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DBC1 (Deleted in Breast Cancer 1) modulates the stability and function of the nuclear receptor Rev-erbα
DBC1 influences the stability and function of the cell's internal clock regulator Rev-erbα
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Abstract
Rev-erbα protein levels decrease significantly upon depletion.
- Rev-erbα is a key regulator of the circadian clock and metabolism.
- DBC1 interacts with Rev-erbα and regulates its repressor function.
- Depletion of DBC1 results in reduced Rev-erbα protein levels without affecting mRNA levels.
- Overexpression of DBC1 enhances Rev-erbα protein stability by inhibiting its degradation.
- Loss of DBC1 leads to a marked decrease in circadian oscillations of Rev-erbα and BMAL1.
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Key numbers
significantly lower levels
Decrease in Rev-erbα Protein Levels
Observed in NIH 3T3 cells treated with siRNA.
1.5 h
Increase in Rev-erbα Half-Life
Half-life increased from approximately 30 min to 1.5 h with overexpression.