Nix Nought Nothing: fairy tale or real deal.
Nix was first described in the heart as the protein product of a differentially expressed mRNA detected by hybridization to a partial cDNA sequence tag on an RNA expression array. Over the subsequent 8 years Nix has become the prototypical transcriptionally-regulated cardiac myocyte "suicide" gene and has been used as a model to interrogate mechanisms of programmed cardiomyocyte death in hypertrophy and heart failure. Nix stimulates conventional apoptosis mediated via the intrinsic mitochondrial pathway, but emerging evidence indicates that Nix also controls programmed necrosis dependent upon sarcoplasmic reticular-mitochondrial tethering, calcium cross-talk, and the mitochondrial permeability transition. Recent studies have also described Nix labeling of senescent cardiomyocyte mitochondria for autophagic elimination, elucidated a physiological mitochondrial quality control Nix function; so-called "mitochondrial pruning". This article is part of a special issue entitled "Key Signaling Molecules in Hypertrophy and Heart Failure."
Dorn
Gerald W
GW
Center for Pharmacogenomics, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, USA. gdorn@dom.wustl.edu
D000818:Animals; D017209:Apoptosis; D006332:Cardiomegaly / Q000378:metabolism / Q000473:pathology; D015870:Gene Expression; D005786:Gene Expression Regulation; D006333:Heart Failure / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D058990:Molecular Targeted Therapy; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000378:metabolism*; D025521:Tumor Suppressor Proteins / Q000235:genetics / Q000378:metabolism*
C116838:BNIP3L protein, human; D008565:Membrane Proteins; D011518:Proto-Oncogene Proteins; D025521:Tumor Suppressor Proteins