ライフサイエンスコーパス: PER

1 PER alone has no effect on CLOCK-BMAL1-activated transcr

2 PER and CRY proteins form heterodimers and suppress the

3 PER and TIM negatively feed back on CLK/CYC transcriptio

4 PER and TIM shift from the cytoplasm to the nucleus dail

5 PER for measuring rates of VF decay is a robust indicato

6 PER fragment alignment increased the coverage 3-fold com

7 PER fragment alignment with long-range splicing confirme

8 PER inhibits the activity of E75 on the Clk promoter, th

9 PER represses by displacing CLOCK-BMAL1 from promoters i

10 PER synthesis happens in a programmable, autonomous, in

11 d sequestered in a strong, approximately 1:1 PER-CLK off-DNA complex.

12 -2 (PET(178)P), but not rat beta-arrestin-1 (PER(177)P).

13 vates the aryl hydrocarbon receptor (AHR), a PER, ARNT, SIM (PAS) family transcription factor that re

14 genome of all PER transcript fragments in a PER dataset.

15 nd potentiated its circadian activation in a PER protein-dependent fashion.

16 ssary, NPF neurons were not able to induce a PER.

17 ic signaling was also sufficient to induce a PER.

18 ts are lost in per (0) mutants, supporting a PER-dependent inhibition of tim mRNA deadenylation by PO

19 se data indicate that TYF potently activates PER translation in pacemaker neurons to sustain robust r

20 s not modulate the clock by simply affecting PER degradation kinetics.

21 tic perturbation of the NRON complex affects PER and CRY protein nuclear translocation, dampens ampli

22 o predict the alignment to the genome of all PER transcript fragments in a PER dataset.

23 The timing of CLK-CYC activation and PER-TIM repression is regulated post-translationally, in

24 The timing of CLK-CYC activation and PER-TIM repression is regulated posttranslationally, in

25 ith vasoactive intestinal peptide, cAMP, and PER at the heart of the SCN pacemaker.

26 nts, we show that the stabilities of CRY and PER are independently regulated, contrary to the expecta

27 this model, the mechanistic roles of CRY and PER are unclear.

28 Both CRY and PER bind to CLOCK and BMAL1 off DNA but, in contrast to

29 In this model, CRY and PER proteins repress their own transcription by suppress

30 pes to characterize the functions of CRY and PER.

31 the turnover rate of the repressors CRY and PER.

32 clock cells, whereas CLK levels decrease and PER and TIM accumulation are delayed when nmo is overexp

33 se is proportional to PER levels on DNA, and PER recruitment probably occurs via CLK.

34 rring through the Helix-Loop-Helix (HLH) and PER-ARNT-SIM (PAS) domains, is needed to convert the AhR

35 CRY proteins determine pacemaker period, and PER/CRY complexes have been proposed to afford mutual st

36 Therefore, interaction between the POR and PER is necessary for context-guided exploratory behavior

37 In addition, TIM and PER are localized in the cytoplasm at all times of day,

38 while allowing robust expression of TIM and PER.

39 y timed nuclear accumulation of both TIM and PER.

40 esults suggest that, in addition to CRYs and PERs, the GM129 protein contributes to the transcription

41 is susceptible to disruption by both FAD and PERs, suggesting a new avenue for pharmacological target

42 edure showed that PER-independent as well as PER-dependent mechanisms could sustain circadian express

43 belong to the basic helix-loop-helix (bHLH)-PER-ARNT-SIM (PAS) family of transcription factors.

44 member of the basic helix-loop-helix (bHLH)/PER-ARNT-SIM (PAS) transcription superfamily, is known t

45 The method was applied to 2 x 35 bp PER datasets from cancer cell lines MCF-7 and SUM-102.

46 In pacemaker cells of the brain, PER and TIM proteins rise to abnormally high levels in t

47 muscle arnt-like 1 and repressors encoded by PER (Period) and Cryptochrome genes.

48 t TIM attenuates transcriptional feedback by PER in cultured cells, suggesting that it holds PER in t

49 s may either be repressed or de-repressed by PER, depending on the particular promoter regulatory ele

50 es by BMAL1-CLOCK complexes is suppressed by PER-CRY complexes.

51 In CK1delta/epsilon-deficient cells, PER phosphorylation is severely compromised and nonrhyth

52 the functional relationship between the CKI-PER and FBXL3-CRY pathways, we generated robust mechanis

53 of the circadian oscillator by altering CLK, PER, and TIM expression, thereby contributing to the gen

54 art through rhythmic phosphorylation of CLK, PER, and TIM [2-4].

