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Article ; Online: Circadian modification network of a core clock driver BMAL1 to harmonize physiology from brain to peripheral tissues.

Tamaru, Teruya / Takamatsu, Ken

2018 Volume 119, Page(s) 11–16

Abstract: Circadian clocks dictate various physiological functions by brain SCN (a central clock) -orchestrating the temporal harmony of peripheral clocks of tissues/organs in the whole body, with adaptability to environments by resetting their timings. ... ...

Abstract	Circadian clocks dictate various physiological functions by brain SCN (a central clock) -orchestrating the temporal harmony of peripheral clocks of tissues/organs in the whole body, with adaptability to environments by resetting their timings. Dysfunction of this circadian adaptation system (CAS) occasionally causes/exacerbates diseases. CAS is based on cell-autonomous molecular clocks, which oscillate via a core transcriptional/translational feedback loop with clock genes/proteins, e.g., BMAL1: CLOCK circadian transcription driver and CRY1/2 and PER1/2 suppressors, and is modulated by various regulatory loops including clock protein modifications. Among mutants with a single clock gene, BMAL1-deficient mice exhibit the most drastic loss of circadian functions. Here, we highlight on numerous circadian protein modifications of mammalian BMAL1, e.g., multiple phosphorylations, SUMOylation, ubiquitination, acetylation, O-GlcNAcylation and S-nitrosylation, which mutually interplay to control molecular clocks and coordinate physiological functions from the brain to peripheral tissues through the input and output of the clocks.
MeSH term(s)	ARNTL Transcription Factors/metabolism ; Animals ; Brain/metabolism ; CLOCK Proteins/metabolism ; Circadian Clocks/physiology ; Circadian Rhythm/physiology ; Humans ; Period Circadian Proteins/metabolism
Chemical Substances	ARNTL Transcription Factors ; Period Circadian Proteins ; CLOCK Proteins (EC 2.3.1.48)
Language	English
Publishing date	2018-01-03
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	283190-9
ISSN	1872-9754 ; 0197-0186
ISSN (online)	1872-9754
ISSN	0197-0186
DOI	10.1016/j.neuint.2017.12.013
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Article ; Online: Circadian adaptation to cell injury stresses: a crucial interplay of BMAL1 and HSF1.

Tamaru, Teruya / Ikeda, Masaaki

The journal of physiological sciences : JPS

2016 Volume 66, Issue 4, Page(s) 303–306

Abstract: The circadian clock system confers daily anticipatory physiological processes with the ability to be reset by environmental cues. This "circadian adaptation system" (CAS), driven by cell-autonomous molecular clocks, orchestrates various rhythmic ... ...

Abstract	The circadian clock system confers daily anticipatory physiological processes with the ability to be reset by environmental cues. This "circadian adaptation system" (CAS), driven by cell-autonomous molecular clocks, orchestrates various rhythmic physiological processes in the entire body. Hence, the dysfunction of these clocks exacerbates various diseases, which may partially be due to the impairment of protective pathways. If this is the case, how does the CAS respond to cell injury stresses that are critical in maintaining health and life by evoking protective pathways? To address this question, here we review and discuss recent evidence revealing life-protective (pro-survival) molecular networks between clock (e.g., BMAL1, CLOCK, and PER2) and adaptation (e.g., HSF1, Nrf2, NF-κB, and p53) pathways, which are evoked by various cell injury stresses (e.g., heat, reactive oxygen species, and UV). The CK2 protein kinase-integrated interplay of the BMAL1 (clock) and HSF1 (heat-shock response) pathways is one of the crucial events in CAS.
MeSH term(s)	ARNTL Transcription Factors/metabolism ; Adaptation, Physiological/physiology ; Animals ; Circadian Clocks/physiology ; Circadian Rhythm/physiology ; Heat-Shock Proteins/metabolism ; Humans ; Oxidative Stress/physiology ; Reactive Oxygen Species/metabolism
Chemical Substances	ARNTL Transcription Factors ; Heat-Shock Proteins ; Reactive Oxygen Species
Language	English
Publishing date	2016-02-24
Publishing country	Japan
Document type	Journal Article ; Review
ZDB-ID	2234472-X
ISSN	1880-6562 ; 1880-6546
ISSN (online)	1880-6562
ISSN	1880-6546
DOI	10.1007/s12576-016-0436-5
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Article ; Online: Class 3 PI3K coactivates the circadian clock to promote rhythmic de novo purine synthesis.

