ライフサイエンスコーパス: calcineurin

1 ulated the phosphatase enzymatic activity of calcineurin.

2 nction as potent physiological inhibitors of calcineurin.

3 pression/activity of the protein phosphatase calcineurin.

4 lcium-dependent serine/threonine phosphatase calcineurin.

5 This process is critically dependent on calcineurin.

6 ion but are then rapidly removed by anchored calcineurin.

7 as also dependent on type 2 NT receptors and calcineurin.

8 pe 2 NT receptor and the protein phosphatase calcineurin.

9 CA encodes the alpha isoform of a subunit of calcineurin.

10 m response factor and the signaling effector calcineurin.

11 d with gene and protein expression levels of calcineurin.

12 dependence of the CaM-dependent phosphatase calcineurin.

13 sitization processes through the phosphatase calcineurin.

14 creased mRNA of the Nfat target regulator of calcineurin 1.

15 forms, protein phosphatase at 14D (Pp2B-14D)/calcineurin A at 14F (CanA-14F), in Toll-mediated immune

16 postnatal splicing transitions of the three calcineurin A genes, calcium-dependent phosphatases that

17 Redirected splicing of calcineurin A to the fetal isoforms in adult muscle and

18 We examined the roles of 2 homologs of Calcineurin A, CanA14F, and Pp2B in the Drosophila cardi

19 ted Kv2.1 channel modulation is dependent on calcineurin, a Ca(2+) -activated phosphatase.

20 regulation of inhibitory GABAA signaling by calcineurin, a calcium- and calmodulin-dependent phospha

21 he present study, we explore the function of calcineurin, a gene candidate we found downregulated in

22 Because FHL2 binds calcineurin, a phosphatase controlling hypertrophic sign

23 Calcineurin, a phosphatase required for the activation o

24 ator of calcineurin (RCAN1), an inhibitor of calcineurin, a well-characterized tau phosphatase.

25 In summary, we have shown that calcineurin Abeta and SORLA are key components in the ph

26 t mice, and a functional interaction between calcineurin Abeta and SORLA was further corroborated by

27 SORLA-deficient mice showed more calcineurin Abeta in the apical region of TAL cells and

28 Here, we identified NKCC2 as a target of the calcineurin Abeta isoform.

29 ed cells reduced the abundance of endogenous calcineurin Abeta.

30 nsights into the kinetics and integration of calcineurin activation in response to myocyte Ca transie

31 r was RCAN1 mRNA level, indicating a lack of calcineurin activation.

32 arization signals, both processes relying on calcineurin activation.

33 aused myofibril disarray, whereas inhibiting Calcineurin activity attenuated FoxO-mediated murf1 expr

34 FAT transcription factors, and inhibition of calcineurin activity by treatment with cyclosporin A (Cs

35 Loss of calcineurin activity impaired phosphorylation of Tyr493

36 te whether FKBP12 plays a role in regulating calcineurin activity in the absence of Tacrolimus.

37 Increased calcineurin activity is associated with alpha-synuclein

38 Calcineurin activity strictly depends on Ca(2+) and Ca(2

39 Thus, FKBP12 can endogenously regulate calcineurin activity with therapeutic implications for t

40 This led to a reduction of calcineurin activity, thereby stabilizing GluA1 phosphor

41 nflux; intracellular Ca2+ concentration; and calcineurin activity.

42 ivated protein kinase activity and increased calcineurin activity; however, the mechanisms controllin

43 Pharmacological inhibition implicated the calcineurin, Akt/protein kinase B, and Ca(2+)/calmodulin

44 nst APP-induced memory defects by correcting calcineurin and cAMP signaling pathways but accelerates

45 first to identify cross-talk between Ca(2+)/calcineurin and Cdc42 signaling and to demonstrate modul

46 tions induce ISC proliferation by regulating Calcineurin and CREB-regulated transcriptional co-activa

47 The calcineurin and Hsp90 cell signaling pathways appear to

48 roblastomas, indicating that deregulation of calcineurin and mitochondrial dynamics contributes to hi

