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 also reduced active cleaved-caspase-1 levels indepen

3 PRL deficiency accelerated liver carcinogenesis in Prl(-

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

5 PRL enhances nociceptive responses by rapidly modulating

6 PRL outer segments became significantly thinner over tim

7 PRL ubiquitinated and accelerated poststimulatory decay

8 PRL-1 knockdown in PDF clock neurons dramatically length

9 PRL-1 mutants exhibit allele-specific interactions with

10 PRL-3 also enhanced matrix metalloproteinase-2 secretion

11 PRL-3 also played a role in the acquired resistance of m

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

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

14 PRL-induced activation of the transcription factor STAT5

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

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

17 hat the Phosphatase of Regenerating Liver-1 (PRL-1) sets period length and behavioral phase gated by

18 Phosphatases of regenerating liver (PRL-1, PRL-2, and PRL-3, also known as PTP4A1, PTP4A2, and PTP4

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

20 16K PRL stimulated the release of miR-146a-loaded exosomes f

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

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

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

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

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

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

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

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

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

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

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

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

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

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

37 Hence, altered PRL-2 expression leads to metabolic reprogramming of the

38 Although PRL is an established chemoattractant for breast cancer

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

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

41 ses of regenerating liver (PRL-1, PRL-2, and PRL-3, also known as PTP4A1, PTP4A2, and PTP4A3) control

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

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

44 thening is suppressed in constant light, and PRL-1 mutants display a delayed phase under short, but n

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

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

47 development through TGF-beta1 production and PRL stimulation leads to SMAD7 activation, repression of

48 Of clinical relevance, STAT3 and PRL-3 expression was positively correlated in five indep

49 rt a feedforward mechanism between STAT3 and PRL-3 that prolongs prosurvival signaling in multiple my

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

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

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

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 hough a compelling connection exists between PRL (phosphatase of regenerating liver) 2 and cancer, ho

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

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

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

61 ipsychotic drugs, such as penfluridol, block PRL signaling in pancreatic cancer cells to reduce their

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

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

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

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

66 not sufficient for the induction of ABCG2 by PRL.

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 ls to bortezomib, which could be overcome by PRL-3 silencing.

70 a magnesium-sensitive mechanism controlling PRL expression, which plays a role in cellular bioenerge

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

72 antipsychotic drugs as agents that decreased PRL-induced JAK2 signaling; incubation of pancreatic can

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

74 eam ORF present in the mRNA leader derepress PRL protein synthesis and attenuate the translational re

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

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

77 s that developed in the presence of elevated PRL.

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

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

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

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

82 ption factor 1 (Pit-1), leading to excessive PRL secretion.

83 l lines aberrantly or ectopically expressing PRLs.

84 eviously undescribed mechanism of action for PRL-3.

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

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

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

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

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

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

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

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

93 Furthermore, PRL-3 could be used as a biomarker to identify high-risk

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

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

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

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

98 Although high PRL levels have been linked to cancer progression, regul

99 significantly enriched in patients with high PRL-3 expression.

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

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

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

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

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

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

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

107 showed statistically significant decrease in PRL, ACTH and non-functional subtypes when compared to L

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

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

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

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

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

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

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

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

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

117 or neurosensory retina, photoreceptor layer (PRL) outer segments, retinal pigment epithelium plus dru

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

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

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

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

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

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

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

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

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

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

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

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

130 Phosphatases of regenerating liver (PRL-1, PRL-2, and PRL-3, also known as PTP4A1, PTP4A2, a

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

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

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

134 y the impaired induction of decidual markers PRL and IGFBP1.

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

136 Mechanistically, PRL induced the protein kinase G (PKG)-mediated phosphor

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

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

139 L1/IGLL5, TNFRSF17, ALDH1A1, KIAA0125, MMP7, PRL, MGC16025, ADAM11, and the most upregulated proteins

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

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

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

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

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

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

146 Abrogation of PRL-3 reduced myeloma cell survival, clonogenicity, and

147 , the regulation and oncogenic activities of PRL-3 in multiple myeloma warrant further investigation.