Alkhoury, Chantal / Henneman, Nathaniel F / Petrenko, Volodymyr / Shibayama, Yui / Segaloni, Arianna / Gadault, Alexis / Nemazanyy, Ivan / Le Guillou, Edouard / Wolide, Amare Desalegn / Antoniadou, Konstantina / Tong, Xin / Tamaru, Teruya / Ozawa, Takeaki / Girard, Muriel / Hnia, Karim / Lutter, Dominik / Dibner, Charna / Panasyuk, Ganna

Nature cell biology

2023 Volume 25, Issue 7, Page(s) 975–988

Abstract: Metabolic demands fluctuate rhythmically and rely on coordination between the circadian clock and nutrient-sensing signalling pathways, yet mechanisms of their interaction remain not fully understood. Surprisingly, we find that class 3 ... ...

Abstract	Metabolic demands fluctuate rhythmically and rely on coordination between the circadian clock and nutrient-sensing signalling pathways, yet mechanisms of their interaction remain not fully understood. Surprisingly, we find that class 3 phosphatidylinositol-3-kinase (PI3K), known best for its essential role as a lipid kinase in endocytosis and lysosomal degradation by autophagy, has an overlooked nuclear function in gene transcription as a coactivator of the heterodimeric transcription factor and circadian driver Bmal1-Clock. Canonical pro-catabolic functions of class 3 PI3K in trafficking rely on the indispensable complex between the lipid kinase Vps34 and regulatory subunit Vps15. We demonstrate that although both subunits of class 3 PI3K interact with RNA polymerase II and co-localize with active transcription sites, exclusive loss of Vps15 in cells blunts the transcriptional activity of Bmal1-Clock. Thus, we establish non-redundancy between nuclear Vps34 and Vps15, reflected by the persistent nuclear pool of Vps15 in Vps34-depleted cells and the ability of Vps15 to coactivate Bmal1-Clock independently of its complex with Vps34. In physiology we find that Vps15 is required for metabolic rhythmicity in liver and, unexpectedly, it promotes pro-anabolic de novo purine nucleotide synthesis. We show that Vps15 activates the transcription of Ppat, a key enzyme for the production of inosine monophosphate, a central metabolic intermediate for purine synthesis. Finally, we demonstrate that in fasting, which represses clock transcriptional activity, Vps15 levels are decreased on the promoters of Bmal1 targets, Nr1d1 and Ppat. Our findings open avenues for establishing the complexity for nuclear class 3 PI3K signalling for temporal regulation of energy homeostasis.
MeSH term(s)	Circadian Clocks/genetics ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Vacuolar Sorting Protein VPS15/genetics ; Vacuolar Sorting Protein VPS15/metabolism ; ARNTL Transcription Factors/genetics ; ARNTL Transcription Factors/metabolism ; Purines ; Lipids
Chemical Substances	Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Vacuolar Sorting Protein VPS15 (EC 2.7.11.1) ; ARNTL Transcription Factors ; Purines ; Lipids
Language	English
Publishing date	2023-07-06
Publishing country	England
Document type	Journal Article
ZDB-ID	1474722-4
ISSN	1476-4679 ; 1465-7392
ISSN (online)	1476-4679
ISSN	1465-7392
DOI	10.1038/s41556-023-01171-3
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Zs.A 5169: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Transgenic rats expressing dominant negative BMAL1 showed circadian clock amplitude reduction and rapid recovery from jet lag.