49 We demonstrate that calcineurin and NFAT factors are constitutively expresse

50 ctivity of the calcium-dependent phosphatase calcineurin and promoting the general amino acid control

51 ng refinement that involves the phosphatases calcineurin and protein phosphatase-1, as well the serin

52 es) further strengthens the understanding of calcineurin and provides a foundation to develop antifun

53 this was accompanied with the activation of calcineurin and subsequent translocation of NFATc4 to th

54 el, sodium-calcium exchanger, phospholamban, calcineurin, and calcium/calmodulin-dependent protein ki

55 a(2+)-sensitive interface between AKAP79 and calcineurin, and increases resting cellular PKA phosphor

56 2+)-dependent signaling molecules, including calcineurin, and inhibition of SOCE or calcineurin impai

57 hospholipase Cbeta, protein kinase Cepsilon, calcineurin, and phospholamban.

58 ctivity of the calcium-activated phosphatase calcineurin, and was opposed by the actions of cyclin-de

59 Drugs targeting calcineurin are potent antifungal agents but also pertur

60 (2016) show that KIF1Bbeta binding releases calcineurin autoinhibition, leading to dephosphorylation

61 ls upon interaction with the calcium sensors calcineurin B like proteins into phosphorylation events

62 logous system showed that the Ca(2+) sensors calcineurin B-like (CBL1), CBL8, CBL9, and CBL10, togeth

63 with CIPK23 requires kinase activity and the calcineurin B-like binding protein CBL1.

64 for plants, it remained unknown if, and how, calcineurin B-like calcium sensors (CBLs) and CBL-intera

65 Using a genetic screen, we found that CALCINEURIN B-LIKE INTERACTING PROTEIN KINASE23 (CIPK23)

66 Calcineurin B-like interacting protein kinases (CIPKs) d

67 -DNA mutant allowed for the isolation of the CALCINEURIN B-LIKE PROTEIN 10 (SlCBL10) gene whose lack

68 Calcineurin B-like proteins (CBLs) and CBL-interacting p

69 In this pathway, the SOS3 and CALCINEURIN B-LIKE10 (CBL10) calcium sensors interact wi

70 le regulator (HIRA), Ubinuclein1 (UBN1), and calcineurin binding protein 1 (CABIN1), deposits histone

71 reens revealed that CEFIP interacts with the calcineurin-binding protein four and a half LIM domains

72 s in a process that is dependent on PERK and calcineurin but not on mTORC1.

73 Further study indicated that inhibition of calcineurin by cyclosporine A or knockdown of NFATc4 usi

74 Calcineurin can be inhibited with Tacrolimus through the

75 ganglion neurons, becomes dysfunctional upon calcineurin (CaN) inhibition.

76 we investigated the role of the phosphatase calcineurin (CaN) using electrophysiological, molecular,

77 Variants near the calcineurin catalytic subunit gamma gene PPP3CC and the

78 We found that knockdown of these calcineurin catalytic subunits caused cardiac restrictio

79 ng pathway (MtRS) involving Ca(+2)-sensitive Calcineurin (Cn) activation as an immediate upstream eve

80 with proteolysis of the protein phosphatase calcineurin (CN) and the elevated expression of the CN-d

81 a activates the Ca(2+)-dependent phosphatase calcineurin (CN) by stabilizing the CN-calmodulin comple

82 ification of substrates of the essential PSP calcineurin (CN) has been exceptionally challenging and

83 Here, we show that a highly active calcineurin (CN) phosphatase fragment and its substrate

84 Increasing evidence suggests that the calcineurin (CN)-dependent transcription factor NFAT (Nu

85 (KB-R7943, YM-244769), or two inhibitors of calcineurin (cyclosporin-A, FK506).

86 ar factor of activated T cells, cytoplasmic, calcineurin-dependent 1 (NFATC1) during osteoclastogenes

87 kinase activation, Ca(2+) mobilization, and calcineurin-dependent activation of NFAT, the master tra

88 adeno-associated virus (AAV) to inhibit the calcineurin-dependent activation of the transcription fa

89 ly encoded calcium sensor, we found that the calcineurin-dependent changes in Kv2.1 probably occur as

90 d that CEFIP overexpression further enhances calcineurin-dependent hypertrophic signal transduction,

91 (2+) concentrations are sufficient to induce calcineurin-dependent Kv2.1 channel dispersal in rat cor

92 quent Adamts-1 induction in aortic wall in a calcineurin-dependent manner.

