ライフサイエンスコーパス: Pin1

1 66 covalently binds to the catalytic site of PIN1.

2 by the peptidyl-prolyl cis-/trans isomerase Pin1.

3 tion sites for the peptidyl-prolyl isomerase Pin1.

4 by the peptidyl-prolyl cis-/trans isomerase Pin1.

5 bution, as well as disturbed localisation of PIN1.

6 rand breaks is regulated by prolyl isomerase Pin1.

7 specific peptidyl-prolyl cis/trans isomerase Pin1.

8 multiple tumor types is the unique isomerase Pin1.

9 otential pS/T-P motifs and binds directly to Pin1.

10 uence of the dynamic modular architecture of Pin1.

11 he phosphorylation-directed prolyl isomerase PIN1.

12 -5p are largely rescued by reconstitution of Pin1.

13 s of fission yeast peptidyl-prolyl isomerase Pin1.

14 er regulated by the unique proline isomerase Pin1.

15 action with the peptidyl prolyl isomerase 1 (Pin1), a critical component of PDPK-mediated regulation.

16 The prolyl isomerase PIN1, a critical modifier of multiple signalling pathway

17 g phosphorylation-dependent interaction with Pin1, a proline isomerase, which mediates cis-trans isom

18 AK1 inhibitors synergized with inhibitors of PIN1, a prolyl isomerase essential for IRAK1 activation

19 In vitro mimicking of haploinsufficiency of PIN1 aberrantly increases tau phosphorylation and aggreg

20 ATRA-induced Pin1 ablation also potently inhibits triple-negative bre

21 Finally, chemical or genetic Pin1 ablation blocked multiple cancer-driving pathways s

22 ATRA-induced Pin1 ablation degrades the protein encoded by the fusion

23 ax2, including increased auxin transport and PIN1 accumulation, and increased lateral root density.

24 ts presented here refute these mechanisms of Pin1 action.

25 with SHFM or EEC syndromes are resistant to Pin1 action.

26 hosphate- and proline-binding pockets in the Pin1 active site.

27 Surprisingly, ablation of Pin1 activity by the chemical juglone or dominant-negati

28 PIN1 activity enhances BRCA1-BARD1 interaction with RAD5

29 inhibitor, which inhibited the intracellular Pin1 activity in cultured mammalian cells but had little

30 Thus, the modulation of Pin1 activity may be a target for the regulation of bone

31 ERK-dependent phosphorylation combined with Pin1 activity promotes REST degradation in neural progen

32 1/864 stabilizes REST, as does inhibition of Pin1 activity.

33 Pin1 acts via isomerization of proline side chains at ph

34 ctional studies, siRNA-mediated knockdown of Pin1 almost completely prevented MPP(+)-induced caspase-

35 PIN1 also catalyses the isomerization of proline 205 of

36 ctions, or "cross-talk." An example is human Pin1, an essential mitotic regulator consisting of a Trp

37 g transcript levels of the auxin transporter PIN1 and derepression of bud outgrowth.

38 Thus, DLX5, p63, Pin1 and FGF8 participate to the same time- and location

39 Furthermore, Pin1 and IL18-related signaling contributed to the obser

40 rabidopsis thaliana auxin efflux transporter pin1 and influx transporter lax2 mutants showed reduced

41 xerted its efficacy likely through degrading Pin1 and inhibiting multiple Pin1-regulated cancer pathw

42 -140-5p directly interacts with the 3'UTR of Pin1 and inhibits Pin1 translation.

43 PRO, is exclusively catalyzed by full-length Pin1 and isolated PPIase domain.

44 e we systematically investigate functions of Pin1 and its inhibitor ATRA in the development and treat

45 nds on a subset of altered proteins, such as Pin1 and Men1, that regulate the host transcription fact

46 Thus, we find that Pin1 and Myc are cooverexpressed in cancer, and this dri

47 e observed a significant correlation between Pin1 and Notch3 expression levels, which may further sug

48 Thus, combined suppression of Pin1 and Notch3 proteins may be exploited as an addition

49 c, as evidenced by differential responses of PIN1 and PIN2 to osmotic stress.

