Proteasome Subunit Alpha Type 7 (PSMA7) Antibody Pair
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Description
PSMA7 Antibody Pair for use in Sandwich ELISA assay development.
Documents del producto
Product specifications
| Category | Antibody Pairs |
| Immunogen Target | Proteasome Subunit Alpha Type 7 (PSMA7) |
| Host | Capture Host: Rabbit Detection Host: Rabbit |
| Reactivity | Human, Mouse, Pig |
| Assay Data | Sandwich |
| Assay Type | Sandwich |
| Clonality | Capture Clonality: Polyclonal Detection Clonality: Polyclonal |
| Conjugation | Biotin |
| Isotype | Capture Isotype: IgG Detection Isotype: IgG |
| Size 1 | 5 × 96 tests |
| Form | Liquid |
| Tested Applications | ELISA |
| Buffer | 0.01 M PBS, pH 7.4, 50% glycerol. |
| Availability | Shipped within 5-10 working days. |
| Dry Ice | No |
| Background | Antibody pair for PSMA7 |
| Status | RUO |
| Note | THIS PRODUCT IS FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC, THERAPEUTIC OR COSMETIC PROCEDURES. NOT FOR HUMAN OR ANIMAL CONSUMPTION. |
Descripción
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PSMA7 antibody
The proteasome is a multicatalytic proteinase complex which is characterized by its ability to cleave peptides with Arg, Phe, Tyr, Leu, and Glu adjacent to the leaving group at neutral or slightly basic pH. The proteasome has an ATP-dependent proteolytic activity. Plays an important role in the regulation of cell proliferation or cell cycle control, transcriptional regulation, immune and stress response, cell differentiation, and apoptosis. Interacts with some important proteins involved in transcription factor regulation, cell cycle transition, viral replication and even tumor initiation and progression. Inhibits the transactivation function of HIF-1A under both normoxic and hypoxia-mimicking conditions. The interaction with EMAP2 increases the proteasome-mediated HIF-1A degradation under the hypoxic conditions. Plays a role in hepatitis C virus internal ribosome entry site-mediated translation. Mediates nuclear translocation of the androgen receptor(AR) and thereby enhances androgen-mediated transactivation. Promotes MAVS degradation and thereby negatively regulates MAVS-mediated innate immune response.
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