ライフサイエンスコーパス: Pin1

1 tween auxin and its transporter PIN-FORMED1 (PIN1).

2 -5p are largely rescued by reconstitution of Pin1.

3 tion sites for the peptidyl-prolyl isomerase Pin1.

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

5 specific peptidyl-prolyl cis/trans isomerase Pin1.

6 multiple tumor types is the unique isomerase Pin1.

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

8 dentify that SENP1 binds to and deSUMOylates Pin1.

9 which is regulated by the action of Cdk1 and Pin1.

10 phorylation and requires a prolyl isomerise, Pin1.

11 er regulated by the unique proline isomerase Pin1.

12 66 covalently binds to the catalytic site of PIN1.

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

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

15 Peptidylprolyl isomerase 1 (Pin1), a protein overexpressed in many tumor types inclu

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

17 Pin1, a major peptidyl-prolyl isomerase, has recently be

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

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

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

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

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

23 ts presented here refute these mechanisms of Pin1 action.

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

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

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

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

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

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

30 1/864 stabilizes REST, as does inhibition of Pin1 activity.

31 Pin1 acts via isomerization of proline side chains at ph

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

33 PIN1 also catalyses the isomerization of proline 205 of

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

35 lphaSer294, and mediates the binding between Pin1 and ERalpha.

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

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

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

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

40 -140-5p directly interacts with the 3'UTR of Pin1 and inhibits Pin1 translation.

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

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

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

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

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

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

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

48 ation showed reduced membrane association of PIN1 and PIN2.

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

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

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

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

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

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

55 Collectively, these data support a role for Pin1 as a central modulator of the intensity and duratio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

73 Pin1 binding and catalysis of phosphorylated tau at the

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

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

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

77 hreonines previously shown to be crucial for PIN1 binding.

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

79 Cellular PPIase Pin1 binds specifically to phosphoserine- or phosphothre

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

81 enetic deletion or cardiac overexpression of Pin1 blunts hypertrophic responses induced by transaorti

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

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

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

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

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

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

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

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

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

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

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

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

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

95 Pin1 deletion increases cellular senescence but not diff

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

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

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

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

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

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

102 phorylated, which occurs simultaneously with Pin1 dephosphorylation.

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

104 trigolactone signalling was found to trigger PIN1 depletion from the plasma membrane of xylem parench

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

106 Mechanistically, we find that Pin1 directly binds to Akt, mitogen activated protein ki

107 PIN1 directly binds to phosphorylated threonine (T) 204

108 Pin1 disrupts ERalpha ubiquitination by interfering with

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

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

111 Pin1 dysregulation is implicated in myriad human cancers

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

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

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

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

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

117 data demonstrate that ERfs are essential for PIN1 expression in the forming midvein of future leaf pr

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

119 has a significant negative correlation with Pin1 expression.

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 or SENP1-mediated deSUMOylation in promoting Pin1 function during tumorigenesis.

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

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

129 about the role of SUMOylation in regulating Pin1 function.

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

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

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

133 Pin1 has been detected in dendritic spines and shafts wh

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

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

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

137 As Pin1 impacts both ERalpha protein levels and transactiva

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

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

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

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

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

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

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

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

146 t to systematically characterize the role of Pin1 in PD using cell culture and animal models.

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

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

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

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

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

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

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

154 ng of Akt and MEK, whereas overexpression of Pin1 increases Raf-1 phosphorylation on the autoinhibito

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

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

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

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

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

165 Previous Pin1 inhibitors contained phosphoamino acids, which are

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

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

168 At this time, the CPEB-Pin1 interaction requires cdk1-catalyzed CPEB phosphoryl

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

170 Therefore, Pin1 is a selective regulator of GR transactivation, act

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

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

173 We show that active Pin1 is driven into nonspecific weak attractive interact

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 diated by a conformational change induced by Pin1 isomerization of CPEB.

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

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

188 1 is required for endogenous CPC response as Pin1 knock-out mice have a reduced number of proliferati

189 Pin1 knockdown potently inhibited HCC cell proliferation

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

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

192 Furthermore, loss of Pin1 leads to diminished hypertrophic signaling of Akt a

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

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

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

196 PIN1 localizations identify basipetal auxin transport in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

215 Pin1 overexpression also impairs proliferation and cause

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

217 Additionally, Pin1 overexpression inhibits replicative senescence, inc

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

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

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

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

222 The substrate recognition site of Pin1 performs specific and nonspecific attractive intera

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

224 PIN1 phosphomimicking mutations, as well as enhanced pho

225 Thereby, PIN1 phosphorylation at all phosphosites generally follo

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

227 PIN1 phosphorylation at the basal and apical plasma memb

228 protein kinases or trafficking mechanisms in PIN1 phosphorylation control.

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

230 erential phosphosite preference for the four PIN1 phosphosites.

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

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

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

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

235 PIN1 polarities are oriented away from regions of high a

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

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

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

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

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

241 horylation, which correlates with changes in PIN1 polarization in epidermal cells during development.

242 Here, we report that the Pin1 prolyl isomerase enhances recruitment of serine 62-

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

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

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

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

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

248 utation and several protein modifications on Pin1 (Q13526), a protein implicated in the development o

249 In addition, Pin1 recognizes four phosphorylated Ser/Thr-Pro motifs i

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

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

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

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

254 The prolyl isomerase Pin1 regulates multiple signaling cascades by modulating

255 Pin1 regulates the levels and functions of phosphoprotei

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

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

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

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

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

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

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

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

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

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

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

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

268 A sub-stoichiometric amount of Pin1 stimulated the dephosphorylation of H1 in vitro and

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

270 phenotypes and residue-specific turnover in Pin1 substrates.

271 fied and phosphorylated forms of PINFORMED1 (PIN1) suggests a tissue-specific difference in phosphory

272 Pin1 SUMOylation inhibits its protein activity and oncog

273 These results not only uncover Pin1 SUMOylation on Lys6/63 as a novel mechanism to inhi

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

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

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

277 uced peptidyl isomerase activity but induced Pin1 to associate with FADD after its phosphorylation at

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

279 ecific kinases and phosphatases, desensitize PIN1 to cytokinin.

280 Binding of Pin1 to RUNX3 suppresses the transcriptional activity of

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

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

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

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

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

286 promoter activity is mediated by functional PIN1 variants.

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

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

289 Pin1 was activated by IL-5, whereas simultaneous IL-5 an

290 However, unlike SEPT9 depletion, Pin1 was not required for the accumulation of the exocys

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

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

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

294 Here, we identify prolyl isomerase Pin1, which is often overexpressed in breast cancer, as

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

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

297 Biochemical evidence associates ABCB19 and PIN1 with sterol- and sphingolipid-enriched PM fractions

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