50 flux (AUX1, LAX1 and LAX2) and auxin efflux (PIN1 and PIN4) carriers by MONOPTEROS helps to maintain

51 Our results identify BRD4 as a new target of PIN1 and suggest that interfering with their interaction

52 bitor, KPT-6566, able to selectively inhibit PIN1 and target it for degradation.

53 catalysis of multiple phosphorylated tau by Pin1 and the need for directly linking biological phenot

54 degradation mediated by the prolyl isomerase Pin1 and the ubiquitin ligase KLHL20.

55 cated auxin efflux transporter PIN-formed 1 (PIN1) and Arabidopsis PM-located auxin efflux transporte

56 dings further emphasize the emerging role of Pin1 as a key modulator of synaptic transmission.

57 Our results identify Pin1 as a new regulator of RUNX3 inactivation in breast

58 Our results implicate Pin1 as a positive effector of 3' processing/termination

59 ansactivation function, these data implicate Pin1 as a potential surrogate marker for predicting outc

60 tify the peptidyl-prolyl cis-trans isomerase Pin1 as an important factor mediating CPEB destruction.

61 PEB during the mammalian cell cycle requires Pin1 as well.

62 for the peptidylprolyl cis/trans isomerase, Pin1, as well as the ERK1/2 kinases.

63 ultiple cellular partners, it is unclear how Pin1 assists in the regulation of ERalpha transactivatio

64 Rta transactivation is enhanced by Pin1 at two delayed early viral promoters in uninfected

65 pid primary response to SL is the removal of PIN1 auxin exporter proteins from the plasma membrane in

66 state and confirm previous findings that the PIN1 auxin transporter is diffusely localized in the dar

67 y (CT) imaging, localization of PIN-FORMED1 (PIN1) auxin transport proteins, and in situ hybridizatio

68 Cytokinin enhances the PIN-FORMED1 (PIN1) auxin transporter depletion at specific polar doma

69 st a key role of the newly identified Notch3-Pin1 axis in T-ALL aggressiveness and progression.

70 global miRNA downregulation, the miR-140-5p/Pin1 axis may play a major role in tumorigenesis and off

71 acellular accumulation, resulting in loss of PIN1 basal polarity at the plasma membrane.

72 arly secretory pathway selectively regulates PIN1 basal polarity establishment in a manner essential

73 n 8 (ES8), which selectively interferes with PIN1 basal polarity without altering the polarity of api

74 Pin1 binding and catalysis of phosphorylated tau at the

75 efuting the commonly accepted model in which Pin1 binding and catalysis on the A180 epitope restores

76 nal domain of Runx2 that are responsible for Pin1 binding and structural modification.

77 la (Kv4.2TA) mutation that abolished dynamic Pin1 binding to Kv4.2.

78 ivity-induced Kv4.2 phosphorylation triggers Pin1 binding to, and isomerization of, Kv4.2 at the pThr

79 ression of mutant SEPT9 that is defective in Pin1 binding was unable to rescue cytokinesis defects ca

80 hreonines previously shown to be crucial for PIN1 binding.

81 Substitution of BRD4 with PIN1-binding-defective BRD4-T204A mutant in gastric canc

82 Cellular PPIase Pin1 binds specifically to phosphoserine- or phosphothre

83 nd CDK kinase activity assays, we found that PIN1 binds the phosphorylated Thr(187)-Pro motif in p27

84 affect recycling or vacuolar trafficking of PIN1 but leads to its intracellular accumulation, result

85 expression of miR-140-5p not only eliminates Pin1, but also inhibits cells growth and metastasis.

86 Inactivation of Pin1 can establish BRCAness in cancer cells and thus sen

87 Here, we demonstrate that Pin1 can increase ERalpha protein without affecting ESR1

88 previously published models for the role of Pin1 catalysis of tau in Alzheimer's disease.

89 eries of proposed molecular mechanism of how Pin1 catalysis of tau results in biological phenotypes.

