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SMC-617

Alpha Synuclein Antibody (Aggregate-Specific)

Eine Lieferung in diese Region ist nicht möglich.

SKU:
SMC-617
Zusätzliche Namen:
Alpha Synuclein, A Alpha-Synuclein, SNCA, Snca, SYN, alphaSYN, NACP, Non-A beta component of AD amyloid, Non-A4 component of amyloid precursor, Parkinson disease familial 1, PARK1, PARK 1, PARK4, PARK 4, Parkinson disease (autosomal dominant, Lewy body) 4, Lewy body 4, Synuclein-alpha, PD1
Anwendung:
IHC, WB, IF, ICC, IP, Dot blot
Konzentration:
1 mg/ml
Spezies-Reaktivität:
Mouse
Aufreinigung:
Protein G Purified
Lagerbedingungen:
-20[o]C
Hersteller:
StressMarq Biosciences
Host:
Mouse
Reaktivitäten:
Human, Mouse
ABP:
IMP-GEN-2015-06 < 10% Serum <100ml
Buffer:
PBS pH7.4, 50% glycerol, 0.09% sodium azide
Immunogen:
Mouse alpha synuclein fibrils
Klon:
2F11
Uniprot:
O55042
Synonyme:
al;alp;alpha-Syn;alpha-synuclein;alphaSYN;NACP;non-A beta component of AD amyloid;non-A4 component of amyloid;Non-A4 component of amyloid precursor
Weitere Details:
Alpha-synuclein (SNCA) is a presynaptic neuronal protein abundantly expressed in the brain, particularly within the olfactory bulb, hippocampus, striatum, and thalamus (1,2). Localized to both synaptic terminals and mitochondria, alpha-synuclein plays a critical role in synaptic vesicle regulation and cytoskeletal dynamics through its interaction with tubulin (3), suggesting a potential function as a microtubule-associated protein. It is also essential for cognitive development, with SNCA inactivation linked to deficits in spatial learning and working memory (4). Pathologically, alpha-synuclein aggregates are a defining feature of several neurodegenerative diseases. These fibrillar inclusions constitute the major non-AB Beta component of amyloid plaques in Alzheimer's disease and are the principal constituents of Lewy bodies in Parkinson's disease (PD). In PD, progressive accumulation of alpha-synuclein and ubiquitin-positive inclusions in dopaminergic neurons is closely associated with motor and cognitive decline (5,6). Alpha-synuclein aggregation is not merely a byproduct of disease but a driver of neurotoxicity, mitochondrial dysfunction, and synaptic failure. Its central role in disease pathogenesis has made it a high-priority target for biomarker development and therapeutic intervention. Covered by US patent family US11,098,108B2 (7).
Versandbedingungen:
Blue Ice