Cet anticorps anti-USP7 est un anticorps Souris Monoclonal détectant USP7 dans WB et ELISA. Adapté pour Humain. Ce Primary Antibody a été cité dans 2+ publications.
USP7
Reactivité: Humain, Souris, Rat
WB, IHC, IF, IC
Hôte: Lapin
Polyclonal
unconjugated
Indications d'application
ELISA: 1/10000
Restrictions
For Research Use only
Format
Liquid
Buffer
Ascitic fluid containing 0.03 % sodium azide.
Agent conservateur
Sodium azide
Précaution d'utilisation
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Stock
4 °C,-20 °C
Stockage commentaire
Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles.
Becker, Marchenko, Maurice, Moll: "Hyperubiquitylation of wild-type p53 contributes to cytoplasmic sequestration in neuroblastoma." dans: Cell death and differentiation, Vol. 14, Issue 7, pp. 1350-60, (2007) (PubMed).
Lu, Ma, Nguyen, Jones, Oren, Donehower: "The Wip1 Phosphatase acts as a gatekeeper in the p53-Mdm2 autoregulatory loop." dans: Cancer cell, Vol. 12, Issue 4, pp. 342-54, (2007) (PubMed).
Antigène
USP7
(Ubiquitin Specific Peptidase 7 (Herpes Virus-Associated) (USP7))
Autre désignation
HAUSP
Sujet
USP7 or HAUSP is a ubiquitin specific protease or a deubiquitylating enzyme that cleaves ubiquitin from its substrates. Since ubiquitylation (polyubiquitination) is most commonly associated with the stability and degradation of cellular proteins, HAUSP acitivity generally stabilizes its substrate proteins. HAUSP is most popularly known as a direct antagonist of Mdm2, the E3 ubiquitin ligase for the tumor suppressor protein, p53.Normally, p53 levels are kept low in part due to Mdm2-mediated ubiquitylation and degradation of p53. Interestingly, in response to oncogenic insults, HAUSP can deubiquitinate p53 and protect p53 from Mdm2-mediated degradation, indicating that it may possess a tumor suppressor function for the immediate stabilization of p53 in response to stress. Another important role of HAUSP function involves the oncogenic stabilization of p53. Oncogenes such as Myc and E1A are thought to activate p53 through a p19 alternative reading frame (p19ARF, also called ARF)-dependent pathway, although some evidence suggests ARF is not essential in this process. An intriguing possibility is that HAUSP provides an alternative pathway for safeguarding the cell against oncogenic insults.