|Positive WB detected in||Neuro-2a cells, C6 cells, fetal human brain tissue, mouse brain tissue, PC-12 cells, pig brain tissue, Y79 cells, Pig cerebellum tissue, Rat brain tissue, Rat cerebellum tissue, Mouse cerebellum tissue|
|Positive IHC detected in||human hypothalamus tissue, human brain tissue, mouse brain tissue|
Note: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0
|Positive IF detected in||SH-SY5Y cells|
|Western Blot (WB)||WB : 1:20000-1:100000|
|Immunohistochemistry (IHC)||IHC : 1:500-1:2000|
|Immunofluorescence (IF)||IF : 1:200-1:800|
|Sample-dependent, check data in validation data gallery|
66230-1-Ig targets UCHL1/PGP9.5 in WB, IHC, IF,ELISA applications and shows reactivity with human, mouse, pig, rat samples.
|Tested Reactivity||human, mouse, pig, rat|
|Host / Isotype||Mouse / IgG1|
|Immunogen||UCHL1/PGP9.5 fusion protein Ag6547|
|Full Name||ubiquitin carboxyl-terminal esterase L1 (ubiquitin thiolesterase)|
|Calculated molecular weight||25 kDa|
|Observed molecular weight||27 kDa|
|GenBank accession number||BC000332|
|Gene ID (NCBI)||7345|
|Purification Method||Protein G purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
Ubiquitin C-terminal hydrolase L1 (UCHL1) was originally identified as a neuronal protein that accounts for nearly 2% of total brain proteins. UCHL1 activity protects neurons from hypoxic injury, and binding of stroke-induced reactive lipid species to the cysteine 152 (C152) of UCHL1 unfolds the protein and disrupts its function. Reduced hydrolytic activity of mutant UCHL1 is implicated in the pathophysiologic process of Parkinson's and Alzheimer's disease due to abnormal neurotoxic protein aggregation. (PMID: 31356902, PMID: 30760601)
ORL J Otorhinolaryngol Relat Spec
Role of the Ubiquitin C-Terminal Hydrolase L1-Modulated Ubiquitin Proteasome System in Auditory Cortex Senescence.
UCH-L1-mediated Down-regulation of Estrogen Receptor α Contributes to Insensitivity to Endocrine Therapy for Breast Cancer.