By Ethan D. Buhr, Joseph S. Takahashi (auth.), Achim Kramer, Martha Merrow (eds.)
This e-book offers the reader with a latest and accomplished evaluate in regards to the molecular, mobile and system-wide rules of circadian clock rules. Emphasis is put on the significance of circadian clocks for the timing of healing interventions.
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Extra info for Circadian Clocks
Nature 434:640–644 Xu Y, Toh KL, Jones CR, Shin JY, Fu YH, Ptacek LJ (2007) Modeling of a human circadian mutation yields insights into clock regulation by PER2. Cell 128:59–70 Yamaguchi S, Isejima H, Matsuo T, Okura R, Yagita K, Kobayashi M, Okamura H (2003) Synchronization of cellular clocks in the suprachiasmatic nucleus. Science 302:1408–1412 Yamazaki S, Kerbeshian MC, Hocker CG, Block GD, Menaker M (1998) Rhythmic properties of the hamster suprachiasmatic nucleus in vivo. J Neurosci 18:10709–10723 Yamazaki S, Numano R, Abe M, Hida A, Takahashi R, Ueda M, Block GD, Sakaki Y, Menaker M, Tei H (2000) Resetting central and peripheral circadian oscillators in transgenic rats.
However, cells have evolved several mechanisms to repair the damaged DNA. Recent results suggest that one such repair mechanism, the nucleotide excision repair pathway, displays circadian oscillation in mouse brain, possibly through oscillation in the expression of the DNA damage-recognition protein xeroderma pigmentosum A (XPA) (Kang et al. 2009). XPA levels also oscillate in mouse liver (Kang et al. 2009), suggesting that the circadian nucleotide excision repair might also be operating in peripheral tissues.
These mice demonstrate a shorter period, increased energy expenditure and are resistant to diet-induced obesity (Alenghat et al. 2008). HDAC3 recruitment to the genome was recently shown to be rhythmic in liver (high during the day and low at night) (Feng et al. 2011). At these HDAC3 binding sites, REV-ERBα and NCoR1 recruitment were in phase with HDAC3 recruitment, whereas histone acetylation and RNA polymerase II recruitment were anti-phasic. Depletion of either HDAC3 or REV-ERBα was shown to cause fatty liver phenotype, such as increased hepatic lipid and triglyceride content (Feng et al.