A mutation in a mitochondrial transmembrane protein is responsible for the pleiotropic hemotological and skeletal phenotype of flexed-tail (f/f) mice

Article Abstract:

A mutation in a mitochondrial transmembrane protein is discussed in this research communication. The mutation has been found to be the source of the pleiotropic hematological/skeletal phenotype of mutant mice of the flexed tail (f/f) type. Positional cloning techniques were used to identify a frameshift mutation in a mitochondrial transmembrane protein. Sfxn1 is the mutated gene and is the prototype for a novel family of proteins evolutionarily conserved in eukaryotes.

Abnormalities, Anemia, Iron in the body, Iron (Nutrient), Eukaryotic cells, Cells (Biology), Eukaryotes, Membrane proteins, Erythrocytes, Red blood cells, Heme

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The expanding role of mitochondria in apoptosis

Article Abstract:

The role of mitochondria in apoptosis is discussed in this review article. Mitochondrial proteins able to activate cellular apoptotic programs directly either activate caspases and nucleases or neutralize cytosolic inhibitors of the process. Mitochondrial and cytosolic proapoptotic proteins interact with antiapoptotic proteins. Each cell's life or death is in the balance, in a complex picture.

Cell death

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IKK1-deficient mice exhibit abnormal development of skin and skeleton

Article Abstract:

IKK1-deficient mice have abnormal development of skeleton and skin. The mutant mice, which are perinatally lethal and have a wide variety of developmental defects, were generated to examine in vivo functions of IKK1. It appears from the results that IKK1 has a role in NF-kappaB activation and is involved in development of skeleton and skin. Two related kinases seem to have distinct functions and cannot be substituted for one another.

Skin, Biological models, Protein kinases, Extremities (Anatomy), Genetic research

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