By Michelle L. Gumz
This publication sheds new mild at the molecular mechanisms that generate circadian rhythms. It examines how organic rhythms effect physiological procedures akin to sleep, hormone synthesis and secretion, immunity, kidney functionality, the cardiovascular approach, blood strain, and the digestive process. scientific implications are thought of whereas exploring the effect of rhythms on neuropsychiatric issues and chronotherapy’s power for decreasing cardiovascular possibility. delivering a cross-section of workmanship in either uncomplicated and translational (bench-to-bedside) learn, this e-book serves as a consultant for physicians and scientists who desire to research extra concerning the impression of circadian rhythms on physiological tactics in well-being and disorder.
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Additional info for Circadian Clocks: Role in Health and Disease
Depletion of CIPC shortens the circadian period length. Heat-shock factor 1 (HSF1) and Upstream Stimulating Factor 1 (USF1) have been identified as circadian transcription factors (Reinke et al. 2008; Buhr et al. 2010; Shimomura et al. 2013). Buhr et al. (2010) propose that glucocorticoids and temperature, which both impact the circadian clock in peripheral tissues, do so through modulation of HSF1 activity. USF1 expression differs in a straindependent manner and contributes to strain-dependent suppression of the longperiod phenotype in ClockΔ19/+ (Shimomura et al.
2007) and identification of the transcription factor zinc finger homeobox 3 (Zfhx3) as the gene mutated in the Short-circuit (Sci) mutant line, as discussed earlier (Parsons et al. 2014). Whether the other mutants identified in these screens represent new mutations in known clock genes, or new clock genes, remains to be determined. This abundant pipeline of yet-to-be-identified mutants affecting circadian rhythms, plus the continuing identification of novel circadian regulatory mechanisms (most recently, LHX1, ZFHX1, and CHRONO), indicates that there is potential for significant, continuing growth in our understanding of circadian clock mechanisms.
Bmal1 appears to be an exception to this redundancy-of-function rule, as mice with disruption of Bmal1 alone are arrhythmic (Bunger et al. 2000). The closely related gene, Bmal2 (Mop9), is a CLOCK:BMAL1 target, however, so Bmal2 expression is greatly reduced in BMAL1-deficient mice (Shi et al. 2010). There is loss of expression of both genes when Bmal1 alone is targeted. Indeed, when BMAL2 is overexpressed from a promoter not requiring CLOCK:BMAL1 for expression, BMAL2 can restore rhythmicity in BMAL1-deficient cells (Shi et al.
Circadian Clocks: Role in Health and Disease by Michelle L. Gumz