Minami, Yoichi / Yoshikawa, Tomoko / Nagano, Mamoru / Koinuma, Satoshi / Morimoto, Tadamitsu / Fujioka, Atsuko / Furukawa, Keiichi / Ikegami, Keisuke / Tatemizo, Atsuhiro / Egawa, Kentaro / Tamaru, Teruya / Taniguchi, Taizo / Shigeyoshi, Yasufumi

The European journal of neuroscience

2021 Volume 53, Issue 6, Page(s) 1783–1793

Abstract: The circadian rhythms are endogenous rhythms of about 24 h, and are driven by the circadian clock. The clock centre locates in the suprachiasmatic nucleus. Light signals from the retina shift the circadian rhythm in the suprachiasmatic nucleus, but there ...

Abstract	The circadian rhythms are endogenous rhythms of about 24 h, and are driven by the circadian clock. The clock centre locates in the suprachiasmatic nucleus. Light signals from the retina shift the circadian rhythm in the suprachiasmatic nucleus, but there is a robust part of the suprachiasmatic nucleus that causes jet lag after an abrupt shift of the environmental lighting condition. To examine the effect of attenuated circadian rhythm on the duration of jet lag, we established a transgenic rat expressing BMAL1 dominant negative form under control by mouse Prnp-based transcriptional regulation cassette [BMAL1 DN (+)]. The transgenic rats became active earlier than controls, just after light offset. Compared to control rats, BMAL1 DN (+) rats showed smaller circadian rhythm amplitudes in both behavioural and Per2 promoter driven luciferase activity rhythms. A light pulse during the night resulted in a larger phase shift of behavioural rhythm. Furthermore, at an abrupt shift of the light-dark cycle, BMAL1 DN (+) rat showed faster entrainment to the new light-dark cycle compared to controls. The circadian rhythm has been regarded as a limit cycle phenomenon, and our results support the hypothesis that modification of the amplitude of the circadian limit cycle leads to alteration in the length of the phase shift.
MeSH term(s)	ARNTL Transcription Factors ; Animals ; Circadian Clocks ; Circadian Rhythm ; Jet Lag Syndrome ; Mice ; Rats ; Rats, Transgenic ; Suprachiasmatic Nucleus
Chemical Substances	ARNTL Transcription Factors ; Arntl protein, rat
Language	English
Publishing date	2021-02-25
Publishing country	France
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	645180-9
ISSN	1460-9568 ; 0953-816X
ISSN (online)	1460-9568
ISSN	0953-816X
DOI	10.1111/ejn.15085
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Article ; Online: Cooperative interaction among BMAL1, HSF1, and p53 protects mammalian cells from UV stress.

Kawamura, Genki / Hattori, Mitsuru / Takamatsu, Ken / Tsukada, Teruyo / Ninomiya, Yasuharu / Benjamin, Ivor / Sassone-Corsi, Paolo / Ozawa, Takeaki / Tamaru, Teruya

Communications biology

2018 Volume 1, Page(s) 204

Abstract: The circadian clock allows physiological systems to adapt to their changing environment by synchronizing their timings in response to external stimuli. Previously, we reported clock-controlled adaptive responses to heat-shock and oxidative stress and ... ...

Abstract	The circadian clock allows physiological systems to adapt to their changing environment by synchronizing their timings in response to external stimuli. Previously, we reported clock-controlled adaptive responses to heat-shock and oxidative stress and showed how the circadian clock interacts with BMAL1 and HSF1. Here, we present a similar clock-controlled adaptation to UV damage. In response to UV irradiation, HSF1 and tumor suppressor p53 regulate the expression of the clock gene
Language	English
Publishing date	2018-11-22
Publishing country	England
Document type	Journal Article
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-018-0209-1
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Article ; Online: Cooperative interaction among BMAL1, HSF1, and p53 protects mammalian cells from UV stress

Genki Kawamura / Mitsuru Hattori / Ken Takamatsu / Teruyo Tsukada / Yasuharu Ninomiya / Ivor Benjamin / Paolo Sassone-Corsi / Takeaki Ozawa / Teruya Tamaru

Communications Biology, Vol 1, Iss 1, Pp 1-

2018 Volume 13

Abstract: Genki Kawamura et al. demonstrate that cells are protected against UV stress through cooperative interactions among circadian clock, heat shock response, and a tumor suppression mechanism. This study reports another protective role of circadian clock as ... ...

