ライフサイエンスコーパス: PRL

1 PRL activates the serine/threonine kinase NEK3, which wa

2 PRL deficiency accelerated liver carcinogenesis in Prl(-

3 PRL dose-dependently induced ABCG2 expression in T-47D h

4 PRL enhances nociceptive responses by rapidly modulating

5 PRL posttranscriptionally increased nuclear cyclin D3 pr

6 PRL ubiquitinated and accelerated poststimulatory decay

7 PRL-2 knockdown by RNA interference markedly inhibited c

8 PRL-2 suppression by siRNA decreased p130Cas and vinculi

9 PRL-3 also enhanced matrix metalloproteinase-2 secretion

10 PRL-3, a metastasis-associated phosphatase, is known to

11 PRL-3, an oncogenic dual-specificity phosphatase, is ove

12 PRL-induced activation of the transcription factor STAT5

13 PRL-targeted therapy may hold promise for reducing the b

14 PRL/p53(-/-) carcinomas also exhibited selectively alter

15 rating liver (PRL) family, comprising PRL-1, PRL-2 and PRL-3, is a group of prenylated phosphatases t

16 Microarray analysis identified 120 PRL-induced genes up-regulated by wild type but not PRLr

17 16K PRL stimulated the release of miR-146a-loaded exosomes f

18 he 16-kDa N-terminal prolactin fragment (16K PRL), the underlying molecular mechanisms are poorly und

19 hat miR-146a is a downstream-mediator of 16K PRL that could potentially serve as a biomarker and ther

20 We found that 16K PRL induced microRNA-146a (miR-146a) expression in ECs,

21 cogenic phosphatase of regenerating liver 2 (PRL-2) has been shown to regulate intracellular magnesiu

22 itor of phosphatase of regenerating liver 3 (PRL-3) that could reduce the level of soluble ULBP2 in t

23 ociated phosphatase of regenerating liver-3 (PRL-3) has pleiotropic effects in driving cancer progres

24 tly induced expression of approximately 4700 PRL-induced genes, whereas PRLrYDmut ablated induction o

25 FAs, 7 ACTH-secreting, 7 GH-secreting, and 5 PRL-secreting adenomas) and 10 normal pituitaries.

26 mance (sensitivity, 94%; specificity, 85.7%; PRL, 6.58; and NLR, 0.07) as compared with the best RNFL

27 h neither ERalpha nor PR was identified as a PRL target gene, a TAD mutation significantly impaired E

28 dependent growth conditions, demonstrating a PRL-2.CNNM3 complex-dependent oncogenic advantage in a m

29 We have identified a PRL-1-binding peptide (Peptide 1) that shares high seque

30 1 matched normal controls (NCs) performing a PRL task in an MRI scanner.

31 catalytic cavity of PRL-2, we showed that a PRL inhibitor could abrogate complex formation, resultin

32 eurons remained electrically responsive to a PRL stimulus, with PRL inducing an acute increase in the

33 Aberrant PRL expression is associated with progression and metast

34 ne environment in normal pregnancy, we added PRL and IGFBP1, which enhanced invasion.

35 loss of one cyclin D1 allele did not affect PRL-induced mammary lesions in nonparous females, the co

36 d 398 significantly perturbed proteins after PRL-3 overexpression.

37 the machine learning technique of Li et al. (PRL 114, 2015) for molecular dynamics simulations.

38 tin increased ACTH-release and did not alter PRL/LH/FSH/TSH-secretion.

39 Although PRL is an established chemoattractant for breast cancer

40 Altogether, PRL-induced transient signaling in sensory neurons is go

41 rations of total testosterone (P = 0.05) and PRL (P<0.01) were lower while the values of TSH (P = 0.0

42 er (PRL) family, comprising PRL-1, PRL-2 and PRL-3, is a group of prenylated phosphatases that are ca

43 roves that the interaction between CNNM2 and PRL-1 occurs via the catalytic domain of the phosphatase

44 altered cell proliferation, cell death, and PRL release.