55 art through rhythmic phosphorylation of CLK, PER, and TIM.

56 he negative elements of the circadian clock (PER-TIM) regulate the positive elements (CLK-CYC).

57 ns accumulate, form a large nuclear complex (PER complex), and bind the transcription factor CLOCK-BM

58 ns accumulate, form a large nuclear complex (PER complex), and repress their own transcription.

59 uRD) are part of the nuclear PERIOD complex (PER complex).

60 xic lesions to the POR and the contralateral PER.

61 We found that rats with contralateral PER-POR lesions were impaired in object-context recognit

62 Although kinases that control PER and TIM levels and subcellular localization have bee

63 Although kinases that control PER, TIM, and CLK levels, activity, and/or subcellular l

64 Perirhinal cortex (PER) has a well established role in the familiarity-base

65 Perirhinal cortex (PER) has a well established role in the familiarity-base

66 The perirhinal cortex (PER) is known to process object information, whereas the

67 mparable with that of the perirhinal cortex (PER) with regard to the lateral entorhinal cortex (LEC).

68 The perirhinal cortex (PER), which is critical for associative memory and stimu

69 K and BMAL1 off DNA but, in contrast to CRY, PER does not bind to the CLOCK:BMAL1:E-box complex.

70 OCK-BMAL1 transcriptional activators and CRY-PER transcriptional repressors.

71 by a "blocking"-type mechanism and that CRY-PER inhibits CLOCK-BMAL1 by a "displacement"-type mechan

72 Here, we show that CRY-PER participates in the displacement-type repression by

73 th in vitro and in vivo experiments, the CRY-PER-mediated repression in vivo seemed in conflict with

74 In the cytoplasm, PERs, CRYs, and CK1delta were distributed into several c

75 ngle-particle EM of two purified cytoplasmic PER complexes revealed approximately 20-nm and approxima

76 onflict with the in vitro data demonstrating PER removes CRY from the CLOCK-BMAL1-E-box complex.

77 1Asil) (CK1epsilon(Tau)), which destabilizes PER, thereby accelerating the clock.

78 t (DBT(S)), all mutants produce differential PER degradation profiles that show direct correspondence

79 teracts mainly with PER proteins and directs PER/CRY nuclear transport in a circadian fashion.

80 However, when PP1 is disrupted, PER phosphorylation is dramatically accelerated; the sam

81 The HK2-ASO1/DPI/PER triple-combination achieved synthetic lethality in m

82 Dimerization of Drosophila PER influences nuclear translocation, repressor activity

83 ms were eliminated and rhythms in endogenous PER abundance and phosphorylation were severely compromi

84 ny by increasing cAMP and PKA, which enhance PER stability and decrease clock speed in intrinsically

85 gthen circadian period by directly enhancing PER stability.

86 ption and the known role of PDF in enhancing PER/TIM stability occur via independent pathways downstr

87 and epsilon (CK1delta/epsilon) are essential PER kinases, but it is clear that additional, unknown me

88 on PER-dependent behavioral tasks and fewer PER principal neurons are activated by stimuli, but the

89 First, PER is recruited to circadian promoters, which leads to

90 an active translation complex important for PER expression and circadian rhythms.

91 ATX2 was necessary for PER accumulation in circadian pacemaker neurons and thus

92 le of DEWs which are very poor substrate for PER.

93 Projections from PER to LEC exert a main inhibitory influence, which may

94 (2), and with the de novo recalculation from PER predictions were 2.95 dB and 17.49 dB(2), respective

95 tor consisting of two basic helix-loop-helix PER-ARNT-SIM (bHLH-PAS) domain protein subunits, CLOCK a

96 leep-wake cycle via 2 basic helix-loop-helix PER-ARNT-SIM (bHLH-PAS) domain proteins-CLOCK and BMAL1.

97 r and a member of the basic helix-loop-helix PER/ARNT/SIM family of chemosensors and developmental re

98 S3 are members of the basic helix-loop-helix-PER-ARNT-SIM (bHLH-PAS) family, and their genetic defici

99 in cultured cells, suggesting that it holds PER in the cytoplasm.