Abstract	Genki Kawamura et al. demonstrate that cells are protected against UV stress through cooperative interactions among circadian clock, heat shock response, and a tumor suppression mechanism. This study reports another protective role of circadian clock as an adaptation strategy against cellular stress.
Keywords	Biology (General) ; QH301-705.5
Language	English
Publishing date	2018-11-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
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Article ; Online: The clock components Period2, Cryptochrome1a, and Cryptochrome2a function in establishing light-dependent behavioral rhythms and/or total activity levels in zebrafish.

Hirayama, Jun / Alifu, Yikelamu / Hamabe, Rin / Yamaguchi, Sho / Tomita, Jun / Maruyama, Yusuke / Asaoka, Yoichi / Nakahama, Ken-Ichi / Tamaru, Teruya / Takamatsu, Ken / Takamatsu, Nobuhiko / Hattori, Atsuhiko / Nishina, Sachiko / Azuma, Noriyuki / Kawahara, Atsuo / Kume, Kazuhiko / Nishina, Hiroshi

Scientific reports

2019 Volume 9, Issue 1, Page(s) 196

Abstract: The circadian clock generates behavioral rhythms to maximize an organism's physiological efficiency. Light induces the formation of these rhythms by synchronizing cellular clocks. In zebrafish, the circadian clock components Period2 (zPER2) and ... ...

Abstract	The circadian clock generates behavioral rhythms to maximize an organism's physiological efficiency. Light induces the formation of these rhythms by synchronizing cellular clocks. In zebrafish, the circadian clock components Period2 (zPER2) and Cryptochrome1a (zCRY1a) are light-inducible, however their physiological functions are unclear. Here, we investigated the roles of zPER2 and zCRY1a in regulating locomotor activity and behavioral rhythms. zPer2/zCry1a double knockout (DKO) zebrafish displayed defects in total locomotor activity and in forming behavioral rhythms when briefly exposed to light for 3-h. Exposing DKO zebrafish to 12-h light improved behavioral rhythm formation, but not total activity. Our data suggest that the light-inducible circadian clock regulator zCRY2a supports rhythmicity in DKO animals exposed to 12-h light. Single cell imaging analysis revealed that zPER2, zCRY1a, and zCRY2a function in synchronizing cellular clocks. Furthermore, microarray analysis of DKO zebrafish showed aberrant expression of genes involved regulating cellular metabolism, including ATP production. Overall, our results suggest that zPER2, zCRY1a and zCRY2a help to synchronize cellular clocks in a light-dependent manner, thus contributing to behavioral rhythm formation in zebrafish. Further, zPER2 and zCRY1a regulate total physical activity, likely via regulating cellular energy metabolism. Therefore, these circadian clock components regulate the rhythmicity and amount of locomotor behavior.
MeSH term(s)	Animals ; CLOCK Proteins/physiology ; Circadian Clocks/physiology ; Cryptochromes/physiology ; Light ; Locomotion ; Period Circadian Proteins/physiology ; Single-Cell Analysis ; Zebrafish/metabolism ; Zebrafish Proteins/metabolism ; Zebrafish Proteins/physiology
Chemical Substances	Cryptochromes ; Period Circadian Proteins ; Zebrafish Proteins ; cry1a protein, zebrafish ; CLOCK Proteins (EC 2.3.1.48)
Language	English
Publishing date	2019-01-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-37879-8
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Article ; Online: CRY Drives Cyclic CK2-Mediated BMAL1 Phosphorylation to Control the Mammalian Circadian Clock.

Tamaru, Teruya / Hattori, Mitsuru / Honda, Kousuke / Nakahata, Yasukazu / Sassone-Corsi, Paolo / van der Horst, Gijsbertus T J / Ozawa, Takeaki / Takamatsu, Ken

PLoS biology

2015 Volume 13, Issue 11, Page(s) e1002293

Abstract: Intracellular circadian clocks, composed of clock genes that act in transcription-translation feedback loops, drive global rhythmic expression of the mammalian transcriptome and allow an organism to anticipate to the momentum of the day. Using a novel ... ...