45 )s(-1), respectively, for EPO, IL4, hGH, and PRL agree well with experimental results.

46 crease as dramatically during pregnancy, and PRL fails to activate proliferation in human islets in v

47 Using PRL receptor-deficient (Prlr(-/-)) and PRL-deficient (Prl(-/-)) mice, we show that PRL plays a

48 In ACTH-secreting and PRL-secreting adenomas, 12 and 7 genes were significantl

49 f a positive feedback loop between STAT5 and PRL that promotes angiogenesis.

50 racterized by reduced basal testosterone and PRL levels and increased TSH levels.

51 ual marker genes, including IGFBP1, WNT4 and PRL.

52 ocations and sizes of subjects' scotomas and PRLs were mapped with a scanning laser ophthalmoscope.

53 sis of the phosphatase PTP4A3 (also known as PRL-3) demonstrated its requirement for G1-S cell-cycle

54 Ptp4a3 (commonly known as PRL-3) is an enigmatic member of the Ptp4a family of pre

55 he -434 GAS element significantly attenuated PRL-stimulated activity of a luciferase reporter driven

56 We report a positive correlation between PRL-3 expression and mTOR phospho-activation in clinical

57 ral basis underlying the interaction between PRL phosphatases and CNNM transporters and provides a hy

58 trongly support a critical interplay between PRL and estrogen via PAK1 and suggest that ligand-indepe

59 plex 1 (mTORC1), but a coherent link between PRL-3 and activation of mTOR has not yet been formally d

60 p115 RhoGAP directly binds PRL-1 in vitro and in cells via its SH3 domain.

61 n is achieved when cells are exposed to both PRL and estrogen.

62 CNNM3 levels correlate positively with both PRL-2 expression and the tumor proliferative index.

63 ficantly decreased the induction of ABCG2 by PRL without altering STAT5 recruitment to the GAS elemen

64 TAT5) also blunted the induction of ABCG2 by PRL, suggesting a role for the JAK2/STAT5 pathway in PRL

65 not sufficient for the induction of ABCG2 by PRL.

66 nown MAPK phosphatases not to be affected by PRL, suggesting a role of unidentified phosphatase(s).

67 regulation of intracellular Mg(2+) levels by PRL and CNNM4 is linked to energy metabolism and AMPK/mT

68 osphorylation of HSP60 which was mediated by PRL-3.

69 regenerating liver (PRL) family, comprising PRL-1, PRL-2 and PRL-3, is a group of prenylated phospha

70 educed STAT5 activation results in decreased PRL-induced transcription and cell proliferation, knockd

71 to Prl promoter, and its knockdown decreases PRL expression and secretion in a lactotrope cell line M

72 amino acids was found to completely disrupt PRL-2.human Cyclin M 3 (CNNM3) complex formation.

73 eral molecular cancer subtypes, and elevated PRL expression and loss of p53 have been observed in som

74 s that developed in the presence of elevated PRL.

75 We propose that elevated PRL-3 expression is an important clinical predictive bio

76 clinical significance, we verified elevated PRL-3 expression as a predictive marker for favorable th

77 e described a novel mechanism where elevated PRL-3 protein increases JMJD2C histone demethylase occup

78 ll lines, the interaction between endogenous PRL-2 and CNNM3 was markedly increased.

79 ion of PRL2, the most ubiquitously expressed PRL family member, leads to impaired placental developme

80 l lines aberrantly or ectopically expressing PRLs.

81 eviously undescribed mechanism of action for PRL-3.

82 Like TP53 mutations, evidence for PRL activity is evident across several molecular cancer

83 Here, we provide evidence for PRL-3-induced hyperactivation of EGFR and its downstream

84 merization-dependent signaling mechanism for PRL and offer proof of concept for trimerization inhibit

85 ntrol animals, indicating a pivotal role for PRL-2 in regulating cellular magnesium homeostasis.

