Proteasome Subunit Alpha Type-7 (PSMA7) Antibody
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Description
Proteasome Subunit Alpha Type-7 (PSMA7) Antibody is a Rabbit polyclonal antibody for the detection of Human Proteasome Subunit Alpha Type-7 (PSMA7).
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Product specifications
| Category | Primary Antibodies |
| Immunogen Target | Proteasome Subunit Alpha Type-7 (PSMA7) |
| Host | Rabbit |
| Reactivity | Human |
| Recommended Dilution | Optimal dilutions/concentrations should be determined by the end user. |
| Clonality | Polyclonal |
| Conjugation | Unconjugated |
| Isotype | IgG |
| Size 1 | 50 µg |
| Size 2 | 100 µg |
| Form | Liquid |
| Tested Applications | ELISA, WB, IHC |
| Buffer | 0.01 M PBS, pH 7.4, 50% glycerol, 0.05% Proclin-300. |
| Availability | Shipped within 5-12 working days. |
| Storage | Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles. |
| Dry Ice | No |
| UniProt ID | O14818 |
| Gene ID | 5688 |
| NCBI Accession | NP_002783.1 |
| Background | Antibody anti-PSMA7 |
| Status | RUO |
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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