Key features and details
- Mouse monoclonal [P-syn/81A] to Alpha-synuclein (phospho S129)
- Suitable for: IHC-P
- Reacts with: Human
- Isotype: IgG2a
Product nameAnti-Alpha-synuclein (phospho S129) antibody [P-syn/81A]
See all Alpha-synuclein primary antibodies
DescriptionMouse monoclonal [P-syn/81A] to Alpha-synuclein (phospho S129)
Tested applicationsSuitable for: IHC-Pmore details
Species reactivityReacts with: Human
Predicted to work with: Rat, Cow, Pig, Chimpanzee, Cynomolgus monkey, Rhesus monkey, Gorilla, Orangutan
- IHC-P: Diseased human brain tissue.
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Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferPreservative: 0.1% Sodium azide
Concentration information loading...
Our Abpromise guarantee covers the use of ab184674 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IHC-P||1/500 - 1/1000. Retrieve antigens with 70% Formic acid for 10-30 minutes at room temperature before commencing with IHC staining protocol.|
FunctionMay 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 specificityExpressed principally in brain but is also expressed in low concentrations in all tissues examined except in liver. Concentrated in presynaptic nerve terminals.
Involvement in diseaseGenetic 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 similaritiesBelongs to the synuclein family.
DomainThe '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.
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 localizationCytoplasm, cytosol. Membrane. Nucleus. Cell junction, synapse. Secreted. Membrane-bound in dopaminergic neurons.
- Information by UniProt
- Alpha synuclein antibody
- Alpha-synuclein antibody
- Alpha-synuclein, isoform NACP140 antibody
ab184674 has been referenced in 12 publications.
- Stevenson TJ et al. a-synuclein inclusions are abundant in non-neuronal cells in the anterior olfactory nucleus of the Parkinson's disease olfactory bulb. Sci Rep 10:6682 (2020). PubMed: 32317654
- Patterson JR et al. Time course and magnitude of alpha-synuclein inclusion formation and nigrostriatal degeneration in the rat model of synucleinopathy triggered by intrastriatal a-synuclein preformed fibrils. Neurobiol Dis 130:104525 (2019). PubMed: 31276792
- Du T et al. Injection of a-syn-98 Aggregates Into the Brain Triggers a-Synuclein Pathology and an Inflammatory Response. Front Mol Neurosci 12:189 (2019). PubMed: 31447645
- Duffy MF et al. Lewy body-like alpha-synuclein inclusions trigger reactive microgliosis prior to nigral degeneration. J Neuroinflammation 15:129 (2018). PubMed: 29716614
- Uemura N et al. Inoculation of a-synuclein preformed fibrils into the mouse gastrointestinal tract induces Lewy body-like aggregates in the brainstem via the vagus nerve. Mol Neurodegener 13:21 (2018). IHC-FoFr ; Mouse . PubMed: 29751824