86 logous expression system and TG neurons from PRL receptor (PRLR)-null mutant mice by expressing rat P

87 ons, one of which is a paucity of functional PRL receptors, and that murine Stat5 overexpression is a

88 Functionally, PRL-3-induced hyperactivation of EGFR correlated with in

89 Furthermore, PRL-3 and Leo1 levels were positively associated in AML

90 U1F1 present with combined deficiency of GH, PRL and TSH.

91 of several pituitary hormones (specially GH/PRL), which was accompanied by increased sst2/sst5/D2 ex

92 troph lineages and in the activation of GH1, PRL and TSHbeta transcription.

93 interference RNA (siRNA)-resistant vector HA-PRL-2m.

94 f CNNM3 that exists only in organisms having PRL orthologs.

95 However, how PRL-3 mediates these functions in AML is not known.

96 lls, the precise molecular mechanisms of how PRL regulates breast cancer cell motility and invasion a

97 However, PRL lacking the CAAX motif can still associate indiscrim

98 However, PRL-induced secretion of dopamine (DA) at the median emi

99 To determine why, we explored the human PRL-prolactin receptor (hPRLR)-Janus kinase 2 (JAK2)-sig

100 is of stage-specific antigens (i.e., IGFBP1, PRL).

101 ling cascade in human brain EC and implicate PRL and VEGF as autocrine regulators of EC migration, in

102 To examine the importance of cyclin D1 in PRL-induced pathogenesis, we generated transgenic mice (

103 Knockdown of H1 rescues the decrease in PRL-induced transcription following HMGN2 knockdown, and

104 poptotic effect of cytokines was enhanced in PRL receptor-null (Prlr(-/-)) mice.

105 Furthermore, in PRL-2 knockout mice, serum magnesium levels were signifi

106 gesting a role for the JAK2/STAT5 pathway in PRL-induced ABCG2 expression.

107 To allow this rise in PRL, TIDA neurons are thought to become unresponsive to

108 Local treatment with PRL or increasing PRL circulating levels also prevented chondrocyte apopto

109 MGA decreased with increasing PRL bivariate normal ellipse area, and visual reaction t

110 modimer of CNNM2BAT bound to two independent PRL-1 molecules, each one located at opposite tips of th

111 also inhibited rapid (</= 1 min) E2-induced PRL release.

112 cts of G protein blockade on ethanol-induced PRL production and cell proliferation in these cells.

113 STAT5A-induced PRL in the conditioned medium can activate STAT5, STAT1,

114 R signaling opens new avenues for inhibiting PRL-3-driven cancer progression.

115 rning, like probabilistic reversal learning (PRL), but the neural bases for those impairments are not

116 Ningyou7 had a shorter primary root length (PRL), greater lateral root density (LRD) and a greater s

117 California, USA) and phakic refractive lens (PRL), both for posterior chamber, significantly lower va

118 on of early-stage PDAC or precursor lesions (PRLs) and improves the prognosis.

119 rs, and accumulating epidemiologic data link PRL to breast cancer development and progression.

120 is developed, named photo-roll lithography (PRL), by integrating photolithography with rollable proc

121 amily of phosphatases of regenerating liver (PRL) are infamously oncogenic members of the PTP superfa

122 Phosphatase of Regenerating Liver (PRL) family members have emerged as molecular markers th

123 The phosphatase of regenerating liver (PRL) family, comprising PRL-1, PRL-2 and PRL-3, is a gro

124 Phosphatase of regenerating liver (PRL) oncoproteins are phosphatases overexpressed in nume

125 The Phosphatase of Regenerating Liver (PRL) proteins promote cell signaling and are oncogenic w

126 ux, binds phosphatase of regenerating liver (PRL), which is frequently overexpressed in malignant hum

127 he human phosphatases of regenerating liver (PRL-1, -2, and -3) that regulate the proliferation, diff

128 Phosphatases of regenerating liver (PRLs), the most oncogenic of all protein-tyrosine phosph

129 on a CAAX motif that is required to localize PRL to the apical edge of the lateral membrane.

