RNA Binding Motif Protein 17 (RBM17) Antibody
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Description
Rabbit Polyclonal against the RBM17 protein.
Documents del producto
Product specifications
| Category | Primary Antibodies |
| Immunogen Target | Target: RNA Binding Motif Protein 17 (RBM17) Immunogen: Recombinant fragment corresponding to 196-375 AA of human RBM17. |
| Host | Rabbit |
| Reactivity | Human |
| Assay Type | Concentration: Lyophilized form: Not applicable. After reconstitution: 1 mg/ml. |
| Recommended Dilution | ELISA: 1/20000 - 1/80000, WB: 1/500 - 1/2000, IHC: 1/100 - 1/200. Optimal dilutions/concentrations should be determined by the end user. |
| Clonality | Polyclonal |
| Conjugation | Unconjugated |
| Isotype | IgG |
| Observed MW | Observed MW: 45 kDa |
| Purification | Purified by antigen affinity column chromatography. |
| Size 1 | 100 µg |
| Size 2 | 1 mg |
| Form | Lyophilized |
| Tested Applications | ELISA, WB, IHC |
| Buffer | Prior to lyophilization: 1% BSA and 0.02% NaN3. |
| Availability | Shipped within 7-15 working days. |
| Storage | Store at -20 °C. Avoid repeated freeze/thaw cycles. |
| Dry Ice | No |
| NCBI Accession | BC007871 |
| Background | Antibody anti-RBM17 |
| 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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RBM17 antibody
Splice factor that binds to the single-stranded 3'AG at the exon/intron border and promotes its utilization in the second catalytic step. Involved in the regulation of alternative splicing and the utilization of cryptic splice sites. Promotes the utilization of a cryptic splice site created by the beta-110 mutation in the HBB gene. The resulting frameshift leads to sickle cell anemia.
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Splice factor that binds to the single-stranded 3'AG at the exon/intron border and promotes its utilization in the second catalytic step. Involved in the regulation of alternative splicing and the utilization of cryptic splice sites. Promotes the utilization of a cryptic splice site created by the beta-110 mutation in the HBB gene. The resulting frameshift leads to sickle cell anemia.
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