93 yocyte hypertrophy in vitro and in vivo in a calcineurin-dependent manner.

94 ut mice to test whether SORLA is involved in calcineurin-dependent modulation of NKCC2.

95 activity and was sensitive to inhibition of calcineurin-dependent NFAT activation.

96 induction of the IP-10 gene was mediated by calcineurin-dependent NFAT signaling in pancreatic beta-

97 Activation of calcineurin-dependent nuclear factor of activated T cell

98 This results in permanent activation of the calcineurin-dependent pathway in these cells.

99 We show that FKBP12 profoundly affects the calcineurin-dependent phosphoproteome, promoting the dep

100 ytosolic Ca(2+) transients, which leads to a calcineurin-dependent redistribution of Kv2.1 channels f

101 the in vivo relevance of HDAC1 and identify calcineurin-dependent serine dephosphorylation as the si

102 This activation triggers calcineurin-dependent TFEB-nuclear translocation, autoph

103 al context for this regulation and show that calcineurin dephosphorylates and positively regulates Rg

104 ses hypertension predominantly by inhibiting calcineurin directly in cells expressing NCC, indicating

105 2 mutant that is defective for regulation by calcineurin display increased gene expression in respons

106 Effects of calcineurin down-regulation and of phosphorylated RIC-3

107 Calcineurin encodes a calcium- and calmodulin-dependent

108 Whether calcineurin/FKBP12 represents a native physiologically r

109 m/calmodulin-dependent phosphatase 2B (PP2B, calcineurin) focuses and insulates termination of local

110 disrupts myofibril integrity by activating a Calcineurin-FoxO-MuRF1-proteosome signaling pathway.

111 of myogenesis and as the enzyme that opposes calcineurin function.

112 the NHE3 intracellular C-terminus, including calcineurin homologous protein, the NHERF family and SNX

113 molecules of the PKC-alpha/IkappaBalpha- and calcineurin/IkappaB-beta-dependent NF-kappaB signaling p

114 in AIAD via the PKC-alpha/IkappaB-alpha- and calcineurin/IkappaB-beta-dependent NF-kappaB signaling p

115 -alpha (PKC-alpha/IkappaB-alpha)-mediated or calcineurin/IkappaB-beta-dependent, NF-kappaB-dependent

116 uding calcineurin, and inhibition of SOCE or calcineurin impairs antigen-dependent T cell proliferati

117 Our results suggest a key role for calcineurin in cardiac remodeling during long-term hypox

118 This specific role of calcineurin in coordinating physical interactions with h

119 it is not known whether there is a role for calcineurin in Dorsal/Dif immune signaling.

120 We therefore investigated the role of calcineurin in intestinal tumor development.

121 Whereas depletion of calcineurin in late-stage schizonts demonstrated its cri

122 te lymphoblastic leukemia (T-ALL) cells upon calcineurin inactivation, among other phenotypic traits

123 Our data also revealed a role for miRNAs in calcineurin-independent regulation of JNK and p38 MAPKs

124 efined may represent novel targets to reduce calcineurin induced nephrotoxicity.

125 A-mediated inhibition of NFATc revealed that calcineurin inhibition decreases HNF1B expression in epi

126 Likewise, calcineurin inhibition did not prevent the Ito,f reducti

127 ly, transient Nebula/DSCR1 overexpression or calcineurin inhibition in aged flies ameliorates APP-med

128 Accordingly, in vivo calcineurin inhibition leads the most self-reactive naiv

129 disease, with proposed mechanisms including calcineurin inhibition, induction of autophagy, and redu

130 [AOR], 6.23; P = .03) and discontinuation of calcineurin inhibitor (AOR, 5.11; P = .02) were independ

131 ntly associated with longer exposure to high calcineurin inhibitor (CNI) concentrations (hazard ratio

132 Interestingly, the calcineurin inhibitor (CNI) cyclosporine A (CsA), an imm

133 aracterization of the HNF1B expression after calcineurin inhibitor (CNI) exposure.