130 s of receptors, the short (PRL-RS) and long (PRL-RL) form.

131 nctional plasticity allows a change from low PRL secretion in the non-pregnant state to the condition

132 and prolactinomas should be treated to lower PRL levels, decrease tumor size, and restore gonadal fun

133 We demonstrated that mammary PRL decreased the latency of tumors in the absence of p5

134 fluorescent caspase substrates, and measured PRL release by radioimmunoassay.

135 Mechanistically, PRL-3-induced activation of EGFR was attributed primaril

136 R-S, but not PRLR-L, is capable of mediating PRL-induced transient enhancement of capsaicin responses

137 the rational design of compounds modulating PRL-1 and CNNM2 activities.

138 Moreover, PRL-3 induced cellular addiction to EGFR signaling, as e

139 Moreover, PRL/p53(-/-) carcinomas displayed higher rates of prolif

140 In this report, a novel PRL-inducible regulatory phosphorylation site within the

141 hogenesis, we generated transgenic mice (NRL-PRL) that overexpress PRL in mammary epithelial cells, w

142 Nevertheless, NRL-PRL/D1(-/-) females developed significantly more preneop

143 Corroborating these findings, we observed PRL-stimulated STAT5 recruitment to a region containing

144 The ability of PRL to inhibit growth under normal conditions is depende

145 The ability of PRL to promote claudin-low carcinomas demonstrates that

146 e that this fundamental regulatory aspect of PRL-2 in cancer cells could potentially lead to broadly

147 ad no effect, indicating that the binding of PRL-2 to CNNM3 is important for the activity of the comp

148 wn of PRL expression by shRNA or blocking of PRL activity with neutralizing antibodies removed the CA

149 in CNNM3 buries into the catalytic cavity of PRL-2, we showed that a PRL inhibitor could abrogate com

150 hey also rule out a possible contribution of PRL secreted by immune cells to the modulation of autore

151 in that binds to the intracellular domain of PRL-RS and identified it as dual specific phosphatase DU

152 hese results reveal the protective effect of PRL against inflammation-induced chondrocyte apoptosis a

153 PRL2 knock-out mice to study the effects of PRL deletion in a genetically controlled, organismal mod

154 ransgenic Drosophila to study the effects of PRL overexpression in a genetically controlled, organism

155 itment and promote the biological effects of PRL signaling.

156 The downstream effects of PRL-3 were maintained even under conditions of environme

157 This first examination of PRL in a model organism demonstrates that PRL performs a

158 and determined the intrinsic excitability of PRL and IL pyramidal neurons in adolescent rats 24 h fol

159 s have documented that altered expression of PRL-1 or PRL-3 can influence cell proliferation, migrati

160 We found that stable expression of PRL-3 confers cytokine independence and growth advantage

161 ression of wild-type but not mutant forms of PRL-2 caused ERK phosphorylation and nuclear translocati

162 knowledge about the biological functions of PRL-2.

163 The identification of PRL-3-driven EGFR hyperactivation and consequential addi

164 Knockdown of PRL expression by shRNA or blocking of PRL activity with

165 Inhibition or gene knockdown of PRL-3 did not reduce ULBP2 shedding, but rather suppress

166 by comparing ethanol effects on the level of PRL production gene transcription rate cellular protein,

167 Elevated levels of PRL associate with metastasis and poor clinical outcomes

168 e normal cellular response to high levels of PRL is growth suppression and furthermore, that PRL can

169 progression, yet the signaling mechanisms of PRL-3 are still not fully understood.

170 omplex, is a novel and important mediator of PRL-3 oncogenic activities in AML.

