Anti-Alpha-synuclein (phospho S129) antibody [MJF-R13 (8-8)] (Ab168381)

NACP, PARK1, SNCA, Alpha-synuclein, Non-A beta component of AD amyloid, Non-A4 component of amyloid precursor

反应种属:Human
抗原名称:SNCA phospho S129
应用:WB, IHC

详细信息

免疫原The exact immunogen used to generate this antibody is proprietary information.
宿主/亚型Rabbit / IgG
抗体类型Monoclonal
产品形式Liquid
纯化方式Affinity purification Protein A
储存缓冲液Preservative: 0.01% Sodium azide Constituents: PBS, 40% Glycerol (glycerin, glycerine), 0.05% BSA
储存条件运输条件: Conditional Ambient 推荐的短期储存时间: 1-2 weeks 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: Avoid freeze / thaw cycle
无载体蛋白No

特异性

This antibody only detects alpha Synuclein phosphorylated on Ser129.

背景信息

Anti-Alpha-synuclein (phospho S129) antibody [MJF-R13 (8-8)] (ab168381) was developed by Abcam using patented rabbit monoclonal antibody technology and is validated for use in IHC-P, WB in human samples. Anti-Alpha-synuclein (phospho S129) antibody [MJF-R13 (8-8)] (ab168381) has been cited over 40 times in peer reviewed journals and is trusted by the scientific community. Abcam's high quality manufacturing and validation processes ensure Anti-Alpha-synuclein (phospho S129) antibody (Anti-pS129 alpha-synuclein antibody) [MJF-R13 (8-8)] (ab168381) has high sensitivity and specificity alongside high lot-to-lot consistency and reproducibility. Anti-Alpha-synuclein (phospho S129) antibody [MJF-R13 (8-8)] (ab168381) has 4 independent reviews from customers. Anti-Alpha-synuclein (phospho S129) antibody [MJF-R13 (8-8)] (ab168381) specifically detects Alpha-synuclein Phospho-S129 (UniProt ID: P37840; Molecular weight: 14kDa) and is sold in 100 µL and 1 mL selling sizes. Anti-Alpha-synuclein (phospho S129) antibody [MJF-R13 (8-8)] (ab168381) was developed by Abcam in partnership with the Michael J. Fox Foundation for Parkinson's Research. Alpha-synuclein phosphorylated at serine 129 (pS129; SNCA/NACP) is a key pathological marker in neurodegenerative diseases such as Parkinson's disease. This phosphorylation event is associated with the abnormal aggregation of alpha-synuclein into Lewy bodies, which are indicative of disease. Studies have shown that pS129 not only promotes the aggregation of alpha-synuclein but also increases its neurotoxicity, contributing to neuronal death and disease progression Alpha-synuclein was the first gene to be linked to Parkinson's disease (PD) and remains the most promising link to PD pathogenesis, where there is genetic evidence that it may play a causal role. In the brain, alpha-synuclein is concentrated in presynaptic nerve terminals. The deposition of the abundant presynaptic brain protein alpha-synuclein as fibrillary aggregates in neurons or glial cells is a hallmark lesion in a subset of neurodegenerative disorders. These disorders include Parkinson's disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy, collectively referred to as synucleinopathies. Parkinson's disease (PD) is a common neurodegenerative disorder characterized by the progressive accumulation in selected neurons of protein inclusions containing alpha-synuclein and ubiquitin. Recent studies also indicate that alpha-synuclein undergoes post-translational modification. Though the role of many of these modifications is still under investigation, phosphorylation at Serine 129 may affect alpha-synuclein aggregations and may also serve as marker of disease pathogenesis. With the advent of this phospho-specific Serine 129 antibody, The Michael J. Fox Foundation hopes to ensure that the putative role of this modification can be further examined by all researchers. Patented technology Our RabMAb ® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb ® patents. What are the advantages of a recombinant monoclonal antibody? This product is a recombinant monoclonal antibody, which offers several advantages including - High batch-to-batch consistency and reproducibility - Improved sensitivity and specificity - Long-term security of supply - Animal-free batch production For more information, read more on recombinant antibodies. Collaborations This antibody was developed with support from The Michael J. Fox Foundation.

文献引用 (57)

Tubulin transforms Tau and α-synuclein condensates from pathological to physiological.

微管蛋白将 Tau 蛋白和 α-突触核蛋白凝聚体从病理状态转化为生理状态。

Lucas Lathan, Tsoi Phoebe S, Quan My Diem, Choi Kyoung-Jae, Ferreon Josephine C, Ferreon Allan Chris M

Olfactory sensory map is perturbed in a human wild-type α-synuclein overexpressing transgenic mouse model of Parkinson's disease.

