Hrk BH3 Domain Antibody
Affinity Purified Rabbit Polyclonal Antibody (Pab)
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- 实验流程
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Application
| WB, IHC-P, E |
|---|---|
| Primary Accession | O00198 |
| Other Accession | NP_003797 |
| Reactivity | Human, Mouse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 9884 Da |
| Antigen Region | 15-50 aa |
| Gene ID | 8739 |
|---|---|
| Other Names | Activator of apoptosis harakiri, BH3-interacting domain-containing protein 3, Neuronal death protein DP5, HRK, BID3 |
| Target/Specificity | This Hrk BH3 Domain antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 15-50 amino acids from human Hrk BH3 Domain. |
| Dilution | WB~~1:1000 IHC-P~~1:100~500 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 | Hrk BH3 Domain Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | HRK |
|---|---|
| Synonyms | BID3 |
| Function | Promotes apoptosis. |
| Cellular Location | Membrane; Single-pass membrane protein. Mitochondrion |
For Research Use Only. Not For Use In Diagnostic Procedures.

Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Activator of apoptosis Hrk regulates apoptosis through interaction with death-repressor proteins Bcl-2 and Bcl-X(L). The HRK protein lacks significant homology to other BCL2 family members except for an 8-amino acid region that was similar to the BCL2 homology domain-3 (BH3) motif of BIK. HRK interacts with BCL2 and BCLXL via the BH3 domain, but not with the death-promoting BCL2-related proteins BAX, BAK, or BCLXS. HRK localizes to membranes of intracellular organelles in a pattern similar to that previously reported for BCL2 and BCLXL.
REFERENCES
Wakabayashi, T., et al., Neurosci. Lett. 318(2):77-80 (2002).
Inohara, N., et al., EMBO J. 16(7):1686-1694 (1997).
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