90 Importantly, site-specific measurements of Pin1-catalysis of CDK2/CycA-phosphorylated full-length t

91 reated with the pharmacological inhibitor of Pin1 catalytic activity PiB.Our data indicate that Pin1

92 uired for cell cycle progression and loss of Pin1 causes cell cycle arrest in the G1 phase in CPCs, c

93 g functions are split between the SoPIN1 and PIN1 clades in grasses.

94 atalytic activity PiB.Our data indicate that Pin1 controls synaptic content of NMDARs via PSD-95 prol

95 leaves shows that they arise by formation of PIN1 convergence sites within a proximodistal polarity f

96 By interacting with PSD-95, Pin1 dampens PSD-95 ability to complex with NMDARs, thus

97 ATRA-induced Pin1 degradation inhibited the growth of HCC cells, alth

98 Pin1 deletion increases cellular senescence but not diff

99 eam target of DLX5 and that FGF8 counteracts Pin1-DeltaNp63alpha interaction.

100 olyl cis-trans isomerase NIMA-interacting 1 (Pin1)-dependent mechanism that regulates the association

101 igand-binding domain, providing evidence for Pin1-dependent allosteric regulation of ERalpha function

102 known to regulate phyllotactic patterns via PIN1-dependent auxin polar transport, and studies of mai

103 Moreover, miR-140-5p inhibits multiple Pin1-dependent cancer pathways and suppresses tumor grow

104 Accordingly, KPT-6566 treatment impairs PIN1-dependent cancer phenotypes in vitro and growth of

105 In this study, we found that Pin1-dependent isomerization of Runx2 is the critical st

106 phase compared with Pin1-null fibroblasts or PIN1-depleted hepatoma cells.

107 Consistently, Pin1 depletion in a mouse model of Notch3-induced T-ALL,

108 PIN1 directly binds to phosphorylated threonine (T) 204

109 Pin1 disrupts ERalpha ubiquitination by interfering with

110 sphosites generally followed the predominant PIN1 distribution but was not restricted to specific pol

111 Surprisingly, we discover that Pin1 does not promote phosphorylated tau-induced MT form

112 Pin1 dysregulation is implicated in myriad human cancers

113 the shoot apical meristem, the PIN-FORMED1 (PIN1) efflux carrier concentrates auxin into local maxim

114 by the chemical juglone or dominant-negative Pin1 enhanced late gene expression and production of inf

115 The prolyl isomerase Pin1 enhanced p53-dependent BAX activation by catalyzing

116 nstrated that ERalphaSer294 is essential for Pin1-ERalpha interaction and modulates ERalpha phosphory

117 Here, we confirmed that PIN1-expressing cells exhibit higher p27 levels but have

118 ng the associated increase in the p27 level, PIN1 expression promotes rather than retards cell prolif

119 iquitin ligase at serine 308, which recruits PIN1 for cis-trans isomerization of TRIM59, leading to T

120 tarting point for development of therapeutic Pin1-FOXM1 inhibitors to target metastatic melanoma.

121 urther underscoring the beneficial effect of Pin1-FOXM1 inhibitory peptides as anti-melanoma drugs.

122 The Pin1-FOXM1 interaction was enhanced by BRAF(V600E), the

123 Importantly, cell-permeable Pin1-FOXM1-blocking peptides repressed the proliferation

124 rate of removal of the auxin export protein, PIN1, from the plasma membrane can reproduce both the au

125 Inactivation of PIN1 function conversely curbs tumour growth and cancer

126 similar to Arabidopsis atpin1, while loss of PIN1 function in Brachypodium has little effect on organ

127 uired specificity and potency for inhibiting Pin1 function in vivo.

128 ng in interdomain interactions important for Pin1 function.

