| Code | CSB-RA021912A129phHU |
| Size | US$210 |
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| Application | Recommended Dilution |
|---|---|
| IHC | 1:50-1:200 |
| IF | 1:20-1:200 |
Alpha-synuclein phosphorylated at serine 129 represents one of the most significant post-translational modifications in neurodegenerative disease research. While only a small fraction of alpha-synuclein is phosphorylated at this site under normal physiological conditions, phospho-S129 accumulates dramatically in Lewy bodies, the pathological hallmarks of Parkinson's disease and dementia with Lewy bodies. This modification is thought to influence protein aggregation, toxicity, and clearance mechanisms, making it an essential marker for investigating synucleinopathy progression and potential therapeutic interventions.
This recombinant monoclonal antibody, generated against a synthetic phosphopeptide corresponding to the human phospho-SNCA S129 region, offers the reproducibility and consistency that phospho-specific detection demands. Because recombinant production ensures sequence-defined specificity and eliminates the lot-to-lot variability inherent in traditional hybridoma-derived antibodies, researchers can confidently compare results across extended studies and between laboratories.
The antibody has been validated for immunohistochemistry and immunofluorescence applications, providing flexibility for both tissue-based and cellular investigations. Immunohistochemical staining in paraffin-embedded human brain tissue demonstrates effective detection using citrate buffer antigen retrieval at dilutions between 1:50 and 1:200, enabling visualization of phospho-synuclein distribution in clinically relevant samples. Immunofluorescence validation in HeLa cells confirms utility for subcellular localization studies, with recommended dilutions ranging from 1:20 to 1:200.
For researchers investigating alpha-synuclein pathobiology, Parkinson's disease mechanisms, or screening compounds that modulate synuclein phosphorylation, this antibody provides a reliable tool for detecting this critical disease-associated modification in human samples.
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