ライフサイエンスコーパス: CLOCK protein

1 a in the C-terminal activation domain of the CLOCK protein.

2 by a transcriptional complex containing the CLOCK protein.

3 define important functional domains of this clock protein.

4 ipping and deletion of 51 amino acids in the CLOCK protein.

5 y to fulfill the biological function of this clock protein.

6 eightened state and if there is a functional CLOCK protein.

7 he presence of period 2 (PER2), another core clock protein.

8 he nuclear translocation and/or stability of clock proteins.

9 ses regulating the function and stability of clock proteins.

10 Y 1 and CRY 2, are known to function as core clock proteins.

11 odicity from posttranslational regulation of clock proteins.

12 ong-term perturbation in the cycles of these clock proteins.

13 d through post-translational modification of clock proteins.

14 cell-autonomous circadian clocks composed of clock proteins.

15 ed molecular feature in repressive circadian clock proteins.

16 h no credible homology between the different clock proteins.

17 mporal, intracellular behaviors of mammalian clock proteins.

18 pon rewarming allowing synthesis of specific clock proteins.

19 been identified that selectively target core clock proteins.

20 enges requires assessing levels of circadian clock proteins.

21 cterize antibodies against several circadian clock proteins.

22 n precise adjustment of expression levels of clock proteins.

23 ty and subcellular localization of essential clock proteins.

24 ver, nucleocytoplasmic translocation of core clock proteins, a key step in circadian timekeeping, is

25 coexpressed in each PER-positive neuron, and clock protein and mRNA oscillations are all suppressed i

26 simodo mutants elicit rhythmic expression of clock proteins and behavior in LL.

27 Formation of a stable complex between clock proteins and CK1 is a conserved feature in eukaryo

28 iotemporal organization and dynamics of core clock proteins and genes affect circadian rhythms in Dro

29 es have helped to expand the architecture of clock proteins and have revealed the abundance of the on

30 gen-dependent prolyl hydroxylases, circadian clock proteins and metabolic intermediates control the a

31 have also revealed novel interactions among clock proteins and new partners that couple the clock to

32 Here, we have purified all of the core clock proteins and performed in vitro and in vivo bioche

33 other hand, a similarity between eukaryotic clock proteins and the cyanobacterial KaiC protein is th

34 CYC, determined the interactions of the four clock proteins, and calculated their absolute levels as

35 al modifications (such as ubiquitination) of clock proteins are critical in maintaining the precision

36 Most clock proteins are degraded through the ubiquitin/26S pr

37 Circadian clock proteins are endogenous timing mechanisms that con

38 The genes encoding clock proteins are expressed throughout the brain, thoug

39 All major clock proteins are highly phosphorylated, and many kinas

40 Circadian clock proteins are modified in many different ways.

41 t because few simple models exist, and known clock proteins are not conserved across phylogenetic kin

42 At the molecular level, circadian clock proteins are transcriptional factors that regulate

43 system against specific pathogens, the core-clock proteins as well as cells in which they are expres

44 whereby PERIOD (PER) and CRYPTOCHROME (CRY) clock proteins associate and translocate to the nucleus

45 he second example of a PAS domain-containing clock protein (besides Drosophila PERIOD), which suggest

46 nd CRY2G351D; the former shows deficiency in clock protein binding and is required for repression by

47 fic uORF through which DENR acts to regulate CLOCK protein biosynthesis.

48 The clock protein BMAL1 (brain and muscle Arnt-like protein

49 Here we show that loss of the core clock protein BMAL1 in macrophages confers protection ag

50 Here, we report that deletion of the master clock protein BMAL1 in mice robustly increases expressio

51 The circadian clock protein BMAL1 modulates glial activation and amylo

52 The core clock protein BMAL1 serves as the primary positive circa

53 suggest a model in which repurposing of the clock protein BMAL1 to synapses locally gates the circad

54 The epithelial clock protein Bmal1 was required to regulate neutrophil

55 ins to interact with the canonical basic HLH clock proteins BMAL1 and CLOCK.