129 thermore, we show that polar localisation of PIN1 generates an auxin flux circuit that not only stabi

130 d by expression of the auxin reporters pPIN1:PIN1:GFP and DR5:YFP Upon auxin microapplication, both l

131 auxin-related reporters PIN-FORMED1 (PIN1)::PIN1::GFP (for green fluorescent protein), DR5:GFP, DR5:

132 avitropic root growth and caused a switch in PIN1-HA polarity from the basal to apical side of root e

133 erformed a forward genetic screening of PIN2:PIN1-HA;pin2 Arabidopsis (Arabidopsis thaliana) plants,

134 Pin1 has been detected in dendritic spines and shafts wh

135 In conclusion, Pin1 has pleiotropic roles in CPCs and may be a molecula

136 Because both ERalpha and Pin1 have multiple cellular partners, it is unclear how

137 identified an angiosperm PIN clade sister to PIN1, here termed Sister-of-PIN1 (SoPIN1), which is pres

138 As Pin1 impacts both ERalpha protein levels and transactiva

139 protein is post-translationally regulated by Pin1 in a proportion of breast carcinomas.

140 of the correlation data, interference with\ Pin1 in BRAF(V600E)-driven metastatic melanoma cells imp

141 ted because ATRA selectively inhibits active Pin1 in cancer cells.

142 ng to evaluate the significance of targeting Pin1 in cancer treatment until the recent identification

143 we examine the heretofore unexplored role of Pin1 in CPCs.

144 are positively regulated by prolyl isomerase PIN1 in gastric cancer cells.

145 Here, we uncover a new role of Pin1 in glutamatergic signaling.

146 tu assessments of ERalpha protein, ESR1, and Pin1 in human tumors from a retrospective cohort show th

147 ally express predominantly basally localized PIN1 in root epidermal cells, leading to agravitropic ro

148 a homologue of the peptidyl-prolyl isomerase PIN1 in T. annulata (TaPIN1) that is secreted into the h

149 ly, we identified a conserved duplication of PIN1 in the grasses: PIN1a and PIN1b.

150 e that the combined inhibition of Notch3 and Pin1 in the Notch3-overexpressing human leukemic TALL-1

151 trongly stimulated the focal accumulation of Pin1 in the subnuclear area, which recruited Runx2.

152 human peptidyl-prolyl cis-trans isomerase 1 (Pin1) in complex with the peptide derived from the C-ter

153 s demonstrates that stable overexpression of Pin1 increases endogenous ERalpha DNA binding activity w

154 nclusion, our results indicate that although PIN1 increases p27 levels, it also attenuates p27's inhi

155 the conformation of its protein substrates, PIN1 increases the activities of key proteins that promo

156 gradation in ccRCC by SCP1 overexpression or Pin1 inhibition enhanced the tumor-suppressive effects o

157 ationale for a therapeutic strategy based on PIN1 inhibition.

158 the CSC-selective agent Salinomycin and the Pin1 inhibitor Juglone.

159 f all-trans retinoic acid (ATRA) as a potent Pin1 inhibitor provides a promising candidate for HCC ta

160 s the molecular insight and rationale to use Pin1 inhibitor(s) for targeted therapies of PrCa patient

161 reening, we have identified a novel covalent PIN1 inhibitor, KPT-6566, able to selectively inhibit PI

162 Dipentamethylene thiuram monosulfide, a Pin1 inhibitor, strongly attenuated their focal accumula

163 d bicyclic peptide as a potent and selective Pin1 inhibitor, which inhibited the intracellular Pin1 a

164 ation of all-trans retinoic acid (ATRA) as a Pin1 inhibitor.

165 Notwithstanding, potent PIN1 inhibitors are still missing from the arsenal of an

166 Previous Pin1 inhibitors contained phosphoamino acids, which are

167 However, available Pin1 inhibitors lack the required specificity and potenc

168 Thus, Pin1 inhibitors promote SPOP-mediated destruction of Nan

169 -parasite drug buparvaquone (and other known PIN1 inhibitors) and is mutated in a drug-resistant stra

170 Accordingly, we have investigated Pin1 interdomain interactions using NMR paramagnetic rel

171 PIN1 is a peptidyl-prolyl isomerase that catalyzes the c

172 Our data thus suggest that Pin1 is a unique, dose-dependent molecular timer that en

173 We show that in infected cells, endogenous Pin1 is active during reactivation and enhances Rta-depe

174 Pin1 is expressed in CPCs in vitro and in vivo and is as

175 w that the turnover efficiency at pSER235 by Pin1 is independent of both the WW domain and phosphoryl

