Sample type Serum, Plasma, Cell Culture Supernatant, Other liquid samples
Components
Break apart microtiter test strips each coated single wells
8 x 12 (96 Total)
Lyophilized Standard
2 x vial
Biotin-labeled Antibody(Concentrated, 100X)
120 uL
HRP-Streptavidin Conjugate(Concentrated, 100X)
120 uL
Washing solution concentrate (25X)
30 mL
Sample Dilution buffer
20 mL
Antibody Dilution buffer
10 mL
Streptavidin Dilution buffer
10 mL
Stopping solution
10 mL
TMB Substrate (ready-to-use)
10 mL
Plate seals
3
Storage Store at 2-8°C.
target relevance
anti-Cinpanemab antibody Anti-drug antibodies (ADAs) generated in subjects following administration of Cinpanemab.
Cinpanemab Cinpanemab biologic drug binds Homo sapiens SNCA Alpha-synuclein
Homo sapiens SNCA Alpha-synuclein
Protein names Alpha-synuclein
Alternative names Non-A beta component of AD amyloid, Non-A4 component of amyloid precursor
Gene names SNCA
Protein family Belongs to the synuclein family
Function Neuronal protein that plays several roles in synaptic activity such as regulation of synaptic vesicle trafficking and subsequent neurotransmitter release (PubMed:20798282, PubMed:26442590, PubMed:28288128, PubMed:30404828). Participates as a monomer in synaptic vesicle exocytosis by enhancing vesicle priming, fusion and dilation of exocytotic fusion pores (PubMed:28288128, PubMed:30404828). Mechanistically, acts by increasing local Ca(2+) release from microdomains which is essential for the enhancement of ATP-induced exocytosis (PubMed:30404828). Also acts as a molecular chaperone in its multimeric membrane-bound state, assisting in the folding of synaptic fusion components called SNAREs (Soluble NSF Attachment Protein REceptors) at presynaptic plasma membrane in conjunction with cysteine string protein-alpha/DNAJC5 (PubMed:20798282). This chaperone activity is important to sustain normal SNARE-complex assembly during aging (PubMed:20798282). Also plays a role in the regulation of the dopamine neurotransmission by associating with the dopamine transporter (DAT1) and thereby modulating its activity (PubMed:26442590)
Structure Soluble monomer. Homotetramer (PubMed:21841800). A dynamic intracellular population of tetramers and monomers coexists normally and the tetramer plays an essential role in maintaining homeostasis (PubMed:21841800). Interacts with UCHL1 (By similarity). Interacts with phospholipase D and histones. Interacts (via N-terminus) with synphilin-1/SNCAIP; this interaction promotes formation of SNCA inclusions in the cytoplasm (PubMed:19762560). Interacts with CALM1 (PubMed:23607618). Interacts with STXBP1; this interaction controls SNCA self-replicating aggregation (PubMed:27597756). Interacts with SNARE components VAMP2 and SNAP25; these interactions allows SNARE complex assembly and integrity (PubMed:20798282). Interacts with RPH3A and RAB3A (PubMed:15207266). Interacts with SERF1A; this interaction promotes the aggregation of SNCA (PubMed:22854022, PubMed:31034892). Interacts with SEPTIN4 (By similarity). Interacts with DDX10; this interaction causes DDX10 mislocalization to the nucleoplasm and cytoplasmic inclusions (PubMed:33657088)
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 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
Involvement in disease Parkinson disease 1, autosomal dominant 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.
Parkinson disease 4, autosomal dominant A complex neurodegenerative disorder with manifestations ranging from typical Parkinson disease to dementia with Lewy bodies. Clinical features include parkinsonian symptoms (resting tremor, rigidity, postural instability and bradykinesia), dementia, diffuse Lewy body pathology, autonomic dysfunction, hallucinations and paranoia.
Dementia, Lewy body A neurodegenerative disorder characterized by mental impairment leading to dementia, parkinsonism, 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.
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Published literature highly relevant to the biological target of this product and referencing this antibody or clone are retrieved from the PubMed database provided by the United States National Library of Medicine at the National Institutes of Health.
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