100 to afford mutual stabilization, although how PER and CRY proteins with contrasting stabilities intera

101 man A1PI (Hu-recA1PI) expressed in the human PER.C6 cell line using an array of analytical and bioche

102 Elevated levels of ASAT and ALAT in PER groups compared with CTRL group were found.

103 d genetic studies have shown that changes in PER phosphorylation kinetics are associated with changes

104 adian kinase regulating the daily changes in PER stability and phosphorylation.

105 ylation that controls the daily downswing in PER abundance.

106 d levels and a decrease of GSH/GSSG ratio in PER group compared with the CTRL group.

107 BMD values and a decrease of BV/TV value in PER groups.

108 to the timing mechanism by slowly increasing PER susceptibility to degradation.

109 creased the abundance of basal and inducible PER proteins, which facilitated circadian clock resettin

110 horylation at these sites does not influence PER stability, timing of nuclear entry, or transcription

111 onditioning), during shock (remote ischemic "PER"conditioning), or during resuscitation (remote ische

112 e ischemic preconditioning, remote ischemic "PER"conditioning, and remote ischemic "POST"conditioning

113 served carboxy-terminal tail and burying its PER-binding interface.

114 that both proline-rich (PR) and PERIOD-like (PER) domains, in addition to the critical role of C2 dom

115 r members of these phyla, and a new lineage, PER, via cultivation-independent recovery of 49 partial

116 signal (NLS) on the Drosophila melanogaster PER protein.

117 SO1) to validate the safety of mHK2-ASO1/MET/PER combination therapy in mice bearing murine multiple

118 We found that mouse PER complexes include the Mi-2/nucleosome remodelling an

119 We found that mouse PER complexes included RNA helicases DDX5 and DHX9, acti

120 Nonetheless, PER induction in pacemaker neurons can rescue tyf mutant

121 ly burden analysis approach identified novel PERs in protein sequences.

122 We propose that proper level of nuclear PER-TIM accumulation is necessary to facilitate kinase r

123 le electron microscopy (EM) revealed nuclear PER complexes purified from mouse liver to be quasi-sphe

124 e protein kinase encoding gene KERNEL NUMBER PER ROW6 (KNR6) determines pistillate floret number and

125 ehavioral rhythms and decreased abundance of PER.

126 TIM(S1404) promotes nuclear accumulation of PER-TIM heterodimers by inhibiting the interaction of TI

127 independent, additive biochemical actions of PER and CRY in circadian control, and complement genome-

128 at this protein functions as an activator of PER translation in circadian neurons.

129 cted with TWENTY-FOUR (TYF), an activator of PER translation.

130 of TWENTY-FOUR (TYF), a crucial activator of PER translation.

131 n mammals, given the conserved activities of PER, DBT, and CLK orthologs.

132 can regulate temporal abundance/activity of PER by phosphorylation-mediated degradation and cellular

133 Immunocytochemical analysis of PER shows that these dynamics in DD and LP are recapitul

134 at alphaF unlatches to switch association of PER with itself to its partner Timeless.

135 Conservation of PER interaction residues among a family of PAS-AB-contai

136 We analyzed protein constituents of PER complexes purified from mouse tissues and identified

137 a previously proposed de-repressor effect of PER on Clk transcription.

138 er, in the presence of CRY, nuclear entry of PER inhibits transcription by displacing CLOCK-BMAL1 fro

139 n the cytoplasm by blocking nuclear entry of PER proteins in human cells.

140 al role of TIM in the timed nuclear entry of PER.

141 phosphorylation-dependent nuclear export of PER-TIM heterodimers to the maintenance of circadian per

142 he absence of CRY very limited expression of PER in a few dorsal clock neurons is able to mediate beh

143 n light:dark can be rescued by expression of PER in either LNv or DN1p clock cells and does not requi

144 K in these mutants rescues the expression of PER in the central clock, but fails to restore behaviora

145 We also show that a stable form of PER is cytoplasmic in tim-null flies.

146 extracts, we elucidate the dual functions of PER as repressor and de-repressor in a context-dependent

147 NB1 is required for timely nuclear import of PER/CRY in the negative feedback regulation of the circa

148 BMAL1:E-box ternary complex independently of PER.

149 The kinetics of PER degradation with DBT(S) in cell culture resembles th

150 also crucial for regulating the kinetics of PER phosphorylation.

151 is required for the nuclear localization of PER and point to a key role for the TIM NLS in the regul

152 result from the cytoplasmic localization of PER.

153 iven the importance of TIM as a modulator of PER function in the pacemaker.