176 que therapeutic target, the prolyl isomerase Pin1 is overexpressed in a majority of HCCs, whereas the

177 g candidate for HCC targeted therapy because Pin1 is overexpressed in most HCC and activates numerous

178 Pin1 is prevalently overexpressed in human cancers inclu

179 Pin1 is required for cell cycle progression and loss of

180 Pin1 is required for endogenous CPC response as Pin1 kno

181 Here, we show that Pin1 is SUMOylated on Lys6 in the WW domain and on Lys63

182 on of the auxin efflux carrier PIN-FORMED 1 (PIN1) is regulated by the auxin response transcription f

183 EBI2 signaling activated Pin1 isomerase activity through a cascade that was sensi

184 B and a peptidyl-prolyl cis-trans isomerase (Pin1) isomerase resulted in potent, selective, proteolyt

185 These studies reveal that Pin1 isomerization of phosphorylated ERalpha can directl

186 Indeed, Pin1 knock-down abolished ATRA inhibitory effects on HCC

187 1 is required for endogenous CPC response as Pin1 knock-out mice have a reduced number of proliferati

188 Pin1 knockdown potently inhibited HCC cell proliferation

189 Furthermore, like stable Pin1 knockdown, moderate overexpression of miR-140-5p no

190 that a pathogenic brain somatic mutation in PIN1 leads to a loss-of-function mutation.

191 In vivo, lack of Pin1 leads to accumulation of the p63 protein in the emb

192 ent in the MPTP mouse model of PD suppressed Pin1 levels and improved locomotor deficits, dopamine de

193 ization, reducing root auxin concentrations; PIN1 levels are reduced under stress in an ABA-dependent

194 tumors from a retrospective cohort show that Pin1 levels correlate with ERalpha protein but not to ES

195 umps are required for vacuole morphology and PIN1 localisation, thereby controlling vacuole and auxin

196 PIN1 localizations identify basipetal auxin transport in

197 is observed for PAX8, VRK2, and FBXL12/UBL5/PIN1 loci in the CHARGE study (n = 47,180; p < 6.3 x 10(

198 omain/WW domain conformations sampled by apo-Pin1 may already include a range of conformations approp

199 he WW-PPIase domain cross-talk mechanisms of Pin1 may be relevant for their mechanisms as well.

200 gh the concerted action of cytosolic p53 and Pin1 may integrate cell stress signals to induce a direc

201 We have previously shown that efficient PIN1-mediated auxin efflux requires activation through p

202 ent PGK1 S203 phosphorylation and subsequent PIN1-mediated cis-trans isomerization.

203 , suggesting that valve outgrowth depends on PIN1-mediated lateral auxin maxima as well as subsequent

204 These findings reveal a Pin1-mediated mechanism regulating reversal learning and

205 The Pin1-mediated structural modification of Runx2 is an ind

206 detected in hippocampal slices obtained from Pin1(-/-) mice compared with controls.

207 indicate that isomerization is required for Pin1-modulation of ERalpha-DNA interactions.

208 rise we observed a dramatic up-regulation of Pin1 mRNA and protein levels in dopaminergic MN9D neuron

209 n the ligand-binding WW domain of the enzyme Pin1, multistate structures were calculated from exact n

210 iferation rates in the S-phase compared with Pin1-null fibroblasts or PIN1-depleted hepatoma cells.

211 Thus, targeting Pin1 offers a promising therapeutic approach to simultan

212 Here, we tested the specific action of Pin1 on an essential step in ERalpha transactivation, bi

213 d DNA binding affinity is a direct effect of Pin1 on ERalpha because it is observed in solution-based

214 anisms and whether the functional effects of Pin1 on ERalpha signaling are direct or indirect.

