The Claim
In human cell lines, acidosis induces preferential binding of MondoA to the promoters of TXNIP and ARRDC4, resulting in their strong transcriptional upregulation, while other MondoA target genes show minimal response.
What the research says
Supports is higher
Support is ahead, but a single strong opposing study can change this.
These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.
In human cells grown in the lab, low pH conditions cause the MondoA protein to bind more strongly to the regulatory regions of the TXNIP and ARRDC4 genes, leading to increased production of these genes' RNA, while other genes regulated by MondoA show little change.
See the scientific wording
In human cell lines, acidosis induces preferential binding of MondoA to the promoters of TXNIP and ARRDC4, resulting in their strong transcriptional upregulation, while other MondoA target genes show minimal response.
When the inside of a cell becomes too acidic, it forces the mitochondria to produce more energy, which is used to convert glucose into a molecule called glucose-6-phosphate. This molecule binds to a protein complex that moves into the cell's nucleus and turns on only two specific genes, TXNIP and ARRDC4, while leaving all other similar genes untouched. These two genes then reduce the cell's intake of sugar to restore balance.
What the research says
1 studyWhen cells get too acidic, a protein called MondoA turns on just two specific genes—TXNIP and ARRDC4—to slow down sugar intake, and ignores all its other possible targets. The study shows this exact behavior happens in human cells.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting studies
Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.