ELISA/assay

Guinea Pig Synuclein, Alpha ELISA Kit

MBS721294

48-Strip-Wells

470 USD

ELISA Kit

Guinea Pig Synuclein, Alpha ELISA Kit

Synuclein, Alpha

SNCA; Alpha-synuclein; alpha-synuclein; synuclein alpha-140; non A-beta component of AD amyloid; synuclein, alpha (non A4 component of amyloid precursor); Non-A beta component of AD amyloid; Non-A4 component of amyloid precursor

SNCa

SNCA; SNCA; PD1; NACP; PARK1; PARK4; NACP; PARK1; NACP

SYUA_HUMAN

Guinea Pig

This assay has high sensitivity and excellent specificity for detection of alpha-SYN. No significant cross-reactivity or interference between alpha-SYN and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between alpha-SYN and all the analogues, therefore, cross reaction may still exist in some cases.

Store all reagents at 2-8 degree C

Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate. Assay Type: Sandwich. Sensitivity: 1.0 pg/mL.

Intended Uses: This alpha-SYN ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Guinea pig alpha-SYN. This ELISA kit for research use only, not for therapeutic or diagnostic applications!

Neurobiology

Principle of the assay: alpha-SYN ELISA kit applies the quantitative sandwich enzyme immunoassay technique. The microtiter plate has been pre-coated with a monoclonal antibody specific for alpha-SYN. Standards or samples are then added to the microtiter plate wells and alpha-SYN if present, will bind to the antibody pre-coated wells. In order to quantitatively determine the amount of alpha-SYN present in the sample, a standardized preparation of horseradish peroxidase (HRP)-conjugated polyclonal antibody, specific for alpha-SYN are added to each well to "sandwich" the alpha-SYN immobilized on the plate. The microtiter plate undergoes incubation, and then the wells are thoroughly washed to remove all unbound components. Next, substrate solutions are added to each well. The enzyme (HRP) and substrate are allowed to react over a short incubation period. Only those wells that contain alpha-SYN and enzyme-conjugated antibody will exhibit a change in color. The enzyme-substrate reaction is terminated by addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The alpha-SYN concentration in each sample is interpolated from this standard curve.

49456267

CAG46454.1

P37840

14,460 Da

Alpha-synuclein Signaling Pathway (137913); Alzheimer's Disease Pathway (83097); Alzheimer's Disease Pathway (509); Amyloids Pathway (366238); EGFR1 Signaling Pathway (198782); Parkinson's Disease Pathway (83098)

Alpha-synuclein is a member of the synuclein family, which also includes beta- and gamma-synuclein. Synucleins are abundantly expressed in the brain and alpha- and beta-synuclein inhibit phospholipase D2 selectively. SNCA may serve to integrate presynaptic signaling and membrane trafficking. Defects in SNCA have been implicated in the pathogenesis of Parkinson disease. SNCA peptides are a major component of amyloid plaques in the brains of patients with Alzheimer's disease. Four alternatively spliced transcripts encoding two different isoforms have been identified for this gene. [provided by RefSeq, Mar 2009]

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. Subunit structure: Soluble monomer which can form filamentous aggregates. Interacts with UCHL1 . By similarity. Interacts with phospholipase D and histones. Ref.16 Ref.17. Subcellular location: Cytoplasm. Membrane. Nucleus. Cell junction synapse. Note: Membrane-bound in dopaminergic neurons. Ref.17 Ref.21. 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. 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. Ref.22. Post-translational modification: Phosphorylated, 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. Ref.13 Ref.14 Ref.15 Ref.20Hallmark 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 . By similarity. Involvement in disease: Note=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.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. Ref.25 Ref.26 Ref.27Defects 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. Sequence similarities: Belongs to the synuclein family.

48-Strip-Wells

470 USD

96-Strip-Wells

675