215 To explain the paradoxical effects of PIN1 on p27 levels and cell cycle progression, we hypoth

216 rization, thus indicating that the action of Pin1 on PSD-95 is critical for this effect.

217 Notably, we identify the Pin1 oncoprotein as an upstream Nanog regulator that imp

218 ressed by inhibitors of the prolyl isomerase Pin1 or extracellular signal-regulated kinases (ERK) 1/2

219 size was detected in CA1 principal cells of Pin1(-/-) or in Thy-1GFP mice treated with the pharmacol

220 that cell polarity for the auxin transporter PIN1 orients up auxin gradients, as this spontaneously g

221 Pin1 overexpression also impairs proliferation and cause

222 down-regulated and inversely correlated with Pin1 overexpression in HCC tissues and cell lines.

223 Additionally, Pin1 overexpression inhibits replicative senescence, inc

224 indicating that cell cycle arrest caused by Pin1 overexpression is a consequence of differentiation

225 ulation in other cancers and major impact of Pin1 overexpression on activating numerous cancer-drivin

226 ty of HCCs, whereas the mechanism underlying Pin1 overexpression remains elusive.

227 These results unveil a CDK4-PIN1-p53-RS-c-Myc pathway as a novel mechanism for the G

228 lates the activity of PEA3 and ELK-1 via the Pin1-pERK pathway and forms self-regulated feedback loop

229 PIN1 phosphomimicking mutations, as well as enhanced pho

230 Thereby, PIN1 phosphorylation at all phosphosites generally follo

231 We have mapped PIN1 phosphorylation at S1-S4 in situ using phosphosite-

232 PIN1 phosphorylation at the basal and apical plasma memb

233 protein kinases or trafficking mechanisms in PIN1 phosphorylation control.

234 We detected phosphorylation at PIN1 phosphosites at the basal (rootward) as well as the

235 erential phosphosite preference for the four PIN1 phosphosites.

236 of the auxin-related reporters PIN-FORMED1 (PIN1)::PIN1::GFP (for green fluorescent protein), DR5:GF

237 ation and DNA fragmentation, indicating that Pin1 plays a proapoptotic role.

238 Human peptidyl-prolyl isomerase (PPIase) Pin1 plays key roles in developmental processes, cell pr

239 he starvation state and the establishment of PIN1 polar membrane localization consistent with auxin e

240 PIN1 polarities are oriented away from regions of high a

241 ized MP expression is sufficient to instruct PIN1 polarity directions non-cell autonomously, toward M

242 The differential effects of D6PK and PID on PIN1 polarity had so far been attributed to their differ

243 the early secretory pathway in establishing PIN1 polarity in Arabidopsis thaliana by pharmacological

244 lly acts downstream of mechanics to regulate PIN1 polarity response.

245 PID, but not D6PK, can also induce PIN1 polarity shifts, seemingly through phosphorylation

246 the differential effects of D6PK and PID on PIN1 polarity, and suggest that a more complex model is

247 s Ca(2+) response is required for changes in PIN1 polarity, though not sufficient.

248 ired for downstream changes in PIN-FORMED 1 (PIN1) polarity.

249 ed at postsynaptic sites where it sequesters Pin1, preventing its negative action on synaptic transmi

250 wo single nucleotide polymorphisms (SNPs) in PIN1 promoter and nasopharyngeal carcinoma (NPC) risk wi

251 ings suggest that -842G > C and -667C > T in PIN1 promoter are associated with NPC risk; as well as t

252 oriented by a polarity field, highlighted by PIN1 protein localisation, and is modulated by dorsovent

253 , these functions are attributed to a single PIN1 protein.

254 In functional experiments, Pin1 proved to be a main regulator of FOXM1 activity thr

255 Pin1 recruitment by PSD-95 occurs at specific serine-thr

256 Furthermore, Pin1 reduces the cellular levels of RUNX3 in an isomeras

257 rough degrading Pin1 and inhibiting multiple Pin1-regulated cancer pathways and cell cycle progressio

258 Thus, ATRA simultaneously blocks multiple Pin1-regulated cancer-driving pathways, an attractive pr

259 The prolyl isomerase Pin1 regulates multiple signaling cascades by modulating

260 Pin1 regulates the levels and functions of phosphoprotei

261 cell cycle progression, we hypothesized that PIN1 relieves CDK2 inhibition by suppressing the CDK inh

262 Here, we demonstrate that Pin1 residing in postsynaptic structures can interact wi

263 ation of XPO5 is altered by prolyl isomerase Pin1, resulting in reduction of pre-miRNA loading.