56 h the molecular clock, most notably the core clock proteins BMAL1, CLOCK, and REV-ERBalpha, control f

57 ional mechanisms, such as phosphorylation of clock proteins by casein kinase 1 (CK1) and glycogen syn

58 After dawn, the highly expressed circadian clock protein CCA1 brings circadian signals to the regul

59 expressing a mutant form of the Arabidopsis clock protein CCA1 that cannot be phosphorylated by CK2,

60 Arabidopsis circadian clock protein CIRCADIAN CLOCK ASSOCIATED1 (CCA1) binds t

61 log of the Caenorhabditis elegans biological clock protein CLK-2 (HCLK2), associated with and was hyd

62 The central clock protein CLOCK has HAT properties.

63 at this may be via interaction with the bHLH clock proteins CLOCK and BMAL1.

64 Mechanistically, the circadian clock proteins CLOCK, BMAL1, and cryptochromes (CRYs) in

65 ucleus, which is controlled by the circadian clock protein complex PERIOD.

66 cillator in which LdpA is a component of the clock protein complex that senses the redox state of a c

67 nobacteria that forms the core of the KaiABC clock protein complex.

68 Per1-3 in mammals, and the appearance of the clock protein complexes assembled from the proteins they

69 facilitate local translation and assembly of clock protein complexes.

70 meters based on experimental data concerning clock protein concentrations within a cell, we find accu

71 first time that skin cells express circadian clock proteins constitutively although regulation of the

72 clocks, post-translational modifications of clock proteins control the dynamics of circadian rhythms

73 domain of CBP/p300 (activating) and with the clock protein CRY1 (repressing) as well as by the BMAL1

74 mechanism, in which cycling of the essential clock proteins CRY1 and CRY2 is thought to be necessary.

75 ss protein interacts with both the circadian clock protein cryptochrome 2 and with the cell cycle che

76 n in mouse slows the degradation of the core clock protein Cryptochrome, lengthening the period of th

77 Finally, the results show that the core clock proteins cryptochrome (CRY) 1 and 2 repressed infl

78 of a repressive complex, defined by the core clock proteins cryptochrome 1 (CRY1):CLOCK:BMAL1, plays

79 The mammalian clock protein, cryptochrome 1 (CRY1), is degraded via th

80 e in vivo characterization of the Drosophila CLOCK protein (dCLOCK), a transcription factor that is r

81 otein are limited, the mechanisms regulating clock protein degradation are only beginning to be eluci

82 ess is known about phosphatases that control clock protein dephosphorylation.

83 eased in PE placenta, a finding supported by CLOCK protein downregulation in an independent cohort of

84 al role in regulating the expression of core clock proteins driving rhythms in activity and metabolis

85 hythm of KaiC abundance persists; therefore, clock protein expression has a preferred status under a

86 ice and hamsters at peak and trough times of clock protein expression in the suprachiasmatic nucleus

87 Peak PER clock protein expression is elevated in the mutant, indi

88 hat suggests a defect in the rising phase of clock protein expression.

89 the SCN shell and triggers downregulation of clock protein expression.

90 Our results further suggest that clock protein foci might regulate dynamic clustering and

91 l how macromolecular assemblies of dedicated clock proteins form and evolve to contribute to the gene

92 ing homology but do not show similarity with clock proteins found so far from either cyanobacteria or

93 ated degradation of the Neurospora circadian clock protein FREQUENCY (FRQ) is critical for clock func

94 In Neurospora, clock protein FREQUENCY (FRQ) is progressively phosphory

95 In Neurospora, the circadian clock protein FREQUENCY (FRQ) is progressively phosphory

96 Phosphorylation of the Neurospora circadian clock protein FREQUENCY (FRQ) regulates its degradation

97 Phosphorylation of the Neurospora circadian clock protein FREQUENCY by several kinases promotes its

98 graphic structure of the cyanobacterial KaiB clock protein from Synechocystis sp. PCC6803.

99 eptide microarray approach to the disordered clock protein FRQ in Neurospora crassa.