Abstract	Intracellular circadian clocks, composed of clock genes that act in transcription-translation feedback loops, drive global rhythmic expression of the mammalian transcriptome and allow an organism to anticipate to the momentum of the day. Using a novel clock-perturbing peptide, we established a pivotal role for casein kinase (CK)-2-mediated circadian BMAL1-Ser90 phosphorylation (BMAL1-P) in regulating central and peripheral core clocks. Subsequent analysis of the underlying mechanism showed a novel role of CRY as a repressor for protein kinase. Co-immunoprecipitation experiments and real-time monitoring of protein-protein interactions revealed that CRY-mediated periodic binding of CK2β to BMAL1 inhibits BMAL1-Ser90 phosphorylation by CK2α. The FAD binding domain of CRY1, two C-terminal BMAL1 domains, and particularly BMAL1-Lys537 acetylation/deacetylation by CLOCK/SIRT1, were shown to be critical for CRY-mediated BMAL1-CK2β binding. Reciprocally, BMAL1-Ser90 phosphorylation is prerequisite for BMAL1-Lys537 acetylation. We propose a dual negative-feedback model in which a CRY-dependent CK2-driven posttranslational BMAL1-P-BMAL1 loop is an integral part of the core clock oscillator.
MeSH term(s)	ARNTL Transcription Factors/chemistry ; ARNTL Transcription Factors/genetics ; ARNTL Transcription Factors/metabolism ; Animals ; Casein Kinase II/chemistry ; Casein Kinase II/genetics ; Casein Kinase II/metabolism ; Cell Line ; Cells, Cultured ; Circadian Clocks ; Cryptochromes/chemistry ; Cryptochromes/genetics ; Cryptochromes/metabolism ; Embryo, Mammalian/cytology ; Humans ; Mice ; Mice, Knockout ; Mice, Transgenic ; Mutation ; Phosphorylation ; Protein Interaction Domains and Motifs ; Protein Processing, Post-Translational ; Recombinant Fusion Proteins/chemistry ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/chemistry ; Recombinant Proteins/metabolism
Chemical Substances	ARNTL Transcription Factors ; Bmal1 protein, mouse ; Cry1 protein, mouse ; Cry2 protein, mouse ; Cryptochromes ; Recombinant Fusion Proteins ; Recombinant Proteins ; CSNK2A1 protein, human (EC 2.7.11.1) ; Casein Kinase II (EC 2.7.11.1)
Language	English
Publishing date	2015-11-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2126776-5
ISSN	1545-7885 ; 1544-9173
ISSN (online)	1545-7885
ISSN	1544-9173
DOI	10.1371/journal.pbio.1002293
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Zs.A 6193: Show issues

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Article ; Online: Cell-based screen identifies a new potent and highly selective CK2 inhibitor for modulation of circadian rhythms and cancer cell growth.

Oshima, Tsuyoshi / Niwa, Yoshimi / Kuwata, Keiko / Srivastava, Ashutosh / Hyoda, Tomoko / Tsuchiya, Yoshiki / Kumagai, Megumi / Tsuyuguchi, Masato / Tamaru, Teruya / Sugiyama, Akiko / Ono, Natsuko / Zolboot, Norjin / Aikawa, Yoshiki / Oishi, Shunsuke / Nonami, Atsushi / Arai, Fumio / Hagihara, Shinya / Yamaguchi, Junichiro / Tama, Florence /

Kunisaki, Yuya / Yagita, Kazuhiro / Ikeda, Masaaki / Kinoshita, Takayoshi / Kay, Steve A / Itami, Kenichiro / Hirota, Tsuyoshi

Science advances

2019 Volume 5, Issue 1, Page(s) eaau9060

Abstract: Compounds targeting the circadian clock have been identified as potential treatments for clock-related diseases, including cancer. Our cell-based phenotypic screen revealed uncharacterized clock-modulating compounds. Through affinity-based target ... ...