154 circadian rhythms by controlling the pace of PER synthesis and presents a novel layer of regulation f

155 Drosophila and a crucial binding partner of PER.

156 The pattern of PER-, BMAL-, and aryl hydrocarbon receptor-induced P450

157 Early morning phosphorylation of PER by the kinase Doubletime (DBT) and subsequent PER tu

158 fact, much of the reduced phosphorylation of PER in the new tim mutant appears to result from the cyt

159 damentally from the inhibitory projection of PER to LEC.

160 e explained solely by changes in the rate of PER degradation.

161 ces in running speed, as the firing rates of PER interneurons did not show significant velocity modul

162 Recruitment of PER complexes to the elongating polymerase at Per and Cr

163 monstrates that the speed and rhythmicity of PER phosphorylation are controlled by the balance betwee

164 Our findings bring clarity to the role of PER in the dynamic nature of the repressive phase of the

165 ns are activated by stimuli, but the role of PER interneurons in these altered circuit properties in

166 Here, we identified phosphorylation sites of PER-bound TIM by mass spectrometry, given the importance

167 The individual stabilities of PER or CRY proteins determine pacemaker period, and PER/

168 We conclude that optical stimulation of PER at different frequencies can alter visual recognitio

169 findings suggest that optical stimulation of PER at specific frequencies can predictably alter recogn

170 NFAT pathway alter nuclear translocation of PER and CRY proteins and impact circadian rhythms in per

171 With advanced age, rats show deficits on PER-dependent behavioral tasks and fewer PER principal n

172 NEMO/NLK kinase at the "per-short" domain on PER stimulates phosphorylation by DOUBLETIME (DBT/CK1del

173 c cues and suggest that some phosphosites on PER proteins can modulate the pace of downstream behavio

174 ylation by DBT at other more distal sites on PER, including those required for recognition by the F b

175 Many bacteria affiliate with OD1, OP3, OP9, PER, ACD58, WWE3, BD1-5, OP11, TM7 and ZB2.

176 Loss of either NONO or PER abolished this activation and circadian expression o

177 pt fragment using end reads from overlapping PERs, guided by the expected length of the fragment.

178 HIF is a basic helix-loop-helix (bHLH)-PAS (PER-ARNT-SIM) heterodimer composed of an oxygen-labile H

179 drocarbon receptor (AHR) belongs to the PAS (PER-ARNT-SIM) family transcription factors and mediates

180 They contain two PAS (PER-ARNT-SIM) domains (PAS-A and PAS-B), which mediate h

181 acid oxidation (FAO) inhibitor perhexiline (PER).

182 PERIOD (PER) is a critical state-variable in this mechanism, and

183 Period (PER) is the major transcription inhibitor in metazoan ci

184 Period (PER) protein phosphorylation is a critical regulator of

185 se shift in association with altered PERIOD (PER) protein dynamics.

186 how diminished expression of CLK and PERIOD (PER) in the central clock cells.

187 ctivator, and Cryptochrome (CRY) and Period (PER) proteins function as repressors.

188 nd repressors Cryptochrome (CRY) and Period (PER).

189 al repressors cryptochrome (CRY) and period (PER).

190 uent with24 h) clocks in animals are PERIOD (PER) proteins, transcriptional regulators that undergo d

191 LK) and CYCLE (CYC) and repressed by PERIOD (PER) and TIMELESS (TIM) [1].

192 otein NONO as a partner of circadian PERIOD (PER) proteins.

193 of the rate-limiting clock component PERIOD (PER) in Drosophila.

194 ted to the core circadian clock gene PERIOD (PER), results in arrhythmic molts and continuously abnor

195 ME (CRY) dampens temperature-induced PERIOD (PER)-LUCIFERASE oscillations in dorsal clock neurons.

196 n M cells decreases the amplitude of PERIOD (PER) cycling in DN1 neurons, suggesting that SIK3 non-ce

197 is activation delays the decrease of PERIOD (PER) in the middle of the day and propagates to downstre

198 ster, the idea that nuclear entry of PERIOD (PER) is controlled by its partner protein TIMELESS (TIM)

199 drive daily cycles in the levels of PERIOD (PER) proteins.

200 necessary for the phosphorylation of PERIOD (PER), a transcriptional repressor, and CLOCK (CLK), a tr

201 nal/night-biting mosquitoes based on PERIOD (PER) and pigment-dispersing factor (PDF) expression show

202 s in the levels of the clock protein Period (PER) as well as more modest effects on Timeless (TIM).

