Sentence examples for by mitochondrial changes that from inspiring English sources

Survival of tumor cells is favored by mitochondrial changes that make death induction more difficult in a variety of stress conditions, such as exposure to chemotherapeutics.

A pathophysiological adaptation to lipotoxicity was probably represented by the observed mitochondrial changes that were possibly paralleled by changes in muscle composition and function.

It was shown that mitaplatin elicits cytotoxic effects upon cisplatin-resistant head and neck tumour cells [ 31] by a dual killing mode: cisplatin interacts with the DNA while the action of the dichloroacetate is focused on the mitochondria by reversing the mitochondrial changes that confers cancer cells resistance to apoptosis.

Those surviving adaptive cancer cells have successfully responded to the selection pressure of the host microenvironment by subversive molecular changes that impact mitochondrial functions and promote glycolysis.

Therefore the synaptic mitochondrial proteomic changes that occur with aging correlate with preservation of synaptic mitochondrial function.

This process can be mediated by changes in enzyme concentrations and mitochondrial biogenesis, modification of cell and mitochondrial membranes, and conformational changes that optimize enzyme efficiencies at different temperatures [ 1- 3].

This suggests that RANKL probably prevents apoptosis by preventing mitochondrial changes prior to caspase activation, perhaps via members of the Bcl-2 family of proteins that regulate the mitochondrial pathway of apoptosis [ 32, 33].

Activation of Bax and Bak during apoptosis involves multiple conformational changes that are accompanied by their mitochondrial intramembranous homooligomerization [ 6].

Taken altogether, these results indicate that p53 is not required for the mitochondrial changes induced by hyperosmolarity and that the involvement of caspases is cell-type specific.

These experiments strongly suggest that oxidative stress lies at the root of the ER and mitochondrial changes caused by Miner1 deficiency, and importantly that sulphydryl anti-oxidant treatment could be a rational therapeutic approach for treating this syndrome.

By that time, the apoptotic mitochondrial changes such as translocation of Bax to the mitochondria and release of cytochrome c to the cytosol had already occurred in the majority of the neurons and the BH3-only proteins should have been activated, as shown for DP5/Hrk, Bim and PUMA.