The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)



Gene Review

Bnip3l  -  BCL2/adenovirus E1B interacting protein 3...

Mus musculus

Synonyms: BCL2/adenovirus E1B 19 kDa protein-interacting protein 3-like, C86132, D14Ertd719e, NIP3-like protein X, NIP3L, ...
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of Bnip3l


High impact information on Bnip3l

  • A previously undescribed truncated Nix isoform, termed sNix, was not targeted to mitochondria but heterodimerized with Nix and protected against Nix-mediated apoptosis [1].
  • To identify mechanisms of gene regulation for these critical cardiac apoptosis effectors, the determinants of Nix and BNip3 promoter activation were elucidated by luciferase reporter gene expression in neonatal rat cardiac myocytes [2].
  • NixP activity was proportional to the extent of TAC hypertrophy and was inhibited by mithramycin [2].
  • Human Nip3 maps to chromosome 14q11.2-q12, whereas Nix/BNip3L was found on 8q21 [4].
  • Following transfection, Nix protein undergoes progressive proteolysis to an 11-kDa C-terminal fragment, which is blocked by the proteasome inhibitor lactacystin [4].

Biological context of Bnip3l


  1. Mitochondrial death protein Nix is induced in cardiac hypertrophy and triggers apoptotic cardiomyopathy. Yussman, M.G., Toyokawa, T., Odley, A., Lynch, R.A., Wu, G., Colbert, M.C., Aronow, B.J., Lorenz, J.N., Dorn, G.W. Nat. Med. (2002) [Pubmed]
  2. Distinct pathways regulate proapoptotic Nix and BNip3 in cardiac stress. Gálvez, A.S., Brunskill, E.W., Marreez, Y., Benner, B.J., Regula, K.M., Kirschenbaum, L.A., Dorn, G.W. J. Biol. Chem. (2006) [Pubmed]
  3. Physiological growth synergizes with pathological genes in experimental cardiomyopathy. Syed, F., Odley, A., Hahn, H.S., Brunskill, E.W., Lynch, R.A., Marreez, Y., Sanbe, A., Robbins, J., Dorn, G.W. Circ. Res. (2004) [Pubmed]
  4. Nix and Nip3 form a subfamily of pro-apoptotic mitochondrial proteins. Chen, G., Cizeau, J., Vande Velde, C., Park, J.H., Bozek, G., Bolton, J., Shi, L., Dubik, D., Greenberg, A. J. Biol. Chem. (1999) [Pubmed]
WikiGenes - Universities