UCHL1 (D8R2I) Rabbit mAb #11896
- WB
Supporting Data
| REACTIVITY | H M R Mk |
| SENSITIVITY | Endogenous |
| MW (kDa) | 27 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
- Mk-Monkey
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Simple Western™ | 1:50 - 1:250 |
Storage
Protocol
Specificity / Sensitivity
Species Reactivity:
Source / Purification
Background
UCHL1 (PGP 9.5/PARK5) functions as a deubiquitinating enzyme and monoubiquitin stabilizer. In vitro studies have demonstrated that UCHL1 can hydrolyze isopeptide bonds between the carboxy-terminal glycine of Ub and the ε-amino group of lysine on target proteins. UCHL1 is also involved in the cotranslational processing of pro-ubiquitin and ribosomal proteins translated as ubiquitin fusions (5-7). Mice deficient in UCHL1 experience spasticity, suggesting that UCHL1 activity is required for the normal neuromuscular junction structure and function (5-7). Research studies have described loss of UCHL1 expression in numerous human malignancies, such as prostate, colorectal, renal, and breast carcinomas. Investigators have shown that loss of UCHL1 expression in breast carcinomas can be attributed to hyper-methylation of the UCHL1 gene promoter (8). While loss of UCHL1 expression is implicated in human carcinogenesis, mutation of UCHL1 has been implicated in neurodegenerative diseases such as Parkinson's and Alzheimer's (6,7).
- Nijman, S.M. et al. (2005) Cell 123, 773-86.
- Nalepa, G. et al. (2006) Nat Rev Drug Discov 5, 596-613.
- Leroy, E. et al. (1998) Nature 395, 451-2.
- Kurihara, L.J. et al. (2001) Hum Mol Genet 10, 1963-70.
- Todi, S.V. and Paulson, H.L. (2011) Trends Neurosci 34, 370-82.
- Setsuie, R. and Wada, K. (2007) Neurochem Int 51, 105-11.
- Day, I.N. and Thompson, R.J. (2010) Prog Neurobiol 90, 327-62.
- Xiang, T. et al. (2012) PLoS One 7, e29783.
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