DBC1 Antibody (N-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
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- 实验流程
- 背景知识
Application
| WB, E |
|---|---|
| Primary Accession | O60477 |
| Other Accession | Q925T8, Q920P3, Q7ZZR3, Q5E9L2 |
| Reactivity | Human, Mouse |
| Predicted | Bovine, Chicken, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 88760 Da |
| Antigen Region | 85-111 aa |
| Gene ID | 1620 |
|---|---|
| Other Names | BMP/retinoic acid-inducible neural-specific protein 1, Deleted in bladder cancer protein 1, BRINP1, DBC1, DBCCR1, FAM5A |
| Target/Specificity | This DBC1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 85-111 amino acids from the N-terminal region of human DBC1. |
| Dilution | WB~~1:1000 E~~Use at an assay dependent concentration. |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | DBC1 Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | BRINP1 |
|---|---|
| Synonyms | DBC1, DBCCR1, FAM5A |
| Function | Plays a role in neurogenesis and brain development (By similarity). May suppress cell cycle progression in postmitotic neurons by inhibiting G1/S transition (PubMed:11420708). |
| Cellular Location | Cytoplasm |
| Tissue Location | Highly expressed in brain. Weakly expressed in heart, lung, skeletal muscle, kidney, thymus, prostate, testis and small intestine. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
DBC1 is located within a chromosomal region that shows loss of heterozygosity in some bladder cancers. It contains a 5' CpG island that may be a frequent target of hypermethylation, and it may undergo hypermethylation-based silencing in some bladder cancers.
REFERENCES
Koyama, S., et al. Biochem. Biophys. Res. Commun. 392(3):357-362(2010)
Gronbaek, K., et al. Mod. Pathol. 21(5):632-638(2008)
Louhelainen, J.P., et al. Oncogene 25(16):2409-2419(2006)
Izumi, H., et al. Hum. Mol. Genet. 14(8):997-1007(2005)
Beetz, C., et al. Oncol. Rep. 13(2):335-340(2005)
Nishiyama, H., et al. Oncogene 20(23):2956-2964(2001)
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