C-terminal fragment C99 (CTFβ). Subsequent cleavage of C99 by γ-secretase releases the amyloid β peptide (Aβ) and AICD. Aβ accumulation in the cortical and hippocampal regions of the brain is a major pathological feature of Alzheimer′s disease (AD).
~110/120/130 kDa observed.

Other Notes

Concentration: Please refer to lot specific datasheet.

Legal Information

ALEXA FLUOR is a trademark of Life Technologies

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存储类别

12 - Non Combustible Liquids

wgk

WGK 2

flash_point_f

Not applicable

flash_point_c

Not applicable

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Pamela R Westmark et al.
Frontiers in molecular neuroscience, 14, 751307-751307 (2021-10-26)
Glycogen synthase kinase 3 (GSK3) is a proline-directed serine-threonine kinase that is associated with several neurological disorders, including Alzheimer's disease and fragile X syndrome (FXS). We tested the efficacy of a novel GSK3 inhibitor AFC03127, which was developed by Angelini
Güliz Gürel Özcan et al.
iScience, 27(2), 108870-108870 (2024-02-06)
Amyloid precursor protein (APP) is a brain-rich, single pass transmembrane protein that is proteolytically processed into multiple products, including amyloid-beta (Aβ), a major driver of Alzheimer disease (AD). Although both overexpression of APP and exogenously delivered Aβ lead to changes

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Neuroscience Solutions for productive research

Alzheimer’s Disease is a progressively deteriorating disease. It manifests itself with memory loss, confusion, problems with judgment, planning, concentration, and personality changes; and in it’s later stages, a decline in physical abilities. The disease’s causes, cures, and preventions are unknown; however, key proteins likely involved in the degenerative mechanism have been identified. Alzheimer’s Disease is characterized by neuronal loss, alterations in neurotransmitter systems, and the presence of neurofibrillary tangles composed of abnormally hyperphosphorylated tau proteins. A prominent feature of Alzheimer’s Disease is the formation of senile plaques in selected regions of the brain. The center of these plaques are composed mainly of fibrillary aggregates of a common, but not well understood, b amyloid peptides (Aβ). The Aβ peptides are generated from the larger amyloid-β precursor protein (APP) by the sequential action of β- and γ-secretase, and it is generally accepted that oligomeric forms of this Aβ are neurotoxic, resulting in disease progression.

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