100 Levels of the clock protein FRQ were measured in Neurospora at various

101 necessary for rhythms in accumulation of the clock protein FRQ, indicating that clock control of eEF-

102 We propose that CK1 and the clock proteins FRQ and PERs form functionally equivalent

103 Her1 and Her7 clock proteins generate oscillatory expression of their

104 The cycling of the PER and CRY clock proteins has been thought to be necessary to keep

105 s post-translational processes that regulate clock protein homeostasis.

106 yzed sequence identities and similarities of clock protein homologues and immunostained brains of 10

107 bodies; (ii) wild-type virus stabilizes the CLOCK protein; (iii) overexpression of CLOCK partially c

108 KaiA is a two-domain circadian clock protein in cyanobacteria, acting as the positive e

109 us PCC 7942 (KaiC) is an essential circadian clock protein in cyanobacteria.

110 encode the N-terminus of the TIMELESS (TIM) clock protein in Drosophila simulans and D. yakuba.

111 Lack of Bmal1, a circadian clock protein in renal collecting ducts disrupted the cl

112 We show that the clock protein in the donor tubules cycled out of phase w

113 e in modulating the stabilities of circadian clock proteins in a manner specific to the time of day.

114 cellular location, and interacts with other clock proteins in a time-dependent manner.

115 d by the intrinsic properties of the central clock proteins in Arabidopsis, but rather by other genes

116 ractions between RUVBL2 orthologues and core clock proteins in humans, Drosophila and the fungus Neur

117 Analysis of clock proteins in mCRY-deficient mice shows that the mCR

118 ave examined posttranslational regulation of clock proteins in mouse liver in vivo.

119 LOCK that are useful for assessing circadian clock proteins in the SCN by immunocytochemistry.

120 -translational feedback loops driven by core clock proteins including BMAL1, CLOCK, PERs, and CRYs.

121 ation of transcription by the core circadian clock proteins including cryptochrome and by regulation

122 n rhythmicity is maintained by a set of core clock proteins including the transcriptional activators

123 post-translational modification of molecular clock proteins influence the temporal expression of SCN

124 Mechanistic studies showed that WT CLOCK protein interacted with the E-box enhancer element

125 mical standpoint and describe their roles in clock protein interactions and circadian timekeeping.

126 contribution of these disordered regions to clock protein interactions had not been elucidated.

127 This suggests that expression of the CLOCK protein is not necessary for normal interval timin

128 Progressive phosphorylation of circadian clock proteins is a hallmark of time-keeping.

129 Posttranslational regulation of clock proteins is an essential part of mammalian circadi

130 The posttranslational modification of clock proteins is critical for the function of circadian

131 delay between the synthesis and function of clock proteins is due to phosphorylation-regulated nucle

132 Versatility of clock proteins is seen in terms of their function in the

133 such that, although PER2(Edo) complexes with clock proteins, its vulnerability to degradation mediate

134 The other essential clock proteins KaiA and KaiB modulate the status of KaiC

135 are generated by the purified cyanobacterial clock proteins, KaiA, KaiB, and KaiC, through rhythmic i

136 ter kaiABC encodes three essential circadian clock proteins: KaiA, KaiB and KaiC.

137 e the BRET technique to demonstrate that the clock protein KaiB interacts to form homodimers.

138 asein, and apomyoglobin as well as circadian clock protein KaiB isolated from Escherichia coli.

139 esign feat by using functionalized circadian clock proteins, KaiB and KaiC, to engineer time-dependen

140 ch we ectopically express the cyanobacterial clock protein KaiC in cells from which the clock genes k

141 modeling and apply it to study the hexameric clock protein KaiC in Cyanobacteria.

142 llations in the phosphorylation state of the clock protein KaiC.

143 nct functions for two domains of the central clock protein KaiC: the C-terminal autokinase domain int

144 Significantly higher BMAL1 and CLOCK protein levels and lower REV-ERBalpha were present

145 anisms that control the cycling of circadian clock protein levels are not known.

146 res precisely calibrated degradation of core clock proteins, like PERIOD.