134 T, with particular emphasis on the choice of calcineurin inhibitor (CNI) immunosuppressive therapy.

135 en used in liver transplantation to overcome calcineurin inhibitor (CNI) nephrotoxicity but the evide

136 to 14 weeks after transplant to convert from calcineurin inhibitor (CNI) to everolimus or remain on s

137 new immunosuppression strategies to minimize calcineurin inhibitor (CNI) toxicity while effectively p

138 the setting of solid-organ transplantation, calcineurin inhibitor (CNI)-based therapy remains the co

139 e-arm, 2-step prospective trial of bottom-up calcineurin inhibitor (CNI)-free de novo immunosuppressi

140 with poor renal response when switching to a calcineurin inhibitor (CNI)-lowered or CNI-free immunosu

141 Finally, beta cell cytotoxicity of the calcineurin inhibitor and immunosuppressant tacrolimus (

142 HD) prophylaxis with PT-Cy with or without a calcineurin inhibitor and mycophenolate.

143 ansplant Everolimus De Novo Study With Early Calcineurin Inhibitor Avoidance trial, where de novo HTx

144 of rapamycin inhibitor and reduced-exposure calcineurin inhibitor does not appear to alter the risk.

145 The calcineurin inhibitor FK506 (tacrolimus) reduced cell de

146 The calcineurin inhibitor FK506 prevented contrast-induced a

147 tor, was suppressed by coincubation with the calcineurin inhibitor FK506, suggesting involvement of D

148 To reduce calcineurin inhibitor immunosuppression and preserve kid

149 for the diagnosis and monitoring of chronic calcineurin inhibitor nephrotoxicity.

150 inhibition of cathepsin K, or treatment with calcineurin inhibitor rescued cells from high-glucose tr

151 ation, has been assessed as a substitute for calcineurin inhibitor therapy after low-to-moderate risk

152 interstitial fibrosis/tubular atrophy versus calcineurin inhibitor therapy.

153 In multivariable analysis, high calcineurin inhibitor trough levels in the month before

154 mozygotes were less likely to report topical calcineurin inhibitor use (OR, 0.16; 95% CI, 0.06-0.42),

155 cy for improving renal function and reducing calcineurin inhibitor use, attenuating cardiac allograft

156 essive weaning protocols, particularly early calcineurin inhibitor withdrawal without lymphocyte-depl

157 115 days posttransplant to convert from CNI (calcineurin inhibitor)/MMF to sirolimus (SRL)/MMF had a

158 4s with the immunosuppressant cyclosporin, a calcineurin inhibitor, robustly inhibited HIV-1 reactiva

159 sus-host disease (GVHD) prophylaxis included calcineurin inhibitor, short-course methotrexate, and me

160 The MSD group received calcineurin inhibitor-based GVHD prophylaxis.

161 prophylaxis, whereas URD recipients received calcineurin inhibitor-based prophylaxis.

162 th the highest remission rates achieved with calcineurin inhibitor-based protocols.

163 wer risk of CMV disease than a standard-dose calcineurin inhibitor-based regimen.

164 Altogether, these results might suggest that calcineurin inhibitor-induced tubular SNAI1 protein cyto

165 ly evident in biopsy specimens obtained from calcineurin inhibitor-treated patients, which might be b

166 28-CD80/86 costimulatory pathway, allows for calcineurin-inhibitor free immunosuppressive therapy in

167 nt of tumor-specific T cell responses due to calcineurin inhibitors (CNI) could contribute to SCC dev

168 The contribution of calcineurin inhibitors (CNI) nephrotoxicity to progressi

169 plantation (LT) is presently based on use of calcineurin inhibitors (CNI), although they are associat

170 such as polyomavirus-associated nephropathy, calcineurin inhibitors (CNI), and genetic factors.

