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Hrk BH3 Domain Antibody
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS: 1
- PROTOCOLS
- BACKGROUND
Application 
| IHC-P, WB, 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 | IHC-P~~1:10~50 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 | 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 |
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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