|Tested species reactivity||Human|
|Host / Isotype||Rabbit / IgG|
|Immunogen||Synthetic peptide corresponding to internal region of human BNIP3L protein.|
|Purification||Antigen affinity chromatography|
|Storage buffer||PBS, pH 7.6, with 1% BSA|
|Contains||<0.1% sodium azide|
|Storage Conditions||4° C, do not freeze|
|Tested Applications||Dilution *|
|Immunohistochemistry (Paraffin) (IHC (P))||1:100|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
Heat-mediated antigen retrieval is recommended prior to staining, using a 10mM citrate buffer, pH 6.0, for 10 minutes followed by cooling at room temperature for 20 min. Following antigen retrieval, incubate samples with primary antibody for 30 min at room temperature. A suggested positive control is breast carcinoma.
Members in the BCL-2 family are critical regulators of apoptosis by either inhibiting or promoting cell death. BCL-2 homology 3 (BH3) domain is a potent death domain. BH3 domain containing pro-apoptotic proteins, including BAD, BAX, BID, BIK, HRK, NIP3, and BIM, form a growing subclass of the BCL-2 family. A novel BH3 domain containing protein was recently identified and designated Bnip3L, Bnip3, and NIX (for NIP3-like protein X). Bnip3L/Bnip3/Nix is a homolog of the E1B 19K/BCL-2 binding and pro-apoptotic protein Bnip3. Overexpression of Bnip3L induces apoptosis. Bnip3L interacts with and overcomes suppression by BCL-2 and BCL-XL. Bnip3L is localized in mitochondria. The messenger RNA of Bnip3L is ubiquitously expressed in human tissues. Bnip3L and Bnip3 form a new subfamily of the pro-apoptotic mitochondrial proteins.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.