171 an important, but not essential, mediator of PRL-induced mammary proliferation and pathology in FVB/N

172 ch may have missing or mutated modulators of PRL function.

173 amily of PRL phosphatases, overexpression of PRL-2 in breast cancer cells has been shown to promote t

174 pecific p53 loss and local overexpression of PRL.

175 his issue by exploiting a unique property of PRL phosphatases, namely, that they may function as homo

176 current study we have evaluated the role of PRL-2 in cell migration and invasion in human cancer cel

177 Supporting the role of PRL-2 in cellular magnesium transport is the observation

178 s on PAK1, we identified Tyr285 as a site of PRL-dependent phosphorylation of PAK1 by JAK2.

179 of Gs expression resulting in stimulation of PRL synthesis and cell proliferation in lactotropes.

180 Here, we describe the crystal structure of PRL-1 in complex with the Bateman module of CNNM2 (CNNM2

181 Among the subfamily of PRL phosphatases, overexpression of PRL-2 in breast canc

182 t CNNM3 is not a phosphorylated substrate of PRL-2, and that the interaction occurs through a loop un

183 Cyclin D1 is a major downstream target of PRL in lobuloalveolar development during pregnancy and i

184 However, our understanding of PRL function came primarily from studies with cultured c

185 lved in the regulation of ethanol actions on PRL production and cell proliferation in lactotropes.

186 ion of STAT5A, and VEGF induction depends on PRL expression.

187 In summary, we demonstrate that oncogenic PRL-2 controls tumor growth by modulating intracellular

188 and outer nuclear/photoreceptor layers (ONL+PRL) were measured and compared in MS versus control eye

189 y shown that transgenic mice expressing only PRL-RS (PRLR(-/-)RS) display abnormal follicular develop

190 cumented that altered expression of PRL-1 or PRL-3 can influence cell proliferation, migration and in

191 gG Ab responses were not affected by PRLR or PRL deficiency.

192 cer cells, including A549 cells, overexpress PRL-2 when compared with normal lung cells.

193 d transgenic mice (NRL-PRL) that overexpress PRL in mammary epithelial cells, with wild-type, heteroz

194 Conversely, pharmacologic PRL mobilization using the dopamine D2 receptor antagoni

195 he GTPases RalA and RalB and the phosphatase PRL-3, proteins terminating in a CCaX motif.

196 rating liver) protein tyrosine phosphatases (PRL-1, -2 and -3) have been identified as key contributo

197 ns have been proposed to promote (prelimbic, PRL) or inhibit (infralimbic, IL) these behaviors.

198 s well as siRNA to DUPD1, completely prevent PRL-mediated MAPK inhibition in ovarian cells.

199 In principle, PRL phosphatases offer appealing therapeutic targets, bu

200 y were observed in layer 2/3 NAcc projecting PRL (PRL2/3) neurons.

201 d adolescent rats, layer 5/6 NAcc projecting PRL (PRL5/6) neurons fired fewer action potentials and t

202 Prolactin (PRL) is essential for normal reproduction and signals th

203 Prolactin (PRL) regulates activity of nociceptors and causes hypera

204 , human growth hormone (hGH), and prolactin (PRL) all form four-helix bundles and bind to type I cyto

205 feration, caspase activation, and prolactin (PRL) release.

206 ion of pituitary hormones such as prolactin (PRL), growth hormone (GH), adrenocorticotropic hormone (

207 ve revealed an important role for prolactin (PRL) in breast cancer.

208 ting evidence supports a role for prolactin (PRL) in the development and progression of human breast

209 The hormone prolactin (PRL) contributes to breast cancer pathogenesis through v

210 The hormone prolactin (PRL) frequently increases in the circulation of patients

211 The hormone prolactin (PRL) has long been debated as a potential immune-stimula

212 he role of the lactogenic hormone prolactin (PRL) in the regulation of ABCG2.

