stabilizing fatty acid synthase (FAS), often overexpressed in biologically aggressive tumors(in prostate cancer)
USP2a and USP2c, two isoforms of the ubiquitin-specific protease USP2, cause cell death upon ectopic expression
13
-
3013
45
396
. localized to peroxisomes in hepatocytes through a canonical peroxisome-targeting motif at its C-terminus
2012
22659130
USP2b, (USP2-45)
is a deubiquitinase that regulates hepatic gluconeogenesis and glucose metabolism
is in a complex with several clock components and regulates the stability and turnover of ARNTL, which in turn alters the expression of several PER/ARNTL controlled genes
12
-
2933
-
362
-
2012
22659130
USP2c
USP2a and USP2c, two isoforms of the ubiquitin-specific protease USP2, cause cell death upon ectopic expression
having a direct proapoptotic activity additionally tightening the connection between apoptosis and the ubiquitin-proteasome system
implicated as a novel positive regulator of TNF-induced NFKB signaling and show that its expression is altered in tumor cells
de-ubiquitinylates and stabilizes target proteins, is rhythmically expressed in multiple tissues including the SCN
potentially mediates circadian disruption by suppressing the CRY1 degradation during inflammation
role for the rhythmically-expressed deubiquitinating enzyme ubiquitin specific peptidase 2 (USP2) in clock function
CELLULAR PROCESS
cell life, cell death/apoptosis
protein, degradation
protein, ubiquitin dependent proteolysis
PHYSIOLOGICAL PROCESS
PATHWAY
metabolism
signaling
a component
new core component of the clock machinery and potential role for deubiquitination in the regulation of the circadian clock, both at the level of the core pacemaker and its response to external cues
INTERACTION
DNA
RNA
small molecule
protein
STUB1 and USP2 show antagonistic functions in the control of AIFM1-mediated cell death, and implicate the role of the enzymes as a switch for cells to live or die under stresses that cause truncated AIFM1 release
mediates mitotic progression by regulating the stability of Aurora-A
interacts with CRY1 and enhances its protein stability via deubiquitination upon serum shock
cell & other
REGULATION
ASSOCIATED DISORDERS
corresponding disease(s)
Susceptibility
Variant & Polymorphism
Candidate gene
Marker
Therapy target
ANIMAL & CELL MODELS
mice with a deletion of the Usp2 gene (Usp2 KO) display a longer free-running period of locomotor activity rhythms and altered responses of the clock to light