171 esized that conventional immunosuppressives, calcineurin inhibitors (CNi), and mammalian target of ra

172 Tacrolimus (Tac) and Cyclosporine A (CyA) calcineurin inhibitors (CNIs) are 2 effective immunosupp

173 Calcineurin inhibitors (CNIs) are among the most effecti

174 ir effect on renal function in comparison to calcineurin inhibitors (CNIs) defined by measured GFR.

175 Calcineurin inhibitors (CNIs) have failed to improve lon

176 cation of effort in trials assessing topical calcineurin inhibitors and corticosteroids as treatment

177 at least partly related to administration of calcineurin inhibitors and diminution of NETs production

178 al existing immunosuppressive drugs, such as calcineurin inhibitors and mammalian target of rapamycin

179 ng withdrawal of the carcinogenic effects of calcineurin inhibitors and/or their impact on chronic (o

180 The administration of calcineurin inhibitors appeared to play an important rol

181 Calcineurin inhibitors are imperfect long-term maintenan

182 High-dose steroids and calcineurin inhibitors are ineffective in the treatment

183 Calcineurin inhibitors are known to be nephrotoxic.

184 us) are best placed to determine how topical calcineurin inhibitors compare with established clinical

185 Treatment of neurons with the calcineurin inhibitors FK506 or cyclosporin A resulted i

186 ght to explore the architecture of trials of calcineurin inhibitors for atopic eczema to document the

187 he activity of calcineurin was elevated, and calcineurin inhibitors improved contractility and amelio

188 therapeutic target and supports the study of calcineurin inhibitors in acute KD.

189 Calcineurin inhibitors induce nephrotoxicity through poo

190 Calcineurin inhibitors induce production of renin in the

191 Calcineurin inhibitors might be developed to prevent pos

192 ical corticosteroids with or without topical calcineurin inhibitors where inadvisable for topical cor

193 th either topical corticosteroids or topical calcineurin inhibitors) in mild AD cases or the preventi

194 o 100% with regimens using dose increases of calcineurin inhibitors, and 55% with IL-2 antagonists.

195 rly, potentially related to corticosteroids, calcineurin inhibitors, and mechanistic target of rapamy

196 sted of plasma exchanges (PE), high doses of calcineurin inhibitors, and steroids.

197 ion, which is partly explained by the use of calcineurin inhibitors, data on the consequences of acut

198 equired the use of topical steroids, topical calcineurin inhibitors, or other medications within the

199 g all patients that had discontinued topical calcineurin inhibitors, those with the rs1898671 single-

200 with A. fumigatus, as well as the impact of calcineurin inhibitors, through a combination of single-

201 uppression toward lower doses especially for calcineurin inhibitors.

202 ications for immunosuppressive therapy using calcineurin inhibitors.

203 cations, especially glucocorticosteroids and calcineurin inhibitors.

204 nosuppressive agents were antimetabolites or calcineurin inhibitors.

205 rapidly released Gal-3, which was blocked by calcineurin inhibitors.

206 ure to environmental stress, the phosphatase calcineurin inhibits Hcm1 by specifically removing activ

207 Calcineurin is a phosphatase whose primary targets in T

208 Calcineurin is an essential Ca(2+)-dependent phosphatase

209 Calcineurin is known to be critical in cardiac hypertrop

210 inhibitory toward Cki3 kinase activity, and calcineurin is responsible for its dephosphorylation.

211 onstrate a previously unknown specificity of calcineurin isoforms as well as the broader impact of al

212 icle, we demonstrate involvement of specific calcineurin isoforms, protein phosphatase at 14D (Pp2B-1

213 d by a single gene, GmHs1-1, which encodes a calcineurin-like metallophosphoesterase transmembrane pr

214 tion lid above the conserved architecture of calcineurin-like phosphoesterases.

215 rom endoplasmic reticulum stores, leading to calcineurin-mediated dephosphorylation and activation of

216 show that CRTC-1 specifically uncouples AMPK/calcineurin-mediated effects on lifespan from pleiotropi

217 ransmembrane potential and induction of Ca2+/Calcineurin-mediated retrograde signaling.

