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UCH-L1/PGP9.5 Recombinant Rabbit mAb (SDT-1765-88)

UCH-L1/PGP9.5 Recombinant Rabbit mAb (SDT-1765-88)

Catalog Number: S0B3522 Application: ELISA Reactivity: Human Conjugation: Unconjugated Brand: Starter
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Regular price $835 USD
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Product Details

Product Specification


Host Rabbit
Antigen UCH-L1/PGP9.5
Synonyms Ubiquitin carboxyl-terminal hydrolase isozyme L1; UCH-L1; Neuron cytoplasmic protein 9.5; PGP 9.5 (PGP9.5); Ubiquitin thioesterase L1; UCHL1
Immunogen Recombinant Protein
Accession P09936
Clone Number SDT-1765-88
Antibody Type Recombinant mAb
Isotype IgG
Application Sandwich ELISA
Reactivity Hu
Predicted Reactivity Ms, Rt
Cross Reactivity

No cross-reactivity against α-Synuclein, GFAP, UCH-L3

Purification Protein A
Concentration 2 mg/ml
Purity >95% by HPLC
Conjugation Unconjugated
Physical Appearance Liquid
Storage Buffer

PBS pH7.4, 0.03% Proclin 300

Stability & Storage

12 months from date of receipt, 2 to 8 °C as supplied

Background

Ubiquitin C-terminal hydrolase 1 (UCHL1), also known as neuron-specific protein PGP9.5 and Parkin 5, is one of the most abundant proteins in the brain (1–5 % of total soluble protein) (Day and Thompson, 2010, Wang et al., 2017). It is also expressed at high levels in testicular tissue and its expression may be induced in other cell types often associated with oncogenesis and metastasis (Jara et al., 2013, Nakao et al., 2018). Immunochemical experiments demonstrate that UCHL1 is localized predominantly in neurons and axons in the central and peripheral nervous system (Day and Thompson, 2010, Wilson et al., 1988). At a molecular level, UCHL1 is a relatively small protein (27 kDa) composed of 223-amino-acids encoded by 9 exons (Setsuie and Wada, 2007). Although the role of UCHL1 in vivo remains unclear, its great abundance in neurons suggests a significant role in neuronal cell function. UCHL1 variants and modifications have been linked with neurodegenerative disorders such as Parkinson’s disease (PD), Alzheimer’s disease (AD) and brain injury (Leroy et al., 1998, Liu et al., 2019, Mi et al., 2021a, Nakamura et al., 2021). These modifications diminish UCHL1′s functions, alter its solubility, and interfere with its normal interactions with other proteins, resulting in increased production and impaired degradation of misfolded and aggregated proteins, common features shared by many neurodegenerative disorders and brain injury.

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