Key features and details
- Sheep polyclonal to Alpha-synuclein
- Suitable for: WB
- Reacts with: Mouse, Rat, Human
- Isotype: IgG
Product nameAnti-Alpha-synuclein antibody
See all Alpha-synuclein primary antibodies
DescriptionSheep polyclonal to Alpha-synuclein
SpecificityHuman and rat alpha synuclein. Cross reactivity: This antibody is known to react with human, mouse, rat and other rodents. Cross reactivity with other species has not yet been tested.
Tested applicationsSuitable for: WBmore details
Unsuitable for: Flow Cyt or ICC/IF
Species reactivityReacts with: Mouse, Rat, Human
Synthetic peptide corresponding to Human Alpha-synuclein aa 116-131. Synthetic peptide of human synuclein (116-131) coupled to diphtheria toxoid with cysteine residue attached to N-ter of peptide. Conjugate cross-linked by maleimidocaproyl-N-hydroxy succinimide (MSC).
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Add glycerol to a final volume of 50% for extra stability and aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle.
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab6162 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||Use a concentration of 0.5 µg/ml.|
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
ab6162 has been referenced in 22 publications.
- Fragniere AMC et al. Hyperosmotic stress induces cell-dependent aggregation of a-synuclein. Sci Rep 9:2288 (2019). PubMed: 30783136
- Han C et al. Exosomes from patients with Parkinson's disease are pathological in mice. J Mol Med (Berl) 97:1329-1344 (2019). PubMed: 31302715
- Alarcón-Arís D et al. Selective a-Synuclein Knockdown in Monoamine Neurons by Intranasal Oligonucleotide Delivery: Potential Therapy for Parkinson's Disease. Mol Ther 26:550-567 (2018). PubMed: 29273501
- Svarcbahs R et al. Removal of prolyl oligopeptidase reduces alpha-synuclein toxicity in cells and in vivo. Sci Rep 8:1552 (2018). PubMed: 29367610
- Lautenschläger J et al. C-terminal calcium binding of a-synuclein modulates synaptic vesicle interaction. Nat Commun 9:712 (2018). PubMed: 29459792