Anti-Alpha-synuclein antibody [4D6] - BSA and Azide free (ab1903)
Key features and details
- Mouse monoclonal [4D6] to Alpha-synuclein - BSA and Azide free
- Suitable for: WB, IHC-P
- Reacts with: Human
- Isotype: IgG1
Overview
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Product name
Anti-Alpha-synuclein antibody [4D6] - BSA and Azide free
See all Alpha-synuclein primary antibodies -
Description
Mouse monoclonal [4D6] to Alpha-synuclein - BSA and Azide free -
Host species
Mouse -
Tested applications
Suitable for: WB, IHC-Pmore details
Unsuitable for: Flow Cyt or ICC -
Species reactivity
Reacts with: Human -
Immunogen
Recombinant full length protein corresponding to Human Alpha-synuclein.
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General notes
The Life Science industry has been in the grips of a reproducibility crisis for a number of years. Abcam is leading the way in addressing this with our range of recombinant monoclonal antibodies and knockout edited cell lines for gold-standard validation. Please check that this product meets your needs before purchasing.
If you have any questions, special requirements or concerns, please send us an inquiry and/or contact our Support team ahead of purchase. Recommended alternatives for this product can be found below, along with publications, customer reviews and Q&As
Properties
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Form
Liquid -
Storage instructions
Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles. -
Storage buffer
Constituent: PBS -
Carrier free
Yes -
Concentration information loading...
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Purity
Protein A purified -
Purification notes
Ammonium sulfate precipitated and dialyzed tissue culture supernatant. -
Clonality
Monoclonal -
Clone number
4D6 -
Isotype
IgG1 -
Research areas
Associated products
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Compatible Secondaries
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Isotype control
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Recombinant Protein
Applications
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab1903 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Application | Abreviews | Notes |
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WB | (3) |
1/100 - 1/10000. Predicted molecular weight: 16 kDa.
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IHC-P | (1) |
1/100 - 1/1000. Antigen retrieval is not essential but may optimise staining.
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Notes |
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WB
1/100 - 1/10000. Predicted molecular weight: 16 kDa. |
IHC-P
1/100 - 1/1000. Antigen retrieval is not essential but may optimise staining. |
Target
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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
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Database links
- Entrez Gene: 6622 Human
- Omim: 163890 Human
- SwissProt: P37840 Human
- Unigene: 21374 Human
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Alternative names
- Alpha synuclein antibody
- Alpha-synuclein antibody
- Alpha-synuclein, isoform NACP140 antibody
see all
Images
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All lanes : Anti-Alpha-synuclein antibody [4D6] - BSA and Azide free (ab1903) at 5 µg/ml
Lane 1 : A549 (Human lung adenocarcinoma epithelial cell line) Whole Cell Lysate
Lane 2 : SK N BE (Human neuroblastoma) Whole Cell Lysate
Lane 3 : SK N SH (Human neuroblastoma) Whole Cell Lysate
Lysates/proteins at 10 µg per lane.
Secondary
All lanes : Goat polyclonal to Mouse IgG - H&L - Pre-Adsorbed (HRP) at 1/3000 dilution
Predicted band size: 16 kDa
Observed band size: 16 kDa
Additional bands at: 18 kDa (possible post-translational modification), 80 kDa (possible post-translational modification) -
IHC-P using ab1903 showing lewy bodies in a human substantia nigra neuron(x400)
Protocols
Datasheets and documents
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Datasheet download
References (70)
ab1903 has been referenced in 70 publications.
- Ujvári B et al. Neurodegeneration in the centrally-projecting Edinger-Westphal nucleus contributes to the non-motor symptoms of Parkinson's disease in the rat. J Neuroinflammation 19:31 (2022). PubMed: 35109869
- Cao Q et al. Suppression of abnormal α-synuclein expression by activation of BDNF transcription ameliorates Parkinson's disease-like pathology. Mol Ther Nucleic Acids 29:1-15 (2022). PubMed: 35784012
- Toomey CE et al. Mitochondrial dysfunction is a key pathological driver of early stage Parkinson's. Acta Neuropathol Commun 10:134 (2022). PubMed: 36076304
- Dieriks BV et al. Human pericytes degrade diverse α-synuclein aggregates. PLoS One 17:e0277658 (2022). PubMed: 36399706
- Bettencourt C et al. MOBP and HIP1 in multiple system atrophy: New α-synuclein partners in glial cytoplasmic inclusions implicated in the disease pathogenesis. Neuropathol Appl Neurobiol 47:640-652 (2021). PubMed: 33368549