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1 oire of protein targets well beyond mTOR and calcineurin.
2  signaling pathway involving the phosphatase calcineurin.
3 by Galphai/o, novel PKC isoforms, or calcium-calcineurin.
4 x to promote its activation by AKAP-anchored calcineurin.
5 tive feedback loop mediated through CAST and calcineurin.
6 ritical for binding and inhibition of fungal calcineurin.
7 CA encodes the alpha isoform of a subunit of calcineurin.
8 m response factor and the signaling effector calcineurin.
9 d with gene and protein expression levels of calcineurin.
10  dependence of the CaM-dependent phosphatase calcineurin.
11 ia IP(3) and ryanodine receptors to activate calcineurin.
12 creased mRNA of the Nfat target regulator of calcineurin 1.
13  postnatal splicing transitions of the three calcineurin A genes, calcium-dependent phosphatases that
14                       Redirected splicing of calcineurin A to the fetal isoforms in adult muscle and
15       We examined the roles of 2 homologs of Calcineurin A, CanA14F, and Pp2B in the Drosophila cardi
16         Here, we demonstrate that activating calcineurin, a calcium-dependent phosphatase, following
17  that can mediate the induction of ATF4, and calcineurin, a calcium-dependent regulator of NFAT, syne
18                                              Calcineurin, a conserved protein from yeast to humans, i
19 TR is dependent on CFTR dephosphorylation by calcineurin, a protein phosphatase that is upregulated b
20 ator of calcineurin (RCAN1), an inhibitor of calcineurin, a well-characterized tau phosphatase.
21 of pathological myocyte hypertrophy, despite calcineurin Aalpha expression in the same cells.
22                            Overexpression of calcineurin Abeta1 in TMEM43 mutant mice or chemical GSK
23 expression of the calcineurin splice variant calcineurin Abeta1 results in GSK3beta inhibition and im
24 We have recently discovered that TCR-induced calcineurin activates DAPK1, which interacts with TSC2 v
25                 Dephosphorylation of CrzA by calcineurin activates the TF, but the specific phosphory
26 gh NMDA and AMPA mediated calcium influx and calcineurin activation to then oppose further membrane d
27 arization signals, both processes relying on calcineurin activation.
28 red myocytes revealed that Ca(2+) levels and calcineurin activity associated with the CIP4 compartmen
29 aused myofibril disarray, whereas inhibiting Calcineurin activity attenuated FoxO-mediated murf1 expr
30 FAT transcription factors, and inhibition of calcineurin activity by treatment with cyclosporin A (Cs
31                Conversely, Ca(2+) levels and calcineurin activity detected by nonlocalized Forster re
32                                              Calcineurin activity impaired Orm2 export from the endop
33 sfer reporters were used to assay Ca(2+) and calcineurin activity in living cells.
34 te whether FKBP12 plays a role in regulating calcineurin activity in the absence of Tacrolimus.
35                                    Increased calcineurin activity is associated with alpha-synuclein
36       Thus, FKBP12 can endogenously regulate calcineurin activity with therapeutic implications for t
37 acrolimus is an inhibitor of the phosphatase calcineurin, an action shared with cyclosporine.
38                                              Calcineurin anchoring by AKAPs confers specificity to ca
39  first to identify cross-talk between Ca(2+)/calcineurin and Cdc42 signaling and to demonstrate modul
40 els appears to be independent of calmodulin, calcineurin and endocytic pathways.
41 eased cytoplasmic Ca(2+) load that activates calcineurin and induces the second phasic Drp1-dependent
42                    Calcium signaling through calcineurin and its major transcription factor (TF), Crz
43       Pharmacologic or genetic inhibition of calcineurin and NFAT signaling reverses the effects of p
44                            TOX is induced by calcineurin and NFAT2, and operates in a feed-forward lo
45  and tumour cell proliferation by inhibiting calcineurin and NFATc3 activation in mouse and human set
46 h selectively blocks the interaction between calcineurin and NFATc3, through computational and medici
47  this was accompanied with the activation of calcineurin and subsequent translocation of NFATc4 to th
48 a(2+)-sensitive interface between AKAP79 and calcineurin, and increases resting cellular PKA phosphor
49 2+)-dependent signaling molecules, including calcineurin, and inhibition of SOCE or calcineurin impai
50 hospholipase Cbeta, protein kinase Cepsilon, calcineurin, and phospholamban.
