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AB126892

Anti-Amyloid Oligomers抗体

Anti-Amyloid Oligomers antibody

4

(2 Reviews)

|

(11 Publications)

Rabbit Polyclonal Amyloid-beta precursor protein antibody. Suitable for IP, ELISA, Dot, WB, IHC-P, IHC-Fr and reacts with Mouse, Rat, Human samples. Cited in 11 publications.

查看别名

A4, AD1, APP, Amyloid-beta precursor protein, ABPP, APPI, Alzheimer disease amyloid A4 protein homolog, Alzheimer disease amyloid protein, Amyloid precursor protein, Amyloid-beta (A4) precursor protein, Amyloid-beta A4 protein, Cerebral vascular amyloid peptide, PreA4, Protease nexin-II, CVAP, PN-II

关键信息

宿主种属

Rabbit

克隆

Polyclonal

亚型

IgG

不含载体蛋白

No

反应种属

Mouse, Human, Rat

应用

WB, IHC-P, IHC-Fr, IP, ELISA, Dot

applications

特异性

Recognizes all types of amyloid oligomers. Appears to recognize a peptide backbone epitope that is common to amyloid oligomers, but is not found in native proteins, amyloidogenic monomer or mature amyloid fibrils.

反应性数据

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性能和储存信息

形式
Liquid
纯化工艺
Affinity purification Protein A
存储溶液
Preservative: 0.09% Sodium azide Constituents: PBS, 50% Glycerol (glycerin, glycerine)
运输条件
Blue Ice
推荐的短期储存条件
+4°C
推荐的长期储存条件
-20°C
储存信息
Stable for 12 months at -20°C

补充信息

This supplementary information is collated from multiple sources and compiled automatically.

Amyloid oligomers also known as beta amyloid oligomers or oligomeric amyloid beta are protein aggregates that play a significant role in various neurodegenerative processes. These oligomeric formations consist of small soluble assemblies of amyloid beta typically ranging from dimers to dodecamers and often measure approximately 4 to 10 kDa in mass. Amyloid oligomers are usually expressed in the brain particularly in regions associated with memory and cognition such as the hippocampus and cortex.
Biological function summary

Amyloid oligomers interfere with synaptic function leading to a cascade of neuronal dysfunction and cell death. Unlike their fibrillar counterparts these oligomers are not part of larger insoluble plaques and they exhibit more harmful properties to neurons. They may form part of a complex with other proteins such as tau which can exacerbate their toxic effects. Amyloid beta oligomers disrupt cellular function primarily through interaction with synaptic receptors influencing calcium homeostasis and promoting oxidative stress.

Pathways

Amyloid oligomers are integral components of amyloidogenic pathways that influence neuronal communication and survival. The amyloid beta pathway involves the cleavage of amyloid precursor protein (APP) by enzymes such as beta-secretase and gamma-secretase leading to the formation of these toxic oligomers. Related proteins include APP the enzymes mentioned and tau which can further disrupt microtubule stability when amyloid oligomers are present. The accumulation of amyloid oligomers is interlinked with pathways that regulate synaptic plasticity and inflammatory responses.

Amyloid oligomers have strong associations with Alzheimer's disease and mild cognitive impairment. These oligomers are directly linked to synaptic loss and dysfunction which contributes heavily to the progression of Alzheimer's disease. Connections with proteins such as tau and APP highlight their role in forming toxic complexes that lead to neurofibrillary tangles and plaque buildup. Additionally amyloid oligomers may relate to other neurodegenerative disorders where protein aggregation and cognitive deficits are apparent.