203 f closely linked core clock proteins period (PER) and cryptochrome (CRY), respectively.

204 rcadian oscillations of the proteins PERIOD (PER) and TIMELESS (TIM) are hallmarks of a functional cl

205 n Drosophila, key pacemaker proteins PERIOD (PER) and TIMELESS (TIM) are progressively phosphorylated

206 sms by which the circadian repressor PERIOD (PER) inhibits CLOCK/CYCLE (CLK/CYC)-mediated transcripti

207 ter by the transcriptional repressor PERIOD (PER), indicating that the majority of CLK targets are re

208 Mounting evidence suggests that PERIOD (PER) proteins play a central role in setting the speed (

209 imers activate the expression of the period (PER) and cryptochrome (CRY) genes acting as transcriptio

210 In mammals, the PERIOD (PER) and CRYPTOCHROME (CRY) proteins accumulate, form a

211 iptional feedback loop, in which the PERIOD (PER) and TIMELESS (TIM) proteins repress the expression

212 Regulated nuclear entry of the Period (PER) and Timeless (TIM) proteins, two components of the

213 y a feedback loop in which the three PERIOD (PER) proteins, acting in a large complex, inhibit the tr

214 by a negative feedback loop in which PERIOD (PER) proteins accumulate, form a large nuclear complex (

215 epressors (CRYPTOCHROMEs (CRYs) and PERIODs (PERs)).

216 negative elements (FREQUENCY [FRQ], PERIODS [PERs], and CRYPTOCHROMES [CRYs]) are understood to inhib

217 Highly phosphorylated PER has a more open structure, suggesting that progressi

218 with that of rats with ipsilateral POR plus PER lesions and sham-operated rats.

219 tructural and functional capacity to be a PM-PER tether.

220 Additionally, expression of artificial PM-PER tethers is sufficient to restore retention in inp1De

221 e first known plasma membrane-peroxisome (PM-PER) tether by demonstrating that Inp1 meets the predefi

222 e first molecular characterization of the PM-PER tether and show it anchors peroxisomes at the mother

223 raction with its direct target gene products PER and CRY, suggesting that the ratio between the negat

224 onships, a light pulse causes more prominent PER degradation in pdf(01) circadian neurons than in wil

225 The period protein (PER) is a well-studied repressor of clock gene transcrip

226 ilon/delta phosphorylate the period protein (PER) to produce circadian rhythms.

227 ian CRYs associate with the Period proteins (PERs) and together inhibit the transcription of their ow

228 and uncertainty in particle emission rates (PERs, #/min) measured by chamber systems still remain, o

229 ng was observed in both young and aged rats, PER interneurons recorded from old animals had lower fir

230 uce the concept of primer exchange reaction (PER) cascades, which grow nascent single-stranded DNA wi

231 emers generated by primer exchange reaction (PER).

232 The RNA-seq paired-end read (PER) protocol samples transcript fragments longer than t

233 It also dramatically reduced PER protein levels in pigment dispersing factor (PDF) ne

234 ng behavior, the proboscis extension reflex (PER), elicited when external food cues are interpreted a

235 g sites in the hTERT proximal exonic region (PER) and determine their functional relevance in mediati

236 All pathogenic variant enriched regions (PERs) identified are available online through "PER viewe

237 A pointwise exponential regression (PER) model was used to calculate average rates of faster

238 key role for the NRON complex in regulating PER/CRY subcellular localization and circadian timekeepi

239 damage suggests that photoenzymatic repair (PER) is an important DNA repair mechanism used by marine

240 Taken together with a previously reported PER structure in which alphaF extends, these data indica

241 The structure of a central, 346-residue PER fragment reveals two associated PAS (Per-Arnt-Sim) d

242 Two models to resolve PER from the chamber and a model for flow tunnel measure

243 ere, a dynamic analysis of the size-resolved PER is conducted through a comparative study of chamber

244 We observe robust PER degradation in a DBT allele-specific manner.

245 ors (CCCs) interact directly with the second PER-ARNT-SIM (PAS) domain of ARNT (ARNT PAS-B).