218 ssed at P0, and combined Foxc2 deletion with calcineurin-Nfat inhibition disrupted early Prox1(hi) en

219 At later stages of blood flow, Foxc2 and calcineurin-Nfat signaling are each required for growth

220 ercoming cellular senescence, which suggests calcineurin-NFAT signaling as a potential target in prev

221 n addition, we defined the role of VEGF/Flk1-Calcineurin-NFAT signaling cascade in the transcriptiona

222 and its knockdown repressed hypertrophy and calcineurin/NFAT activity.

223 fects mitigated by [Ca(2+)]i chelator BAPTA, calcineurin/NFAT inhibitor VIVIT, and TRPC6 channel knoc

224 However, calcineurin/NFAT regulation did not contribute to consti

225 juvenile islets, Ex-4 induced expression of calcineurin/NFAT signaling components as well as target

226 uncharacterized protein CEFIP that modulates calcineurin/NFAT signaling in cardiomyocytes, a finding

227 mice attenuated cardiac oxidative stress and calcineurin/NFAT signaling in diabetic mice.

228 -regulation of NFAT-c2, reflecting increased calcineurin/NFAT signaling in myocyte hypertrophy.

229 K and those associated with Ca(2+) handling, calcineurin/NFAT signaling, insulin signaling, cardiac a

230 i elevation and the ensuing induction of the calcineurin/NFAT, FasL/Fas, and caspase signaling cascad

231 pes were shown by blocking activation of the calcineurin-NFATc1 pathway.

232 stogenesis, and they serve as inhibitors for calcineurin-NFATc1 signaling both in vivo and in vitro.

233 enafil suppressed ET-1-induced activation of calcineurin/NFATc4 signaling pathway and consequent TRPC

234 stimulates TRPC6 expression by activation of calcineurin/NFATc4 signaling pathway, and inhibition of

235 g pathway, and inhibition of PDE5 suppresses calcineurin/NFATc4- mediated TRPC6 expression in PASMCs

236 , we show that the suppression of astrocytic calcineurin/NFATs helps to protect synaptic function and

237 w that the mitogenic effect of Ex-4 requires calcineurin/nuclear factor of activated T cells (NFAT) s

238 Calcineurin/nuclear factor of activated T cells (Nfat) s

239 eractivation in PPR patients upregulates the calcineurin/nuclear factor of activated T cells signalin

240 ing, we examined the effects of CEFIP on the calcineurin/nuclear factor of activated T-cell (NFAT) pa

241 eted by Cdks during the cell cycle, and that calcineurin opposes Fus3 to activate Rga2 and decrease C

242 s prevented by E-64 but not by inhibition of calcineurin or blockade of transient receptor potential

243 Mutants lacking calcineurin, or its client CrzA, displayed normal alkali

244 used to inhibit CaMKIIdeltac, CaMKIIdeltab, calcineurin, or nuclear factor kappaB (NF-kappaB).

245 by decreased intracellular Ca(2+) levels via calcineurin, p38 mitogen-activated protein kinase (MAPK)

246 onclusion, NF-kappaB, and not CaMKIIdelta or calcineurin, partly mediates the Ito,f reductions induce

247 ty was not increased in HCM, suggesting that calcineurin pathway activation is not an upstream cause

248 rate that calcium-mediated activation of the calcineurin pathway acts as a rheostat to shape both the

249 osphorylation in the brain through the RCAN1-calcineurin pathway.

250 ease from intracellular stores and increased calcineurin phosphatase activity, resulting in NFATc1 nu

251 Inhibition of calcineurin phosphatase has been shown to stimulate tran

252 gnalling, demonstrating the functionality of calcineurin/PKC-modified residues.

253 , and the control of Brg1 phosphorylation by calcineurin, PKCbeta1, and p38 regulates the transition

254 the Ca(2+)/calmodulin-dependent phosphatase calcineurin plays a role in DIF-1 signaling to the DimB

255 Calcineurin (PPP3CB) mRNA was not increased, nor was RCA

256 re we investigated the roles of regulator of calcineurin (RCAN) genes in bone homeostasis.

