Application | Comment | Organism |
---|---|---|
medicine | transient knockdown of NNT in NCI-H295R cells increases intracellular levels of oxidative stress, resulting in a pronounced suppression of cell proliferation, higher apoptotic rates, and sensitization of cells to chemically induced oxidative stress. Steroidogenesis is stimulated by NNT loss. In a stable NNT knockdown model in the same cell line, after long-term culture, cells adapt metabolically to chronic NNT knockdown, restoring their redox balance and resilience to oxidative stress, although their proliferation remains suppressed. This is associated with higher rates of oxygen consumption | Homo sapiens |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | Q13423 | - |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
adrenocortical carcinoma cell | - |
Homo sapiens | - |
NCI-H295R cell | - |
Homo sapiens | - |
General Information | Comment | Organism |
---|---|---|
physiological function | transient knockdown of NNT in NCI-H295R cells increases intracellular levels of oxidative stress, resulting in a pronounced suppression of cell proliferation, higher apoptotic rates, and sensitization of cells to chemically induced oxidative stress. Steroidogenesis is stimulated by NNT loss. In a stable NNT knockdown model in the same cell line, after long-term culture, cells adapt metabolically to chronic NNT knockdown, restoring their redox balance and resilience to oxidative stress, although their proliferation remains suppressed. This is associated with higher rates of oxygen consumption | Homo sapiens |