213 The polypeptide hormone prolactin (PRL) stimulates breast epithelial cell growth, different

214 The lactogenic hormone prolactin (PRL) transcriptionally increases ZnT2 expression through

215 ogen-responsive pituitary hormone prolactin (PRL), signaling through hepatocyte-predominant short-for

216 The mammotrophic hormone, prolactin (PRL), and/or its receptor are also expressed in many bre

217 mainly by the lactogenic hormones prolactin (PRL) and placental lactogens.

218 We identified prolactin (PRL) as a candidate autocrine factor.

219 Most conspicuously, mutations in prolactin (PRL) and its receptor (PRLR) have an impact on thermoreg

220 mption has been shown to increase prolactin (PRL) production and cell proliferation of pituitary lact

221 ons are the central regulators of prolactin (PRL) secretion.

222 atolactotropes, the precursors of prolactin (PRL)-producing lactotropes.

223 entrations of total testosterone, prolactin (PRL), thyroid stimulating hormone (TSH), free triiodothy

224 We have previously shown that the prolactin (PRL)-activated tyrosine kinase JAK2 phosphorylates PAK1

225 ted Ser305-ERalpha in response to prolactin (PRL), implying that maximal ERalpha phosphorylation is a

226 The addition of recombinant PRL restores this activity.

227 We next reconstituted PRL-induced signaling in a heterologous expression syste

228 n to function antagonistically in regulating PRL-induced transcription as well as breast cancer cell

229 the other hand, inhibition of Leo1 reverses PRL-3 oncogenic phenotypes in AML.

230 %) underwent surgical resection for low-risk PRL.

231 went surgery and were found to have low-risk PRL.

232 s through two types of receptors, the short (PRL-RS) and long (PRL-RL) form.

233 ork study identified RAC1, CTGF, SDCBP, SRC, PRL, and SHC1 as major nodes of an Msi1-associated netwo

234 These observations demonstrate a STAT5/PRL/VEGF signaling cascade in human brain EC and implica

235 ot LH/TSH-release; 2) adiponectin stimulated PRL-, inhibited ACTH- and did not alter LH/FSH/TSH-relea

236 Furthermore: 1) Leptin stimulated PRL/ACTH/FSH- but not LH/TSH-release; 2) adiponectin sti

237 CA-STAT5A expression stimulates PRL production at the RNA and protein level, and STAT5A

238 ce rolls over a photoresistcoated substrate, PRL realizes continuous photolithographic fabrication of

239 underwent surgical resection for a suspected PRL, but only four (1.9%) had high-risk lesions (ie, hig

240 iewed together, our results demonstrate that PRL constrains tumor-promoting liver inflammation by inh

241 Here, we demonstrate that PRL inhibits the apoptosis of cultured chondrocytes in r

242 mouse models of cancer and demonstrate that PRL-3 increased downstream signalling to the mTOR substr

243 We demonstrate that PRL/JAK2-dependent phosphorylation of these tyrosines pr

244 ote claudin-low carcinomas demonstrates that PRL can influence this subset of triple-negative breast

245 of PRL in a model organism demonstrates that PRL performs as a tumor suppressor and underscores the n

246 These findings establish that PRL post-translationally regulates ZnT2-mediated zinc se

247 is growth suppression and furthermore, that PRL can counter oncogenic activity of Src.

248 Although previous studies indicate that PRL-1 promotes cell growth and migration by activating b

249 magnesium transport is the observation that PRL-2 knockdown results in a substantial decrease of cel

250 We propose that PRL binds to other membrane-localized proteins that are

251 Herein, we report that PRL post-translationally stimulated ZnT2 ubiquitination,

252 These results reveal that PRL does not play a central role in the development of c

253 cal analyses of cultured cells revealed that PRL prevents CNNM4-dependent Mg(2+) efflux and that regu

