| Overview |
| bs-5798R |
| BNIP3L Polyclonal Antibody |
| ELISA, IHC-P, IHC-F, IF(IHC-P), IF(IHC-F), IF(ICC) |
| Human, Mouse |
| Rat, Cow, Pig, Horse, Rabbit |
| Specifications |
| Unconjugated |
| Rabbit |
| KLH conjugated synthetic peptide derived from human BNIP3L |
| Polyclonal |
| #REF! |
| IgG |
| 1ug/ul |
| Purified by Protein A. |
| 0.01M TBS(pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| Shipped at 4C. Store at -20C for one year. Avoid repeated freeze/thaw cycles. |
| Target |
| 665 |
| O60238 |
| Cytoplasm, Nucleus, Cell membrane |
| NIX; BNIP3a; BCL2/adenovirus E1B 19 kDa protein-interacting protein 3-like; Adenovirus E1B19K-binding protein B5; BCL2/adenovirus E1B 19 kDa protein-interacting protein 3A; NIP3-like protein X; NIP3L; BNIP3L; BNIP3H |
| Induces apoptosis. Interacts with viral and cellular anti-apoptosis proteins. Can overcome the suppressors BCL-2 and BCL-XL, although high levels of BCL-XL expression will inhibit apoptosis. Inhibits apoptosis induced by BNIP3. Involved in mitochondrial quality control via its interaction with SPATA18/MIEAP: in response to mitochondrial damage, participates to mitochondrial protein catabolic process (also named MALM) leading to the degradation of damaged proteins inside mitochondria. The physical interaction of SPATA18/MIEAP, BNIP3 and BNIP3L/NIX at the mitochondrial outer membrane regulates the opening of a pore in the mitochondrial double membrane in order to mediate the translocation of lysosomal proteins from the cytoplasm to the mitochondrial matrix. May function as a tumor suppressor. |
| Application Dilution |
| ELISA |
1:500-1000 |
| IHC-P |
1:200-400 |
| IHC-F |
1:100-500 |
| IF(IHC-P) |
1:50-200 |
| IF(IHC-F) |
1:50-200 |
| IF(ICC) |
1:50-200 |