147 The daily rhythms of circadian clock proteins may coordinate gene expression programs i

148 The rhythmic expression of RORgamma1 by clock proteins may lead to the rhythmic expression of RO

149 s that specifically modulate regulatory core clock proteins may potentially enable better management

150 s effect, posttranslational modifications of clock proteins modulate circadian rhythms and are though

151 xamine the effect of the circadian clock and clock proteins, namely PERIODs and BMAL1, on exercise ca

152 nsists of a feedback loop in which canonical clock proteins negatively regulate transcription of thei

153 The clock proteins of Drosophila and mammals exhibit strikin

154 and epsilon (CK1epsilon) phosphorylate core clock proteins of the mammalian circadian oscillator.

155 s that directly modulate the activity of key clock proteins offer the potential to directly modulate

156 25a is required for temperature-synchronized clock protein oscillations in subsets of central clock n

157 ndependent superimposed oscillations and the clock protein oscillations in the dorsal neuron 1 and 2

158 xpression in LNvs severely dampened Timeless clock protein oscillations, we conclude that the master

159 xpressing immunoreactivity for the circadian clock protein PER is located in the same region as PTTH-

160 ic cells coexpress ghrelin and the circadian clock proteins PER1 and PER2.

161 in a diurnal manner and are dependent on the clock proteins PER1/2.

162 tion due to its reduced affinity to the core clock protein PER2 and defective translocation into the

163 es that implicate heme interactions with the clock proteins PER2 and nPAS2 in biological function.

164 neuropeptide arginine vasopressin (AVP) and clock proteins (PER2 and BMAL1), supporting that paterna

165 ed by marked reductions in the levels of the clock protein Period (PER) as well as more modest effect

166 ity, and altered expression of the circadian clock protein period (Per) in a subset of pacemaker neur

167 ation of excitatory receptors influences the clock protein PERIOD 2 (PER2) in a contractile organ, th

168 Oscillations of the clock protein PERIOD are intact in na mutants, indicatin

169 Oscillations of the clock protein PERIOD are normal in pacemaker neurons lac

170 ile cell number and oscillations of the core clock protein PERIOD are unaffected in the small LNv (sL

171 d by phase-advanced oscillations of the core clock protein PERIOD.

172 system stems from robust degradation of the clock protein PERIOD.

173 odulate the stability of closely linked core clock proteins period (PER) and cryptochrome (CRY), resp

174 localized within clock neurons and that the clock proteins Period (Per) and Timeless (Tim) accumulat

175 Antisera against the circadian clock proteins Period (PER) and Timeless (TIM) were used

176 n techniques, we demonstrate that Drosophila clock proteins (PERIOD and CLOCK) are organized into a f

177 e, these flies express low levels of the two clock proteins, PERIOD (PER) and TIMELESS (TIM), due to

178 gh-fat diet increased phosphorylation of the clock protein PERIOD2 (PER2) on serine 662 (S662), which

179 Bioluminescent recording of circadian clock protein (PERIOD2) output from ex vivo SCN revealed

180 We demonstrate that cryptochrome regulates clock protein phosphorylation by modulating the effect o

181 Within the core molecular clock, protein phosphorylation and degradation play a vi

182 These results demonstrate that clock proteins play a hitherto unexpected role in the su

183 g that the PER NES and the nuclear export of clock proteins play an important role in temperature com

184 Phosphorylation of clock proteins plays a critical role in generating prope

185 y between central brain and peripheral liver clock proteins postulated to be instrumental for linking

186 mong nuclear receptors but common among core clock proteins, protecting the organism from major pertu

187 lings, whereas the levels of closely related clock proteins, PRR3 and PRR7, are unchanged.

188 rosophila, ~150 neurons expressing molecular clock proteins regulate circadian behavior.

189 These core clock proteins regulate thousands of tissue-specific gen

190 ing that the lag in the accumulation of some clock proteins relative to their mRNAs does not arise fr

191 Phosphorylation of circadian clock proteins represents a major regulatory step that c

192 Phosphorylation of clock proteins represents an important mechanism regulat

193 Mutation of the core clock protein REVERBalpha in these cells exacerbated the

194 regulatory loops in which specific proteins (clock proteins) rhythmically repress expression of their

195 tion of qsm in the clock circuit restores LL clock protein rhythms in qsm-negative neurons, indicatin

