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Moreover, rhythms of BMAL1 and blood glucose were altered in KO mice.
AhR/ARNT and the clock proteins (circadian locomotor ourpur cycles kaput; CLOCK) and BMAL1 [brain, muscle ARNT-like protein 1; also called Arntl (aryl hydrocarbon receptor nuclear translocator-like)] share structural similarities and exhibit diurnal changes in multiple tissues (Richardson et al.
Disruption of CLOCK and BMAL1 alters glucose tolerance and regulation of key metabolism genes (Marcheva et al.
In the present study we investigated the involvement of BMAL1 and PPAR-[alpha] in glucose metabolism after manipulation of AhR signaling using small interfering RNA (siRNA) or AhR agonists, as well as in AhR-deficient [knockout (KO)] mice.
To confirm that BMAL1 regulates PPAR-[alpha], we silenced Bmall with siRNA.
Because BMAL1 and AhR both up-regulate PPAR-[alpha], we cotransfecced Ahr siRNA and Small plasmid or Email siRNA and Ahr plasmid and measured Ppara mRNA levels.
Cyplal is suppressed, indicating chat BMAL1 depletion inhibits AhR (Figure 6A).
Schibler and colleagues report similar results, demonstrating that SIRT1 levels rise and fall throughout the day, and that SIRT1, CLOCK and BMAL1 interact in a circadian manner.
Digging deeper into the molecular workings of the clock, Panda and his colleagues found that each morning, JARID1a reactivates CLOCK and BMAL1 by countering the action of a brake protein HDAC1.
They genetically engineered some mice to have defective CLOCK genes and some to also lack the BMAL1 gene.
Young mice lacking the BMAL1 gene only in their pancreas, however, had normal body weight and composition, and their behavior followed normal circadian patterns, although their blood sugar levels were abnormally high, the researchers found.
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