257 A2M gene network that includes regulator of calcineurin (RCAN1), an inhibitor of calcineurin, a well

258 We here report that SOCE and calcineurin regulate cell cycle entry of quiescent T cel

259 physiological and molecular similarities to calcineurin-regulated activity-dependent bulk endocytosi

260 We further demonstrate that calcineurin regulates CXCR4 cell-surface expression in a

261 Calcineurin regulates Dig2 and Rod1/Art4 to inhibit mati

262 Calcineurin regulates size recovery by controlling the a

263 this issue, Wang et al. demonstrate that the calcineurin regulator Down syndrome critical region 1 pr

264 Moreover, we identified the calcineurin regulator Rcn2, the 4E-BP (translation initi

265 Here we demonstrate that activation of calcineurin requires Mid1, an endoplasmic reticulum-loca

266 pregulation of Nebula/DSCR1, an inhibitor of calcineurin, rescues APP-induced memory defects in young

267 We also show that the calcineurin-responsive transcription factor Crz1 undergo

268 n (FDA)-approved compound Tacrolimus, blocks calcineurin's activity toward those proteins and protect

269 In adult myocytes, the calcineurin sensors appear to be localized to the cardia

270 miR-30s also regulated calcium/calcineurin signaling in cardiomyocytes.

271 Calcium/calcineurin signaling is critical for normal cellular ph

272 isms that underlie the regulation of calcium/calcineurin signaling is essential.

273 The ensuing Ca(2+) entry then activates NFAT/calcineurin signaling to induce transcriptional producti

274 e showed that critical components of calcium/calcineurin signaling, including TRPC6, PPP3CA, PPP3CB,

275 membrane depolarization, calcium influx, and calcineurin signaling.

276 tant allows myogenesis despite inhibition of calcineurin signalling, demonstrating the functionality

277 chy governing alkaline tolerance circumvents calcineurin signalling.

278 eractivation, which leads to Hsp90-dependent calcineurin stabilization and thereby increased azole re

279 in (GAP) for the Cdc42 Rho-type GTPase, as a calcineurin substrate.

280 Epithelial calcineurin supports the survival and proliferation of c

281 relaxation, promotes nuclear localization of calcineurin target Nfatc3, and/or affects expression of

282 nds on opposing functions of the phosphatase calcineurin (TAX-6), and of the casein kinase II homolog

283 Calcineurin, the conserved Ca(2+)/calmodulin-activated p

284 Calcineurin, the conserved Ca(2+)/calmodulin-regulated p

285 ygen species that signal to Mid1 to activate calcineurin, thereby inhibiting the GAAC response and au

286 ation to develop antifungal agents targeting calcineurin to deploy against Mucor and other pathogenic

287 cardiac dilation and improves survival in a calcineurin transgenic mouse model, indicating that COUP

288 Cyclosporin A, which inhibits calcineurin upstream of NFATc1, blocked BMP-2-induced NF

289 Calcineurin was also reduced in Q111 compared with Q7 ce

290 mic reticulum was increased, the activity of calcineurin was elevated, and calcineurin inhibitors imp

291 Here we found that calcineurin was recruited to the T cell antigen receptor

292 xtrarenal tissues, and whether inhibition of calcineurin was required.

293 ng of either PKA or the opposing phosphatase calcineurin, we found that CP-AMPARs are recruited to hi

294 ppressive drug that inhibits the phosphatase calcineurin when bound to the 12 kDa FK506-binding prote

295 eover, we show that eCB-tLTD requires active calcineurin whereas eCB-tLTP necessitates the activity o

296 e associated with constitutive activation of calcineurin, whereas nuclear translocation of NFAT is as

297 tive muscle metabolism through activation of calcineurin, which likely confers the protective effect.

298 d intracellular Ca(2+) in the NG, activating calcineurin, which, in turn, bound to an nuclear factor

299 he functional interaction between FKBP12 and calcineurin, with low doses of the Food and Drug Adminis

300 Precisely how TORC2-Ypk1 signaling regulates calcineurin within this pathway remains unknown.