NIX / BNIP3L Antibody (aa77-92)
Rabbit Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB, IHC-P, IF |
---|---|
Primary Accession | O60238 |
Reactivity | Human |
Host | Rabbit |
Clonality | Polyclonal |
Calculated MW | 24kDa |
Dilution | IHC-P (5 µg/ml), WB (0.5-1 µg/ml), |
Gene ID | 665 |
---|---|
Other Names | 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, BNIP3A, BNIP3H, NIX |
Target/Specificity | peptide (daqhesgqsssrgssh) corresponding to amino acids 77 to 92 of human origin, which are identical to those of mouse Bnip3L |
Reconstitution & Storage | Short term 4°C, long term aliquot and store at -20°C, avoid freeze thaw cycles. Store undiluted. |
Precautions | NIX / BNIP3L Antibody (aa77-92) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | BNIP3L |
---|---|
Synonyms | BNIP3A, BNIP3H, NIX |
Function | 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 in 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. |
Cellular Location | Nucleus envelope. Endoplasmic reticulum. Mitochondrion outer membrane. Membrane; Single-pass membrane protein. Note=Colocalizes with SPATA18 at the mitochondrion outer membrane |
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Background
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.
References
Matsushima M.,et al.Genes Chromosomes Cancer 21:230-235(1998).
Yasuda M.,et al.Submitted (JUL-1998) to the EMBL/GenBank/DDBJ databases.
Chen G.,et al.J. Biol. Chem. 274:7-10(1999).
Ohi N.,et al.Cell Death Differ. 6:314-325(1999).
Aerbajinai W.,et al.Blood 102:712-717(2003).
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