产品实验方案

For this product, it's our understanding that no specific protocols are required. You can visit:

靶点信息

Functions as a cell surface receptor and performs physiological functions on the surface of neurons relevant to neurite growth, neuronal adhesion and axonogenesis. Interaction between APP molecules on neighboring cells promotes synaptogenesis (PubMed : 25122912). Involved in cell mobility and transcription regulation through protein-protein interactions. Can promote transcription activation through binding to APBB1-KAT5 and inhibits Notch signaling through interaction with Numb. Couples to apoptosis-inducing pathways such as those mediated by G(o) and JIP. Inhibits G(o) alpha ATPase activity (By similarity). Acts as a kinesin I membrane receptor, mediating the axonal transport of beta-secretase and presenilin 1 (By similarity). By acting as a kinesin I membrane receptor, plays a role in axonal anterograde transport of cargo towards synapses in axons (PubMed : 17062754, PubMed : 23011729). Involved in copper homeostasis/oxidative stress through copper ion reduction. In vitro, copper-metallated APP induces neuronal death directly or is potentiated through Cu(2+)-mediated low-density lipoprotein oxidation. Can regulate neurite outgrowth through binding to components of the extracellular matrix such as heparin and collagen I and IV. The splice isoforms that contain the BPTI domain possess protease inhibitor activity. Induces a AGER-dependent pathway that involves activation of p38 MAPK, resulting in internalization of amyloid-beta peptide and leading to mitochondrial dysfunction in cultured cortical neurons. Provides Cu(2+) ions for GPC1 which are required for release of nitric oxide (NO) and subsequent degradation of the heparan sulfate chains on GPC1.. Amyloid-beta peptides are lipophilic metal chelators with metal-reducing activity. Bind transient metals such as copper, zinc and iron. In vitro, can reduce Cu(2+) and Fe(3+) to Cu(+) and Fe(2+), respectively. Amyloid-beta protein 42 is a more effective reductant than amyloid-beta protein 40. Amyloid-beta peptides bind to lipoproteins and apolipoproteins E and J in the CSF and to HDL particles in plasma, inhibiting metal-catalyzed oxidation of lipoproteins. APP42-beta may activate mononuclear phagocytes in the brain and elicit inflammatory responses. Promotes both tau aggregation and TPK II-mediated phosphorylation. Interaction with overexpressed HADH2 leads to oxidative stress and neurotoxicity. Also binds GPC1 in lipid rafts.. Appicans elicit adhesion of neural cells to the extracellular matrix and may regulate neurite outgrowth in the brain.. The gamma-CTF peptides as well as the caspase-cleaved peptides, including C31, are potent enhancers of neuronal apoptosis.
See full target information APP

文献 (11)

Recent publications for all applications. Explore the full list and refine your search

The Journal of clinical investigation : PubMed41026542

2025

Aggregation shifts amyloid-β peptides from synaptogenic to synaptotoxic.

Applications

Unspecified application

Species

Unspecified reactive species

Alberto Siddu,Silvia Natale,Connie H Wong,Hamidreza Shaye,Thomas C Südhof

Scientific reports 15:4393 PubMed39910105

2025

Amyloids in bladder cancer hijack cancer-related proteins and are positive correlated to tumor stage.

Applications

Unspecified application

Species

Unspecified reactive species

Diego Alem,César X García-Laviña,Francisco Garagorry,Dardo Centurión,Joaquina Farias,Hany Pazos-Espinosa,María Noel Cuitiño-Mendiberry,Carolina Villadóniga,Susana Castro-Sowinski,Martín Fló,Federico Carrión,Brenda Iglesias,Kevin Madauss,Lucía Canclini

Alzheimer's & dementia : the journal of the Alzheimer's Association 20:6094-6106 PubMed38958575

2024

Nanoscale flow cytometry-based quantification of blood-based extracellular vesicle biomarkers distinguishes MCI and Alzheimer's disease.

Applications

Unspecified application

Species

Unspecified reactive species

Thamara Dayarathna,Austyn D Roseborough,Janice Gomes,Reza Khazaee,Carolina R A Silveira,Kathy Borron,Soojung Yu,Kristy Coleman,Sarah Jesso,Elizabeth Finger,Penny MacDonald,Michael Borrie,Jennie Wells,Robert Bartha,Guangyong Zou,Shawn N Whitehead,Hon S Leong,Stephen H Pasternak

Scientific reports 11:8617 PubMed33883656

2021

Optimal allogeneic islet dose for transplantation in insulin-dependent diabetic Macaca fascicularis monkeys.

