Anti-Alpha-synuclein (phospho S129) antibody [EP1536Y] (Ab51253)
NACP, PARK1, SNCA, Alpha-synuclein, Non-A beta component of AD amyloid, Non-A4 component of amyloid precursor
详细信息
特异性
This antibody only detects alpha synuclein phosphorylated on Ser129. IHC-P: This antibody showed no staining in human hippocampus normal brain and showed staining in Parkinson's brain as expected. Mouse and rat species are recommended based on WB results, we do not guarantee IHC-P for mouse and rat.
背景信息
Anti-Alpha-synuclein (phospho S129) antibody [EP1536Y] (ab51253) was developed by Abcam using patented rabbit monoclonal antibody technology and is validated for use in Dot blot, ELISA, IHC-FrFl, IHC-P, WB in human, mouse, rat samples. Anti-Alpha-synuclein (phospho S129) antibody [EP1536Y] (ab51253) has been cited over 373 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 synuclin antibody/ Anti-SNCA antibody) [EP1536Y] (ab51253) has high sensitivity and specificity alongside high lot-to-lot consistency and reproducibility. Anti-Alpha-synuclein (phospho S129) antibody [EP1536Y] (ab51253) has 9 independent reviews from customers. Anti-Alpha-synuclein (phospho S129) antibody [EP1536Y] (ab51253) specifically detects Alpha-synuclein Phospho-S129 (UniProt ID: P37840; Molecular weight: 14kDa) and is sold in 100 µL and 1 mL selling sizes. Conjugation-ready, carrier free format available for antibody clone EP1536Y - ab209422. Antibody clone EP1536Y is also available pre-conjugated to a variety of labels for your convenience - Alexa Fluor® 750, PE, Alexa Fluor® 647, Alexa Fluor® 488, Alexa Fluor® 594, Alexa Fluor® 568 ( ab321645, ab314419, ab225294, ab225295, ab311788, ab313069 ). Alpha-synuclein phosphorylated at serine 129 (pS129; phosphorylated alpha synuclein, SNCA/NACP) is a modified form of the alpha-synuclein protein, which plays a crucial role in the regulation of synaptic vesicle trafficking and neurotransmitter release. This phosphorylation is significantly increased in the brains of patients with Parkinson's disease and other synucleinopathies. The presence of pS129 is associated with the formation of Lewy bodies, a hallmark of Parkinson's disease, and is believed to contribute to the neurotoxic properties of alpha-synuclein, exacerbating disease progression. 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.
文献引用 (534)
Sono-mechanical nanostructures-enabled sustained precise ultrasound brain stimulation.
声机械纳米结构实现了持续、精确的超声波脑刺激。
Anti-TLR2 immunotherapy modulates neuron-to-oligodendrocyte propagation of α-synuclein in mouse and human models.
抗 TLR2 免疫疗法可调节小鼠和人类模型中 α-突触核蛋白从神经元到少突胶质细胞的传播。
Glycerol 3-phosphate acyltransferase exacerbates α-synuclein-induced toxicity by increasing lipid peroxidation.
甘油 3-磷酸酰基转移酶通过增加脂质过氧化作用加剧α-突触核蛋白诱导的毒性。
Mapping cellular vulnerability in Parkinson's disease using retro-AAVs and preformed α-synuclein fibrils.
利用逆转录AAV和预先形成的α-突触核蛋白原纤维绘制帕金森病细胞脆弱性图谱。
Gut-initiated alpha synuclein fibrils drive parkinsonism phenotypes: temporal mapping of REM sleep behavior disorder-like and other non-motor symptoms.
肠道启动的α-突触核蛋白原纤维驱动帕金森病表型:快速眼动睡眠行为障碍样症状和其他非运动症状的时间映射。
Ultrasonic repression of TRPA1-dependent astrocyte reactivity confers neuroprotection in models of Lewy body dementia.
超声波抑制 TRPA1 依赖性星形胶质细胞反应性可在路易体痴呆模型中发挥神经保护作用。
Artificial miRNA-mediated reduction of SNCA for the treatment of α-synucleinopathies.
利用人工 miRNA 介导的 SNCA 减少治疗 α-突触核蛋白病。
The C3-C3aR axis drives rotenone-induced cognitive damage via synaptic engulfment, dark microglia and PANoptosis.
C3-C3aR 轴通过突触吞噬、暗小胶质细胞和 PANoptosis 驱动鱼藤酮诱导的认知损伤。
Microglia-T cell interactions drive α-synuclein pathology in a Parkinson's disease mouse model.
在帕金森病小鼠模型中,小胶质细胞-T细胞相互作用驱动α-突触核蛋白病理。
An autonomous siRNA delivery system targeting NLRP3: implications in Parkinson's disease.
靶向 NLRP3 的自主 siRNA 递送系统:对帕金森病的影响。
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