254 PRL-deficient (Prl(-/-)) mice, we show that PRL plays a redundant role in the development of chronic

255 Here, we show that PRL signaling induces chromatin decompaction at promoter

256 and pharmacological approaches to show that PRL transiently enhanced capsaicin-evoked responses invo

257 Here we show that PRL-2 regulates intracellular magnesium levels by formin

258 We also show that PRL-3 increases mTOR translocation to lysosomes via incr

259 heir phosphorylation status, suggesting that PRL-2 knockdown could inhibit tumor cell migration and i

260 ons of environmental stress, suggesting that PRL-3 provides a strategic survival advantage to tumour

261 iatum (VS) in many SZ patients suggests that PRL deficits may be largely attributable to processes do

262 The PRL (phosphatase of regenerating liver) phosphatases are

263 The PRL phosphatases are oncogenic when overexpressed but th

264 vents STAT5 binding at promoter DNA, and the PRL-induced dissociation of H1 mediated by HMGN2 is nece

265 deletion revealed a requirement for both the PRL-2 catalytic functionality and prenylation site.

266 expressing EC induces phosphorylation of the PRL receptor and activates MAPK.

267 CNNM3 is itself pro-oncogenic, and that the PRL-2/CNNM3 association is important for conferring tran

268 A and protein level, and STAT5A binds to the PRL promoter region, suggesting direct transcriptional r

269 d hGH1 promoter, but not to sites within the PRL promoter, and it selectively increases binding affin

270 owever, the specific in vivo function of the PRLs remains elusive.

271 The ability of the PRLs to suppress PTEN expression underscores the biochem

272 To define the physiological roles of the PRLs, we generated PRL2 knock-out mice to study the effe

273 The three PRL (phosphatases of regenerating liver) protein tyrosin

274 nd-independent activation of ERalpha through PRL/PAK1 may impart resistance to anti-estrogen therapie

275 In contrast to PRL neurons, layer 5 IL (IL5) and layer 2/3 (IL2/3) NAcc

276 eta-cells fail to proliferate in response to PRL for multiple reasons, one of which is a paucity of f

277 mechanisms of NEK3 activation in response to PRL signaling have not been defined.

278 ng copy number dependency in its response to PRL treatment.

279 tion of the linker histone H1 in response to PRL.

280 ity on adult human beta-cells in response to PRL.

281 rescued JAK2-STAT5 signaling in response to PRL.

282 However, contradictory cellular responses to PRL expression have been reported, including the inhibit

283 no data clearly ascribe a pathogenic role to PRL in these diseases.

284 eurons are thought to become unresponsive to PRL at lactation and functionally silenced.

285 ically normal mammary epithelium, transgenic PRL restored it to rates of wild-type females.

286 io) leads to the inhibition of the transient PRL actions.

287 nhibitors as candidate therapeutics to treat PRL-driven cancers.

288 Ectopic expression of wild-type PRL-2, a catalytic inactive C101S mutant and a C-termina

289 The molecular mechanisms underlying PRL-induced transient signaling in neurons are not well

290 Using PRL receptor-deficient (Prlr(-/-)) and PRL-deficient (Pr

291 hesis about the molecular mechanism by which PRL-1, upon binding to CNNM2, might increase the intrace

292 fy an important and novel mechanism by which PRL-3 mediates its oncogenic function in AML.

293 ppressed the growth of cancer cells in which PRL was overexpressed.

294 These results support a model in which PRL-2 promotes cell migration and invasion through an ER

295 he TSD condition (P = 0.61) decreased, while PRL levels increased (P = 0.05) irrespectively of the ex

296 d a mutant form that does not associate with PRL-2 confirm that CNNM3 is itself pro-oncogenic, and th

297 mino acid loop critical for the binding with PRL-2.

298 ctrically responsive to a PRL stimulus, with PRL inducing an acute increase in their firing rate duri

299 Local treatment with PRL or increasing PRL circulating levels also prevented

300 posure differentially affects neurons within PRL and IL regions.