USP7 / HAUSP抗体

USP7 / HAUSP抗体产品信息免疫原 : Recombinant Human USP7 / HAUSP Protein (Catalog #11681-HNCB)

Antibody Type : Mouse Monoclonal Antibody ( Mouse mAb Service Platform )
克隆号 : 7B9H2

抗体宿主 : Mouse IgG2b
缓冲液 : 0.2 μm filtered solution in PBS, 5% trehalose may be added in some batches. Please read the hardcopy of COA or contact our customer service to confirm the formulation.
制备方法 : This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, human cell-derived, recombinant Human USP7 / HAUSP (rh USP7 / HAUSP; Catalog #11681-HNCB; Lys 208- Glu 560; NP_003461.2). The IgG fraction of the cell culture supernatant was purified by Protein A affinity chromatography.
USP7 / HAUSP抗体 Background
Ubiquitin carboxyl-terminal hydrolase 7, also known as Ubiquitin thioesterase 7, Herpesvirus-associated ubiquitin-specific protease, Ubiquitin-specific-processing protease 7, USP7 and HAUSP, is a widely expressed protein which belongs to the peptidase C19 family. USP7 is a member of the family of deubiquitinating enzymes. It is involved in the regulation of stress response pathways, epigenetic silencing and the progress of infections by DNA viruses. USP7 is a protein with a cysteine peptidase core, N- and C-terminal domains required for protein-protein interactions. USP7 contributes to epigenetic silencing of homeotic genes by Polycomb (Pc). USP7 cleaves ubiquitin fusion protein substrates. It deubiquitinates TP53/p53 and MDM2 and strongly stabilizes TP53 even in the presence of excess MDM2. USP7 also induces TP53-dependent cell growth repression and apoptosis. USP7 has key roles in the p53 pathway whereby it stabilizes both p53 and MDM2. Herpes simplex virus type 1 (HSV-1) regulatory protein ICP0 stimulates lytic infection and the reactivation of quiescent viral genomes. ICP0 interacts very strongly with USP7. USP7-mediated stabilization of ICP0 is dominant over ICP0-induced degradation of USP7 during productive HSV-1 infection. The biological significance of the ICP0-USP7 interaction may be most pronounced in natural infection situations, in which limited amounts of ICP0 are expressed.
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