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USP2 encodes a member of the family of de-ubiquitinating enzymes, which belongs to the peptidase C19 superfamily. Additionally we are shipping USP2 Antibodies (147) and and many more products for this protein.
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In general, we collect and summarize the factors involved in the alternative splicing of USP2 in this review to further understand the mechanism behind the USP2's alternative splicing
Authors show here USP2 is expressed in quiescent and activated T-cells and its expression is 50% lower in CTCL (show TSPYL2 Proteins) cell lines (MyLa2000, SeAx and Hut-78) than in normal T-cells.
Data show that ubiquitin variants (Ubvs) that bind to USP2 or USP21 (show USP21 Proteins) contain a similar core functional epitope, or "hot spot," consisting mainly of positions that are conserved as the wild type sequence, but also some positions that prefer mutant sequences.
The results show a connection between miR (show MLXIP Proteins)-125b and USP2 gene the etiology of psoriasis. They proceeded to show that modulation of nuclear factor kappa B-mediated inflammation is the likely mechanism through which this miRNA gene pair function
the deubiquitinase USP2a translocates into the nucleus and binds to pY701-STAT1 (show STAT1 Proteins), and inhibits K48-linked ubiquitination and degradation of pY701-STAT1 (show STAT1 Proteins)
ML364 also caused a decrease in homologous recombination-mediated DNA repair. These effects by a small molecule inhibitor support a key role for USP2 as a regulator of cell cycle (show C13orf15 Proteins), DNA repair, and tumor cell growth.
Identify USP2 as a novel regulator of lipoprotein clearance owing to its ability to control ubiquitylation-dependent degradation of the LDLR (show LDLR Proteins) by IDOL (show MYLIP Proteins).
Data suggest up-regulation of ASAH1 (acid ceramidase (show ASAH1 Proteins)) activity by androgen in androgen-sensitive prostate cancer cells (but not other cancer cells) is mainly due to prolonged stability of ASAH1 (show ASAH1 Proteins) by androgen-stimulated induction of USP2 expression.
Modulation of USP-2 expression plays a crucial role in cell cycle regulation by leptin and adiponectin.
The present study showed that USP2 expression is associated with TNBC cell line's invasiveness and poor survival of breast cancer patients and may serve as a prognostic biomarker and therapeutic target for TNBC
3,3'-Diindolylmethane directly inhibits USP2 deubiquitinase activity in 3T3-L1 pre-adipocytes.
Usp2 is required for the PTH1 (show PTH Proteins)-34-induced proliferation of osteoblasts
Usp2 is a clock output effector related to bodily Ca2 (show CA2 Proteins)+ homeostasis, a feature that is conserved across evolution.
A novel function of USP2 in the molecular clock in which it regulates PER1 (show PER1 Proteins) function.
A role for USP2-45 as a central regulator of MR, able to remove the receptor monoubiquitylation and induced its destabilization.
Data suggest that USP2 does not play a primary role in the control of sodium balance or blood pressure.
a functional liver clock is required for the proper nutritional and circadian regulation of USP2-45 expression; at the molecular level, transcriptional coactivators PGC-1alpha and PGC-1beta and repressor E4BP4 (show NFIL3 Proteins) exert opposing effects on USP2-45 promoter activity
USP2a potentially mediates circadian disruption by suppressing the CRY1 (show CRY1 Proteins) degradation during inflammation.
Rhythmic expression of USP2 in the SCN (show SRI Proteins) and other tissues offers a new level of control of the clock machinery through de-ubiqutinylation and suggests a role for USP2 during circadian adaptation to environmental day length changes
severe defect in the ability of Usp2 -/- spermatozoa to fertilize eggs
This gene encodes a member of the family of de-ubiquitinating enzymes, which belongs to the peptidase C19 superfamily. The encoded protein is a ubiquitin-specific protease which is required for TNF-alpha (tumor necrosis factor alpha) -induced NF-kB (nuclear factor kB) signaling. This protein deubiquitinates polyubiquitinated target proteins such as fatty acid synthase, murine double minute 2 (MDM2), MDM4/MDMX and cyclin D1. MDM2 and MDM4 are negative regulators of the p53 tumor suppressor and cyclin D1 is required for cell cycle G1/S transition. Multiple alternatively spliced transcript variants encoding different isoforms have been identified.
41 kDa ubiquitin-specific protease
, deubiquitinating enzyme 2
, ubiquitin carboxyl-terminal hydrolase 2
, ubiquitin specific protease 12
, ubiquitin specific protease 9
, ubiquitin thioesterase 2
, ubiquitin-specific-processing protease 2
, ubiquitin specific protease 2
, ubiquitin thiolesterase 2
, ubiquitin-specific-processing protease testis
, family of cysteine protease
, ubiquitin specific protease 41
, ubiquitin specific protease 46
, ubiquitin specific protease 52
, ubiquitin specific protease 66