246 Specifically, PER/CRY complexes act at E-box sequences in Per and Cry

247 Mutant TIM can bind to and stabilize PER.

248 d protein kinase A (PKA) activity stabilizes PER, in S2 tissue culture cells and in fly circadian neu

249 time-lapse fluorescence microscopy we study PER stability in the presence of DBT and its short, long

250 In the present study, PER neurons were recorded while rats traversed a circula

251 y the kinase Doubletime (DBT) and subsequent PER turnover is an essential step in the functioning of

252 , additional kinases are predicted to target PER, TIM, and/or CLK to promote time-specific transcript

253 Finally, an SCN graft procedure showed that PER-independent as well as PER-dependent mechanisms coul

254 e nucleus daily, and the length of time that PER and TIM reside in the cytoplasm is an important dete

255 ate molting cycles in much the same way that PER-based oscillators drive rhythmic behaviors and metab

256 The PER complex thus acquires full repressor activity only u

257 everely compromised and nonrhythmic, and the PER proteins are constitutively cytoplasmic.

258 in a loss of the repression mediated by the PER.

259 BMAL1 complex, and a negative component, the PER-CRY complex.

260 n errors for both the MD and VFI favored the PER forecasts (P < 0.001).

261 At the onset of negative feedback, the PER complex delivers the remaining complementary NuRD su

262 These findings provide a function for the PER complex and a molecular mechanism for circadian cloc

263 s on object and pattern information from the PER to encode representations of context.

264 lies on object information received from the PER to form complex representations of context.

265 nd VFI, and (2) calculation de novo from the PER-predicted final thresholds.

266 R to MEC are functionally different from the PER-to-LEC counterpart in providing an excitatory drive

267 molecular event recorder that records in the PER transcript the order in which distinct RNA inputs ar

268 -induced mutation, early doors (Edo), in the PER-ARNT-SIM (PAS) domain dimerization region of period

269 HeLa cells is regulated by sequences in the PER.

270 ations contribute to the oscillations of the PER and TIM proteins but few posttranscriptional mechani

271 his study, we showed that stimulation of the PER could increase or decrease exploration of novel and

272 r cells demonstrate that a sub-region of the PER exhibits strong transcriptional repressive activity.

273 rotein (PYP), a 125-residue prototype of the PER-ARNT-SIM (PAS) domain superfamily of signaling prote

274 rily regulates the accumulating phase of the PER-CRY repressive complex by controlling the nuclear im

275 translocation and repressor function of the PER/CRY complex.

276 Regulated nuclear translocation of the PER/CRY repressor complex is critical for negative feedb

277 Interestingly, KPNB1 regulates the PER/CRY nuclear entry and repressor function, independen

278 criptional inhibitory complexes and that the PER complex thereby rhythmically delivers histone deacet

279 The data indicate that the PER levels bound to CLK change dynamically and are impor

280 ing as transcription factors directed to the PER and CRY promoters via E-box elements.

281 RNAi depletion of KPNB1 traps the PER/CRY complex in the cytoplasm by blocking nuclear ent

282 Deep sampling of the transcriptome using the PER protocol presents the opportunity to reconstruct the

283 Our analysis indicates that PSF within the PER complex recruits SIN3A, a scaffold for assembly of t

284 e found that in mouse liver nuclei all three PERs, both CRYs, and Casein Kinase-1delta (CK1delta) are

285 periodicity is determined primarily through PER phosphorylation kinetics set by the balance between

286 Rs) identified are available online through "PER viewer," a user-friendly online platform for interac

287 complexes and repressed by PERIOD-TIMELESS (PER-TIM) complexes keeps circadian time.

288 LE (CLK-CYC) activators and PERIOD-TIMELESS (PER-TIM) repressors are feedback loop components whose t

289 LE (CLK-CYC) activators and PERIOD-TIMELESS (PER-TIM) repressors to drive rhythmic transcription peak

290 This decrease is proportional to PER levels on DNA, and PER recruitment probably occurs v

291 clear accumulation of both TIM and wild-type PER proteins.

292 ments for different materials underestimated PER by up to an order of magnitude and overestimated par

293 Unexpectedly, PER actually interferes with the binding of CRY to the C

294 te cortical and/or subcortical pathways when PER-POR interaction is not available.

295 Whereas PER phosphorylation has been extensively studied, system

296 n clock is built on a feedback loop in which PER and CRY proteins repress their own transcription.

297 it that CRY is the dominant repressor, while PER may play an accessory role.

298 ow unite REV-ERB-alpha and REV-ERB-beta with PER, CRY and other components of the principal feedback

299 KPNB1 interacts mainly with PER proteins and directs PER/CRY nuclear transport in a

300 CRYs, in complex with PERs, bind to the BMAL1/CLOCK complex and repress E-box-