alpha Synuclein protein (ab51181)
Our Abpromise guarantee covers the use of ab51181 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|SDS-PAGE||SDS-PAGE: Use at an assay dependent dilution.|
- Alpha synucleinAlpha-synucleinAlpha-synuclein, isoform NACP140
- alphaSYNMGC105443MGC110988MGC127560MGC64356NACPNon A beta component of AD amyloidNon A4 component of amyloidNon A4 component of amyloid precursorNon-A beta component of AD amyloidNon-A-beta component of alzheimers disease amyloid , precursor ofNon-A4 component of amyloid precursorOTTHUMP00000218549OTTHUMP00000218551OTTHUMP00000218552OTTHUMP00000218553OTTHUMP00000218554PARK 1PARK 4PARK1PARK4Parkinson disease (autosomal dominant, Lewy body) 4Parkinson disease familial 1PD 1PD1SNCASnca synuclein, alpha (non A4 component of amyloid precursor)Synuclein alphaSynuclein alpha 140Synuclein, alpha (non A4 component of amyloid precursor)SYUA_HUMAN
Defects in SNCA are the cause of Parkinson disease type 1 (PARK1) [MIM:168601]. A complex neurodegenerative disorder characterized by bradykinesia, resting tremor, muscular rigidity and postural instability. Additional features are characteristic postural abnormalities, dysautonomia, dystonic cramps, and dementia. The pathology of Parkinson disease involves the loss of dopaminergic neurons in the substantia nigra and the presence of Lewy bodies (intraneuronal accumulations of aggregated proteins), in surviving neurons in various areas of the brain. The disease is progressive and usually manifests after the age of 50 years, although early-onset cases (before 50 years) are known. The majority of the cases are sporadic suggesting a multifactorial etiology based on environmental and genetic factors. However, some patients present with a positive family history for the disease. Familial forms of the disease usually begin at earlier ages and are associated with atypical clinical features.
Defects in SNCA are the cause of Parkinson disease type 4 (PARK4) [MIM:605543]. A complex neurodegenerative disorder with manifestations ranging from typical Parkinson disease to dementia with Lewy bodies. Clinical features include parkinsonian symptoms (tremor, rigidity, postural instability and bradykinesia), dementia, diffuse Lewy body pathology, autonomic dysfunction, hallucinations and paranoia.
Defects in SNCA are the cause of dementia Lewy body (DLB) [MIM:127750]. A neurodegenerative disorder clinically characterized by mental impairment leading to dementia, parkinsonism, often with fluctuating cognitive function, visual hallucinations, falls, syncopal episodes, and sensitivity to neuroleptic medication. Brainstem or cortical intraneuronal accumulations of aggregated proteins (Lewy bodies) are the only essential pathologic features. Patients may also have hippocampal and neocortical senile plaques, sometimes in sufficient number to fulfill the diagnostic criteria for Alzheimer disease.
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.
References for alpha Synuclein protein (ab51181)
ab51181 has not yet been referenced specifically in any publications.