148 Therapeutic administration of PRL exerted antiinflammatory and antifibrotic actions in

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

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

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

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

153 ium levels correlates with a rapid change of PRL expression by a mechanism involving its 5'UTR mRNA r

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

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

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

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

158 itment and promote the biological effects of PRL signaling.

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

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

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

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

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 ohistochemical analyses to compare levels of PRL and PRLR in multitumor tissue microarrays.

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 ocarcinoma (PDAC) have high plasma levels of PRL.

170 Furthermore, loss of PRL-3 efficiently abolished nuclear localization of STAT

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

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

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

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

175 Overexpression of PRL-3, an oncogenic phosphatase, was identified as a nov

176 pecific p53 loss and local overexpression of PRL.

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

178 The rate of PRL outer segment thinning was higher in eyes with SDDs

179 cts as a direct transcriptional regulator of PRL-3.

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

181 n understanding the female-selective role of PRL/PRLR in nociceptor sensitization and in pathological

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

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

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

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

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

187 Upregulation of PRL-3 increased myeloma cell viability and rephosphoryla

188 T3-dependent transcriptional upregulation of PRL-3, which in turn re-phosphorylates STAT3 and aberran

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

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

191 The clinical implications of the peripheral PRL/PRLR system for the discovery of new therapies for p

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

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

194 ry effect of the sGC stimulator praliciguat (PRL) in the liver.

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

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

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

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

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

200 Prolactin (PRL) signaling is up-regulated in hormone-responsive can

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

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

203 tant prolactinomas display higher prolactin (PRL) levels (p = 0.02) and shorter progression-free surv

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

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

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

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

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

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

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

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

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

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

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

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

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

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

218 Emerging evidence reveals that prolactin (PRL) signaling at its cognate prolactin receptor (PRLR)

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

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

221 tential, but when stimulated with prolactin (PRL) they increased the differentiation of other CD34(+)

222 opic (LH/FSH-secreting) = 17; prolactinomas (PRL-secreting) = 11, Cushing's disease (ACTH-secreting)

223 The addition of recombinant PRL restores this activity.

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

225 n reduces intracellular ATP but up-regulates PRL protein expression via activation of the AMPK/mTORC2

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

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

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

229 %) underwent surgical resection for low-risk PRL.

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

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

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

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

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

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

236 g in multiple myeloma, and suggest targeting PRL-3 as a valid therapeutic opportunity in multiple mye

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

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

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

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

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

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

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

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

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

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

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

248 Thus, our studies reveal that PRL-1-dependent dephosphorylation of TIM is a core mecha

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

250 Both mRNA and protein analyses show that PRL increased mothers against decapentaplegic homolog 7

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

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

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

254 Moreover, we show that PRL-1 promotes TIM accumulation and dephosphorylation.

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

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

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

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

259 The PRL antiinflammatory effect was also associated with sup

260 The PRL antiinflammatory effect was associated with lower F4

261 The PRL phosphatases are oncogenic when overexpressed but th

262 The PRL receptor (PRLR) is a class I cytokine receptor that

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

264 Interestingly, the PRL-1 mutant period lengthening is suppressed in constan

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

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

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

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

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

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

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

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

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

274 PRLR are increased in PDAC, and exposure to PRL increases proliferation and migration of pancreatic

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

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

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

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

279 rescued JAK2-STAT5 signaling in response to PRL.

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

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

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

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

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

285 opolysaccharide plus adenosine triphosphate, PRL inhibited the priming (expression of Il1b and Nlrp3)

286 Compared to LH/FSH-secreting tumors, PRL-secreting tumors showed statistically significant de

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

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

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

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

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

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

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

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

295 final visit (P < 0.001) and correlated with PRL outer segment thickness (r = 0.33; P =0.02).

296 s or small hairpin RNA), were incubated with PRL or penfluridol and analyzed in proliferation and sph

297 Incubation of pancreatic cell lines with PRL activated signaling via JAK2-signal transducer and a

298 hese data indicate that sGC stimulation with PRL exerts antiinflammatory actions in the liver through

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

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

301 posure differentially affects neurons within PRL and IL regions.