Title : BAX supports the mitochondrial network, promoting bioenergetics in nonapoptotic cells.

Pub. Date : 2011 Jun

PMID : 21289292






6 Functional Relationships(s)
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1 Oxygen consumption and cellular ATP levels were reduced in BAX-deficient cells, while glycolysis was increased. Adenosine Triphosphate BCL2 associated X, apoptosis regulator Homo sapiens
2 These results suggested that cells lacking BAX have a deficiency in the ability to generate ATP through cellular respiration. Adenosine Triphosphate BCL2 associated X, apoptosis regulator Homo sapiens
3 Inhibition of BAX with small interfering RNAs reduced intracellular ATP content in BAX-containing cells. Adenosine Triphosphate BCL2 associated X, apoptosis regulator Homo sapiens
4 Inhibition of BAX with small interfering RNAs reduced intracellular ATP content in BAX-containing cells. Adenosine Triphosphate BCL2 associated X, apoptosis regulator Homo sapiens
5 Expression of either full-length or COOH-terminal-truncated BAX in BAX-deficient cells rescued ATP synthesis and oxygen consumption and reduced glycolytic activity, suggesting that this metabolic function of BAX was not dependent upon its COOH-terminal helix. Adenosine Triphosphate BCL2 associated X, apoptosis regulator Homo sapiens
6 Expression of BCL-2 in BAX-containing cells resulted in a subsequent loss of ATP measured, implying that, even under nonapoptotic conditions, an antagonistic interaction exists between the two proteins. Adenosine Triphosphate BCL2 associated X, apoptosis regulator Homo sapiens