Abstract	Compounds targeting the circadian clock have been identified as potential treatments for clock-related diseases, including cancer. Our cell-based phenotypic screen revealed uncharacterized clock-modulating compounds. Through affinity-based target deconvolution, we identified GO289, which strongly lengthened circadian period, as a potent and selective inhibitor of CK2. Phosphoproteomics identified multiple phosphorylation sites inhibited by GO289 on clock proteins, including PER2 S693. Furthermore, GO289 exhibited cell type-dependent inhibition of cancer cell growth that correlated with cellular clock function. The x-ray crystal structure of the CK2α-GO289 complex revealed critical interactions between GO289 and CK2-specific residues and no direct interaction of GO289 with the hinge region that is highly conserved among kinases. The discovery of GO289 provides a direct link between the circadian clock and cancer regulation and reveals unique design principles underlying kinase selectivity.
MeSH term(s)	Animals ; CLOCK Proteins/metabolism ; Carcinoma, Renal Cell/metabolism ; Carcinoma, Renal Cell/pathology ; Casein Kinase II/antagonists & inhibitors ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Circadian Clocks/drug effects ; Circadian Rhythm/drug effects ; Crystallography, X-Ray ; Drug Screening Assays, Antitumor/methods ; HEK293 Cells ; Humans ; Kidney Neoplasms/metabolism ; Kidney Neoplasms/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Phosphorylation/drug effects
Chemical Substances	CLOCK Proteins (EC 2.3.1.48) ; CSNK2A1 protein, human (EC 2.7.11.1) ; Casein Kinase II (EC 2.7.11.1)
Language	English
Publishing date	2019-01-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.aau9060
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Article ; Online: Synchronization of circadian Per2 rhythms and HSF1-BMAL1:CLOCK interaction in mouse fibroblasts after short-term heat shock pulse.

Teruya Tamaru / Mitsuru Hattori / Kousuke Honda / Ivor Benjamin / Takeaki Ozawa / Ken Takamatsu

PLoS ONE, Vol 6, Iss 9, p e

2011 Volume 24521

Abstract: Circadian rhythms are the general physiological processes of adaptation to daily environmental changes, such as the temperature cycle. A change in temperature is a resetting cue for mammalian circadian oscillators, which are possibly regulated by the ... ...

Abstract	Circadian rhythms are the general physiological processes of adaptation to daily environmental changes, such as the temperature cycle. A change in temperature is a resetting cue for mammalian circadian oscillators, which are possibly regulated by the heat shock (HS) pathway. The HS response (HSR) is a universal process that provides protection against stressful conditions, which promote protein-denaturation. Heat shock factor 1 (HSF1) is essential for HSR. In the study presented here, we investigated whether a short-term HS pulse can reset circadian rhythms. Circadian Per2 rhythm and HSF1-mediated gene expression were monitored by a real-time bioluminescence assay for mPer2 promoter-driven luciferase and HS element (HSE; HSF1-binding site)-driven luciferase activity, respectively. By an optimal duration HS pulse (43°C for approximately 30 minutes), circadian Per2 rhythm was observed in the whole mouse fibroblast culture, probably indicating the synchronization of the phases of each cell. This rhythm was preceded by an acute elevation in mPer2 and HSF1-mediated gene expression. Mutations in the two predicted HSE sites adjacent (one of them proximally) to the E-box in the mPer2 promoter dramatically abolished circadian mPer2 rhythm. Circadian Per2 gene/protein expression was not observed in HSF1-deficient cells. These findings demonstrate that HSF1 is essential to the synchronization of circadian rhythms by the HS pulse. Importantly, the interaction between HSF1 and BMAL1:CLOCK heterodimer, a central circadian transcription factor, was observed after the HS pulse. These findings reveal that even a short-term HS pulse can reset circadian rhythms and cause the HSF1-BMAL1:CLOCK interaction, suggesting the pivotal role of crosstalk between the mammalian circadian and HSR systems.
Keywords	Medicine ; R ; Science ; Q
Subject code	571
Language	English
Publishing date	2011-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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