196 Finally, Nobiletin, an agonist of the core-clock proteins RORalpha/gamma, boosted both circadian am

197 Overall, our findings suggest that clock proteins shape exercise capacity in a daytime-depe

198 biquitin-specific proteases can regulate the clock protein stability and circadian pathways remains l

199 from gene expression, the precise control of clock protein stability plays a pivotal role in establis

200 A series of clock protein structures demonstrate that the PAS (Per/A

201 le for the membrane clock, but not in Ca(2+) clock proteins, suggesting that the membrane clock under

202 In Drosophila melanogaster four circadian clock proteins termed PERIOD (PER), TIMELESS (TIM), dCLO

203 yanobacteria, KaiC is an essential hexameric clock protein that forms the core of a circadian protein

204 Cryptochrome (CRY) is a core clock protein that plays an essential role in the repres

205 tify the first phosphorylation sites on core clock proteins that are acutely regulated by photic cues

206 homo and heterodimerization of several core clock proteins that assemble into transcription factors

207 chemical and structural understanding of the clock proteins that constitute the molecular "cogs" of t

208 CYC is by far the most abundant of the four clock proteins that have been examined, PER and TIM appe

209 to be generated by a feedback loop involving clock proteins that inhibit transcription of their own g

210 onally active heterodimer with the circadian CLOCK protein, the structurally related MOP4, and hypoxi

211 contribution to timekeeping than any of the clock proteins they phosphorylate.

212 In addition, the recently identified clock protein TIM (for timeless) interacted with PER in

213 Like CRY, this pathway targets the clock protein TIM.

214 RY promotes the degradation of the circadian clock protein TIMELESS (TIM) and then is itself degraded

215 reviously been reported to interact with the clock protein TIMELESS (TIM) in a light-dependent manner

216 l role in light-dependent degradation of the clock protein Timeless (TIM), a key step in the entrainm

217 YPTOCHROME, which induces degradation of the clock protein TIMELESS (TIM), but temperature cycles are

218 ecause of light-dependent degradation of the clock protein Timeless (Tim), constant illumination (LL)

219 s mediated by proteasomal degradation of the clock protein TIMELESS (TIM).

220 nvolves the light-induced degradation of the clock protein timeless (TIM).

221 s interactions with targets that include the clock protein Timeless (TIM).

222 zing action of the light-sensitive circadian clock protein TIMELESS (TIM).

223 clock via light-dependent degradation of the clock protein TIMELESS (TIM).

224 osophila, light-dependent degradation of the clock protein TIMELESS by the blue light photoreceptor C

225 elegans TIM-1, a paralogue of the Drosophila clock protein TIMELESS, in the regulation of chromosome

226 ing of nuclear accumulation of the circadian clock protein TIMELESS.

227 , as well as altered cycling kinetics of the clock proteins timeless (TIM) and period (PER).

228 y promoting light-induced degradation of the clock proteins Timeless and Period, as well as its own p

229 roteasome-dependent degradation of a central clock protein, TIMING OF CAB EXPRESSION 1 (TOC1).

230 Here we find a novel role for the CLOCK protein to antagonize CREB-mediated transcriptiona

231 lts define a biochemical action for the core clock protein TOC1 and refine our perspective on how pla

232 PIL1, previously shown to interact with the clock protein TOC1.

233 ) that plays an important role in regulating clock protein turnover.

234 lusive whether the deregulation of circadian clock proteins underlies stem cell aging and whether the

235 ities are rescued by expressing a functional CLOCK protein via viral-mediated gene transfer specifica

236 Here, the Drosophila CLOCK protein was shown to induce transcription of the c

237 Clock gene mRNAs and clock proteins were found differentially expressed in th

238 thologous hypoxia, heat-shock, and circadian clock proteins were found to cluster according to habita

239 REV-ERBalpha is a core circadian clock protein which also serves as a nuclear receptor an

240 The clock manifests oscillations of key clock proteins, which are under dynamic control at multi

241 output and decreased expression of the core clock proteins, which regulate many aspects of cellular

242 ity primarily through interaction with other clock proteins, while mPER2 positively regulates rhythmi

243 nd precision of rhythms in PERIOD2 (PER2), a clock protein, within the SCN isolated from embryonic an