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Key Documents

36-011

Sigma-Aldrich

Anti-nitro-α/β-Synuclein Antibody, clone nSyn12

clone nSyn12, Upstate®, from mouse

Přihlásitk zobrazení cen stanovených pro organizaci a smluvních cen


About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

mouse

Quality Level

antibody form

ascites fluid

antibody product type

primary antibodies

clone

nSyn12, monoclonal

species reactivity

human

manufacturer/tradename

Upstate®

technique(s)

immunohistochemistry: suitable
western blot: suitable

NCBI accession no.

UniProt accession no.

shipped in

dry ice

Gene Information

human ... SNCA(6622)

Specificity

α-Synuclein nitrated at Tyr125 and Tyr136
β-Synuclein nitrated at Tyr130

Application

Anti-nitro-α/β-Synuclein Antibody, clone nSyn12 is an antibody against nitro-α/β-Synuclein for use in WB, IH.

Quality

rountinely evaluated on recombinant protein nitrated in vitro

Target description

α-Synuclein, Mr 14.5kDa
β-Synuclein, Mr 17kDa

Physical form

Format: Unpurified

Legal Information

UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany

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Storage Class

10 - Combustible liquids

wgk_germany

WGK 1


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J M Souza et al.
The Journal of biological chemistry, 275(24), 18344-18349 (2000-04-05)
Intracellular proteinaceous aggregates are hallmarks of many common neurodegenerative disorders, and recent studies have shown that alpha-synuclein is a major component of several pathological intracellular inclusions, including Lewy bodies in Parkinson's disease (PD) and glial cell inclusions in multiple system
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Background. Salivary α-synuclein (aSyn) and its nitrated form, or 3-nitrotyrosine-α-synuclein (3-NT-αSyn), hold promise as biomarkers for idiopathic Parkinson's disease (IPD). Nitrative stress that is characterized by an excess of 3-nitrotyrosine proteins (3-NT-proteins) has been proposed as a pathogenic mechanism in
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Journal of neurochemistry, 104(6), 1504-1525 (2007-11-27)
Microglial neuroinflammatory processes play a primary role in dopaminergic neurodegeneration for Parkinson's disease (PD). This can occur, in part, by modulation of glial function following activation by soluble or insoluble modified alpha-synuclein (alpha-syn), a chief component of Lewy bodies that

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