264 trate that the pharmacological inhibition of Pin1 reverses the pathologic phenotypes of neurons knock

265 Pin1's effect, however, suggests a rheostat-like influen

266 nge of conformations appropriate for binding Pin1's numerous substrates.

267 The PREs show that apo-Pin1 samples interdomain contacts beyond the range sugge

268 of permutations of ERalpha-binding elements, Pin1 selectively enhances the binding affinity of ERalph

269 emains elusive--inhibits and degrades active Pin1 selectively in cancer cells by directly binding to

270 roduction of infectious virus, while ectopic Pin1 showed inhibitory effects.

271 d, through G-protein subunit alpha, ERK, and Pin1 signaling, likely participate in the regulation of

272 lost a PIN clade sister to AtPIN1, Sister-of-PIN1 (SoPIN1), which is conserved in flowering plants.

273 clade sister to PIN1, here termed Sister-of-PIN1 (SoPIN1), which is present in all sampled angiosper

274 Moreover, it has been shown that PIN1 stabilizes and increases the level of the cyclin-de

275 cancer cells with impaired Myc degradation, Pin1 still enhances Myc DNA binding, although it no long

276 cells and in animal models by acting on many Pin1 substrate oncogenes and tumor suppressors.

277 phenotypes and residue-specific turnover in Pin1 substrates.

278 A 4.5-mus all-atom MD simulation of apo-Pin1 suggests that the fluctuations of interdomain dista

279 hondrial activity of ATR is downregulated by Pin1 that isomerizes ATR from cis-isomer to trans-isomer

280 oot apex, as judged by altered expression of PIN1, the auxin reporter DR5rev::GFP, and the auxin-indu

281 tive PINOID (PID) phosphorylate and activate PIN1 through phosphorylation at all four phosphosites.

282 iR-140-5p inhibits HCC by directly targeting Pin1 to block multiple cancer-driving pathways.

283 ecific kinases and phosphatases, desensitize PIN1 to cytokinin.

284 strate GC-activated co-recruitment of GR and Pin1 to the GILZ gene promoter.

285 olyl cis-trans isomerase NIMA-interacting 1 (PIN1) to p53-RS, but not the p53 form with mutations of

286 atively regulating the catalytic activity of Pin1 toward PSD-95, facilitates NMDAR synaptic expressio

287 nteracts with the 3'UTR of Pin1 and inhibits Pin1 translation.

288 From these maxima, PIN1 transports auxin into internal tissues along emerge

289 Upon binding, Pin1 triggers structural changes in PSD-95, thus negativ

290 promoter activity is mediated by functional PIN1 variants.

291 However, UV inactivates Pin1 via DAPK1, stabilizing the pro-survival cis-isomeri

292 by the interaction with the prolyl-isomerase Pin1, via proteasome-mediated degradation; p63 mutant pr

293 lation of the expression of prolyl isomerase PIN1, which in turn increases enzyme activity of casein

294 as compared to the fast folding mutant FiP35 Pin1, which introduces a negative charge into the first

295 novel target protein of the prolyl-isomerase Pin1, which is able to regulate Notch3 protein processin

296 substrate for the peptidyl prolyl isomerase, Pin1, which mediates cis-trans isomerization of the pS11

297 ity correlated with expression of the enzyme Pin1, which we found to be indicative of a poor prognosi

298 st HCC tumor growth in mice through reducing Pin1, with a better potency than the slow-releasing ATRA

299 A hyperstable Pin1 WW domain has been circularly permuted via excision

300 The folding of wild type Pin1 WW domain, which has two positively charged residue