在人类野生型α-突触核蛋白过表达的帕金森病转基因小鼠模型中,嗅觉感觉图谱受到干扰。

Biju K C, Hernandez Enrique Torres, Stallings Alison Michelle, Felix-Ortiz Ada C, Hebbale Skanda K, Clark Robert A

Single-cell transcriptomics revealed molecular vulnerability in a human midbrain-like organoid model of Parkinson's disease.

单细胞转录组学揭示了帕金森病人类中脑样类器官模型中的分子脆弱性。

Xie Jessica Jiaxin, Vitkauskas Matas, Do Quyen, Saw Tzuen Yih, Sun Alfred Xuyang, Yang Lin, Soong Tuck Wah, Lim Kah-Leong, Tan Eng-King, Ng Huck-Hui, Liu Jinyue

Sympathetic and parasympathetic subtypes of body-first Lewy body disease observed in postmortem tissue from prediagnostic individuals.

在诊断前个体的尸检组织中观察到交感神经和副交感神经亚型的路易体病

Andersen Katrine B, Krishnamurthy Anushree, Just Mie Kristine, Van Den Berge Nathalie, Skjærbæk Casper, Horsager Jacob, Knudsen Karoline, Vogel Jacob W, Toledo Jon B, Attems Johannes, Polvikoski Tuomo, Saito Yuko, Murayama Shigeo, Borghammer Per

Disrupting α-Synuclein-ClpP interaction restores mitochondrial function and attenuates neuropathology in Parkinson's disease models.

破坏α-突触核蛋白-ClpP相互作用可恢复线粒体功能并减轻帕金森病模型中的神经病理学。

CHCHD2 mutant mice link mitochondrial deficits to PD pathophysiology

CHCHD2突变小鼠将线粒体缺陷与帕金森病病理生理学联系起来

Szu-Chi Liao ,Kohei Kano ,Sadhna Phanse ,Mai Nguyen ,Elyssa Margolis ,YuHong Fu ,Jonathan X Meng ,Mohamed Taha Moutaoufik ,Zac Chatterton ,Tatiana Saccon ,Kirsten Broderick ,Hiroyuki Aoki ,Jeffrey Simms ,Felicia Xaveria Suteja ,Yoshitaka Sei ,Eric J Huang ,Kevin McAvoy ,Giovanni Manfredi ,Glenda Halliday ,Mohan Babu ,Ken Nakamura

Increased burden of rare risk variants across gene expression networks predisposes to sporadic Parkinson's disease.

基因表达网络中罕见风险变异负担的增加会导致散发性帕金森病

Eubanks Elena, VanderSleen Katelyn, Mody Jiya, Patel Neha, Sacks Benjamin, Farahani Mahsa Darestani, Wang Jinying, Elliott Jordan, Jaber Nora, Akçimen Fulya, Bandres-Ciga Sara, Helweh Fadel, Liu Jun, Archakam Sanjana, Kimelman Robert, Sharma Bineet, Socha Philip, Guntur Ananya, Huang Yiming, Ramalingam Nagendran, Guadagno Elyse, Bartels Tim, Dettmer Ulf, Mouradian M Maral, Bahrami Amir Houshang, Dai Wei, Baum Jean, Shi Zheng, Hardy John, Kara Eleanna

Phosphorylated α-synuclein in CSF and plasma does not reflect synucleinopathy

脑脊液和血浆中的磷酸化α-突触核蛋白并不能反映突触核蛋白病。

Giovanni Bellomo # ,Erik Stoops # ,Jeroen Vanbrabant ,Leentje Demeyer ,Cindy Francois ,Melanie Vanhooren ,Yihua Ma ,Carly M Farris ,Luis Concha-Marambio ,Federico Paolini Paoletti ,Lorenzo Gaetani ,Lucilla Parnetti ,Davide Chiasserini

Distinct subcellular localization of tau and alpha-synuclein in lewy body disease

路易体疾病中 tau 和 α-突触核蛋白的不同亚细胞定位

D Luke Fischer, Marissa Menard, Omar Z Abdelaziz, Nicholas M Kanaan, Virginia G Cobbs, Richard E Kennedy, Geidy E Serrano, Thomas G Beach, Laura A Volpicelli-Daley

Piezo1 Mediates Ultrasound-Stimulated Dopaminergic Neuron Protection via Synaptic Vesicle Recycling and Ferroptosis Inhibition.

Piezo1 通过突触囊泡回收和铁死亡抑制介导超声刺激的多巴胺能神经元保护。

Xu Tian, Zhang Li, Lu Xiaoxiao, Ji Wei, Chen Kaidong
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