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Autophagy supports tumor growth by limiting p53 function, maintaining functional mitochondria, supplying metabolites for tumor metabolism, inhibiting senescence, modulating p62 function, preventing diversion of tumor progression to benign oncocytomas, and suppressing immune surveillance.
However, in an established tumor, autophagy promotes cancer progression by providing substrates for metabolism, maintaining functional mitochondria, and fostering survival during and after therapy.
It is known that mitochondrial fission and fusion play critical roles in maintaining functional mitochondria when cells experience metabolic or environmental stresses.
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It is tempting to speculate that these dietary components may stimulate mitochondrial biogenesis through ATM to maintain functional mitochondria and regulate ROS.
mtDNA is extremely compact (93% coding sequence) and the majority of proteins required to build and maintain functional mitochondria is therefore encoded by nuclear DNA, synthesized in the cytosol and imported into mitochondria, where they are targeted to one of the four mitochondrial compartments.
These data provide evidence that the expression of distinct mitochondria-associated genes is important for maintaining functional populations of mitochondria in lens epithelial cells.
To identify those mitochondrial regulatory and degradation genes that maintain functional populations of mitochondria in the lens epithelium and eliminate mitochondria in the lens fiber cells, we used high-throughput mRNA sequencing combined with bioinformatics analysis to determine the entire spectrum and range of transcripts expressed by EC, EQ, FP, and FC cells of the E13 chicken lens.
These results demonstrate that anti-apoptotic Bcl-2 proteins maintain functional integrity of mitochondria in HaCaT-derived SCC.
Maintaining muscle function is vital to maintain functional independence.
The data provide insight into the specific mitochondrial regulatory and degradation pathways operating to maintain functional mitochondrial populations in the lens epithelium and eliminate mitochondria upon lens fiber cell maturation.
Collectively, these results suggest that a balance between different mitophagy mechanisms mirrors the need to maintain functional mitochondrial populations in lens epithelial cells and eliminate mitochondria in lens fiber cells.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com