Applications

Unspecified application

Species

Unspecified reactive species

Geun Soo Kim,Chan Woo Cho,Jong Hyun Lee,Du Yeon Shin,Han Sin Lee,Kyo Won Lee,Yeongbeen Kwon,Jae Sung Kim,Heung-Mo Yang,Sung Joo Kim,Jae Berm Park

PloS one 15:e0237667 PubMed32833960

2020

Protein-conformational diseases in childhood: Naturally-occurring hIAPP amyloid-oligomers and early β-cell damage in obesity and diabetes.

Applications

Unspecified application

Species

Unspecified reactive species

Nelly F Altamirano-Bustamante,Eulalia Garrido-Magaña,Eugenia Morán,Aurora Calderón,Karina Pasten-Hidalgo,Rosa Angélica Castillo-Rodríguez,Gerardo Rojas,Reyna Lara-Martínez,Edgar Leyva-García,Mateo Larralde-Laborde,Guadalupe Domíguez,Chiharu Murata,Yolanda Margarita-Vazquez,Rafael Payro,Manuel Barbosa,Alejandro Valderrama,Hortencia Montesinos,Alejandra Domínguez-Camacho,Víctor H García-Olmos,Regina Ferrer,Patricia G Medina-Bravo,Fernanda Santoscoy,Cristina Revilla-Monsalve,Luis Felipe Jiménez-García,Julio Morán,Jalil Villalobos-Alva,Mario Javier Villalobos,Raúl Calzada-León,Perla Altamirano,Myriam M Altamirano-Bustamante

Scientific reports 10:7103 PubMed32345996

2020

Investigating APOE, APP-Aβ metabolism genes and Alzheimer's disease GWAS hits in brain small vessel ischemic disease.

Applications

Unspecified application

Species

Unspecified reactive species

Sonja Blumenau,Marco Foddis,Susanne Müller,Manuel Holtgrewe,Kajetan Bentele,Daniel Berchtold,Dieter Beule,Ulrich Dirnagl,Celeste Sassi

Scientific reports 9:18465 PubMed31804529

2019

Unpacking the aggregation-oligomerization-fibrillization process of naturally-occurring hIAPP amyloid oligomers isolated directly from sera of children with obesity or diabetes mellitus.

Applications

Unspecified application

Species

Unspecified reactive species

Myriam M Altamirano-Bustamante,Nelly F Altamirano-Bustamante,Mateo Larralde-Laborde,Reyna Lara-Martínez,Edgar Leyva-García,Eulalia Garrido-Magaña,Gerardo Rojas,Luis Felipe Jiménez-García,Cristina Revilla-Monsalve,Perla Altamirano,Raúl Calzada-León

FEBS letters 593:2139-2150 PubMed31211853

2019

Inhibition of amyloid-induced toxicity by ergothioneine in a transgenic Caenorhabditis elegans model.

Applications

Unspecified application

Species

Unspecified reactive species

Irwin K Cheah,Li-Theng Ng,Li-Fang Ng,Vanessa Y Lam,Jan Gruber,Cheryl Y W Huang,Fang-Qin Goh,Keith H C Lim,Barry Halliwell

Journal of neuroscience research 97:492-505 PubMed30461032

2018

Activation of Nrf2/ARE pathway alleviates the cognitive deficits in PS1V97L-Tg mouse model of Alzheimer's disease through modulation of oxidative stress.

Applications

Unspecified application

Species

Unspecified reactive species

Yuanruhua Tian,Wei Wang,Lingzhi Xu,Haitao Li,Yiping Wei,Qiaoqi Wu,Jianping Jia

Cell reports 24:1713-1721.e4 PubMed30110628

2018

Stress-Induced Low Complexity RNA Activates Physiological Amyloidogenesis.

Applications

Unspecified application

Species

Unspecified reactive species

Miling Wang,Xianzun Tao,Mathieu D Jacob,Clayton A Bennett,J J David Ho,Mark L Gonzalgo,Timothy E Audas,Stephen Lee
View all publications

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