Alpha-synuclein (phospho S129) peptide (ab188826)
Key features and details
- Suitable for: Blocking
Description
-
Product name
Alpha-synuclein (phospho S129) peptide
See all Alpha-synuclein proteins and peptides -
Accession
-
Animal free
No -
Nature
Synthetic -
Associated products
-
Corresponding Antibody
Specifications
Our Abpromise guarantee covers the use of ab188826 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
-
Applications
Blocking - Blocking peptide for Anti-Alpha-synuclein (phospho S129) antibody [EP1536Y] (ab51253)
-
Form
Lyophilized -
Additional notes
- First try to dissolve a small amount of peptide in either water or buffer. The more charged residues on a peptide, the more soluble it is in aqueous solutions.
- If the peptide doesn’t dissolve try an organic solvent e.g. DMSO, then dilute using water or buffer.
- Consider that any solvent used must be compatible with your assay. If a peptide does not dissolve and you need to recover it, lyophilise to remove the solvent.
- Gentle warming and sonication can effectively aid peptide solubilisation. If the solution is cloudy or has gelled the peptide may be in suspension rather than solubilised.
- Peptides containing cysteine are easily oxidised, so should be prepared in solution just prior to use. -
Concentration information loading...
Preparation and Storage
-
Stability and Storage
Shipped at 4°C. Store at -20°C.
Information available upon request.
General Info
-
Alternative names
- Alpha synuclein
- Alpha-synuclein
- Alpha-synuclein, isoform NACP140
see all -
Function
May be involved in the regulation of dopamine release and transport. Induces fibrillization of microtubule-associated protein tau. Reduces neuronal responsiveness to various apoptotic stimuli, leading to a decreased caspase-3 activation. -
Tissue specificity
Expressed principally in brain but is also expressed in low concentrations in all tissues examined except in liver. Concentrated in presynaptic nerve terminals. -
Involvement in disease
Genetic alterations of SNCA resulting in aberrant polymerization into fibrils, are associated with several neurodegenerative diseases (synucleinopathies). SNCA fibrillar aggregates represent the major non A-beta component of Alzheimer disease amyloid plaque, and a major component of Lewy body inclusions. They are also found within Lewy body (LB)-like intraneuronal inclusions, glial inclusions and axonal spheroids in neurodegeneration with brain iron accumulation type 1.
Parkinson disease 1
Parkinson disease 4
Dementia Lewy body -
Sequence similarities
Belongs to the synuclein family. -
Domain
The 'non A-beta component of Alzheimer disease amyloid plaque' domain (NAC domain) is involved in fibrils formation. The middle hydrophobic region forms the core of the filaments. The C-terminus may regulate aggregation and determine the diameter of the filaments. -
Post-translational
modificationsPhosphorylated, predominantly on serine residues. Phosphorylation by CK1 appears to occur on residues distinct from the residue phosphorylated by other kinases. Phosphorylation of Ser-129 is selective and extensive in synucleinopathy lesions. In vitro, phosphorylation at Ser-129 promoted insoluble fibril formation. Phosphorylated on Tyr-125 by a PTK2B-dependent pathway upon osmotic stress.
Hallmark lesions of neurodegenerative synucleinopathies contain alpha-synuclein that is modified by nitration of tyrosine residues and possibly by dityrosine cross-linking to generated stable oligomers.
Ubiquitinated. The predominant conjugate is the diubiquitinated form.
Acetylation at Met-1 seems to be important for proper folding and native oligomeric structure. -
Cellular localization
Cytoplasm, cytosol. Membrane. Nucleus. Cell junction, synapse. Secreted. Membrane-bound in dopaminergic neurons. - Information by UniProt
Images
-
To learn more about our protein and peptide range click here.
Protocols
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
Datasheets and documents
-
SDS download
-
Datasheet download
References (5)
ab188826 has been referenced in 5 publications.
- Koss DJ et al. Nuclear alpha-synuclein is present in the human brain and is modified in dementia with Lewy bodies. Acta Neuropathol Commun 10:98 (2022). PubMed: 35794636
- Chen HH et al. Development of a 36-Channel Instrument for Assaying Biomarkers of Ultralow Concentrations Utilizing Immunomagnetic Reduction. ACS Meas Sci Au 2:485-492 (2022). PubMed: 36785659
- Zhao J et al. Apolipoprotein E regulates lipid metabolism and α-synuclein pathology in human iPSC-derived cerebral organoids. Acta Neuropathol 142:807-825 (2021). PubMed: 34453582
- Ardah MT et al. Inhibition of alpha-synuclein seeded fibril formation and toxicity by herbal medicinal extracts. BMC Complement Med Ther 20:73 (2020). PubMed: 32143619
- Martinez-Valbuena I et al. Interaction of amyloidogenic proteins in pancreatic ß cells from subjects with synucleinopathies. Acta Neuropathol N/A:N/A (2018). IHC-P ; Human . PubMed: 29536165