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 PER- and DBT-containing protein complexes feed back to r

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

13 -2 (PET(178)P), but not rat beta-arrestin-1 (PER(177)P).

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

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

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

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

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

19 functioning, and quality of life occur after PER.

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

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

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

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

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

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

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

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

28 the turnover rate of the repressors CRY and PER.

29 pes to characterize the functions of CRY and PER.

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

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

32 Rhythmic ghrelin and PER expression are synchronized to prior feeding, and no

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

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

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

36 daytime levels of nuclear PER proteins, and PER-CRY-CLOCK complexes were elevated.

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 an rhythms when physical interaction between PER and CKIdelta/epsilon was disrupted by overexpressing

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

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

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

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

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

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

50 onal activation is rhythmically repressed by PER or PER-TIM to control circadian gene expression that

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

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

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

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

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

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

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

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

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

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

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

72 1Asil) (CK1epsilon(Tau)), which destabilizes PER, thereby accelerating the clock.

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

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

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

76 important for phosphorylation of Drosophila PER by casein kinase I epsilon (CKI epsilon; doubletime

77 Dimerization of Drosophila PER influences nuclear translocation, repressor activity

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

79 led to dramatically low levels of endogenous PER, while PER-binding, kinase-inactive DN-CKIepsilon di

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

81 gthen circadian period by directly enhancing PER stability.

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

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

84 oups of dorsal neurons (DN1 and DN2) exhibit PER oscillation peaks coinciding with two activity bouts

85 t the domain functions in part to facilitate PER phosphorylation within the cytoplasm, which in turn

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

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

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

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

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

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

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

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

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

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

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

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

98 promotes PER and CLK phosphorylation and how PER and CLK phosphorylation contributes to transcription

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

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

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

102 ylation that controls the daily downswing in PER abundance.

103 decreased S6KII is associated with increased PER repression.

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

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

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

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

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

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

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

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

112 ion on dPER that is conserved with mammalian PERs and contains the major in vivo DBT binding domain,

113 ttp://www.netlab.uky.edu/p/bioinfo/MapSplice/PER.

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

115 Characterization of PER lacking this motif (PER Delta) shows that it is important for phosphorylatio

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

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

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

119 s from these mice, daytime levels of nuclear PER proteins, and PER-CRY-CLOCK complexes were elevated.

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

121 ehavioral rhythms and decreased abundance of PER.

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

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

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

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

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

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

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

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

130 Characterization of PER lacking this motif (PER Delta) shows that it is impo

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

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

133 cts on PER, and TIM regulates the control of PER by PP1, although it does not affect PP2A action on P

134 nized the phosphorylation and degradation of PER, and it damped the oscillation of PER in vivo.

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

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

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

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

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

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

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

142 s study, however, constitutive expression of PER, and not CRY1, severely disrupted the clock in fibro

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

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

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

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

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

148 also crucial for regulating the kinetics of PER phosphorylation.

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

150 result from the cytoplasmic localization of PER.

151 ld for when in a daily cycle the majority of PER proteins are tagged for rapid degradation.

152 ion of PER, and it damped the oscillation of PER in vivo.

153 that is driven primarily by oscillations of PER and CRY, which inhibit their own transcriptional act

154 (S) and tau mutations on the oscillations of PER phosphorylation suggest that the mutations shorten t

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

156 Drosophila and a crucial binding partner of PER.

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

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

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

160 damentally from the inhibitory projection of PER to LEC.

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

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

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

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

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

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

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

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

169 , although it does not affect PP2A action on PER.

170 PP1 also acts on PER, and TIM regulates the control of PER by PP1, althou

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 In contrast, Tik effects on PER are undetectable in a tim(01) background, suggesting

174 horylation is unrelated to direct effects on PER stability.

175 Despite their potentially crucial effects on PER, it has not been demonstrated in a mammalian system

176 ting that TIM is required for CK2 effects on PER.

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

178 on the centrally located DBT docking site on PER and partially counterbalanced by protein phosphatase

179 1772) identify a key phosphorylation site on PER that recruits the F-box protein Slimb to trigger PER

180 high-affinity atypical SLIMB-binding site on PER.

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

182 spectrometry to map phosphorylation sites on PER, leading to the identification of a number of "phosp

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

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

185 tivation is rhythmically repressed by PER or PER-TIM to control circadian gene expression that peaks

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

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

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

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

190 Peak PER clock protein expression is elevated in the mutant,

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

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

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

194 Period (PER) proteins are essential parts of the molecular clock

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

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

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

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

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

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

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

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

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

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

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

206 phosphorylation, and degradation of PERIOD (PER) and TIMELESS (TIM) proteins govern period length.

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

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

209 s the progressive phosphorylation of PERIOD (PER) proteins, which is highly dependent on casein kinas

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

211 the emergence of a novel pattern of period (PER) synchrony whereby two subgroups of dorsal neurons (

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

213 bt mutations have similar effects on period (PER) protein phosphorylation by the fly and vertebrate e

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

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

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

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

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

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

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

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

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

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

224 anscriptional feedback loop in which PERIOD (PER) is rate-limiting for feedback inhibition.

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

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

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

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

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

230 ependent transcription, but how DBT promotes PER and CLK phosphorylation and how PER and CLK phosphor

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

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

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

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

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

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

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

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

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

240 Phosphorylation regulates PER's stability and subcellular localization; however, t

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

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

243 he fraction of the transcriptional repressor PER that is nuclear and suppression of per and tim RNA l

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

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

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

247 as other neuronal subgroups exhibit a single PER peak coinciding with one of the two activity bouts.

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

249 Mutant TIM can bind to and stabilize PER.

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

251 may have a non-catalytic role in stabilizing PER.

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

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

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

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

256 ation or transcriptional repression and that PER phosphorylation is dispensable for repressing CLK-de

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

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

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

260 The PER complex thus acquires full repressor activity only u

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

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

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

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

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

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

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

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

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

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

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

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

273 HeLa cells is regulated by sequences in the PER.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

292 recruits the F-box protein Slimb to trigger PER degradation and set clock speed.

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

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

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

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

297 atically low levels of endogenous PER, while PER-binding, kinase-inactive DN-CKIepsilon did not, sugg

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

299 per and tim transcription is associated with PER-dependent reversal of these events.

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

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