51 lar chaperone Hsp90, the protein phosphatase calcineurin, and the small GTPase Ras1, as well as with
52 e CDI whereas recruitment of the phosphatase calcineurin antagonizes the effect of PKA.
53                              Drugs targeting calcineurin are potent antifungal agents but also pertur
54                       This report implicates calcineurin as an intracellular signaling molecule respo
55 SK3beta inhibition bypassed the calreticulin/calcineurin axis and increased osteoblast output from bo
56           By creating a SC conditional KO of calcineurin B (CnB(scko)), we assessed the effects of Cn
57 neurin in ALL and observed that depletion of calcineurin B (CnB) in leukemia cells dramatically prolo
58 reens and unbiased lipidomics, we identified calcineurin B homologous protein 1 (CHP1) as a major reg
59                           The families of 10 Calcineurin B-Like (CBL) calcium sensors and 26 CBL-Inte
60 with CIPK23 requires kinase activity and the calcineurin B-like binding protein CBL1.
61 for plants, it remained unknown if, and how, calcineurin B-like calcium sensors (CBLs) and CBL-intera
62        Using a genetic screen, we found that CALCINEURIN B-LIKE INTERACTING PROTEIN KINASE23 (CIPK23)
63                         In this pathway, the CALCINEURIN B-LIKE10 (AtCBL10) calcium sensor interacts
64 Calcium-dependent protein kinases (CPKs) and calcineurin-B-like proteins (CBLs) can sense and transla
65 interval 1.09-2.41; P < 0.02) and the use of calcineurin-based therapy maintenance therapy (hazard ra
66 reens revealed that CEFIP interacts with the calcineurin-binding protein four and a half LIM domains
67                             Mutations of the calcineurin-binding sites in the channel (PQAAAS-AQAP) d
68                                 Furthermore, calcineurin blockade synergized with BCL-2 and MCL-1 inh
69   Further study indicated that inhibition of calcineurin by cyclosporine A or knockdown of NFATc4 usi
70                                Inhibition of calcineurin by FK506 results in an increase in the net p
71                                              Calcineurin can be inhibited with Tacrolimus through the
72  and recent literature has demonstrated that calcineurin can regulate autophagy via dephosphorylation
73 lin-dependent protein kinase II (CaMKII) and calcineurin (CaN) both bind open calmodulin, favoring Lo
74 ganglion neurons, becomes dysfunctional upon calcineurin (CaN) inhibition.
75                                              Calcineurin (CaN) phosphatase signaling is regulated by
76  we investigated the role of the phosphatase calcineurin (CaN) using electrophysiological, molecular,
77   The calcium-dependent protein phosphatase, calcineurin (CaN), has been implicated in both the conso
78 rylation by the Ca(2+)-dependent phosphatase calcineurin (CaN).
79 2+)/calmodulin-dependent protein phosphatase calcineurin (CaN, PP2B, and PPP3).
80                               Therefore, the calcineurin cascade is an attractive target in drug deve
81     Here we report the crystal structures of calcineurin catalytic (CnA) and regulatory (CnB) subunit
82 ained paradox is how the beta isoform of the calcineurin catalytic A-subunit (CaNAbeta) is required f
83                            Variants near the calcineurin catalytic subunit gamma gene PPP3CC and the
84             We found that knockdown of these calcineurin catalytic subunits caused cardiac restrictio
85 ng pathway (MtRS) involving Ca(+2)-sensitive Calcineurin (Cn) activation as an immediate upstream eve
86                                              Calcineurin (Cn) is a calcium-activated serine/threonine
87 RBLE-pep, we systematically probe binding of calcineurin (CN), a conserved protein phosphatase essent
88 ng the calcium-activated Ser/Thr phosphatase calcineurin (CN), and its downstream target nuclear fact
89 sis, is regulated by the Ser/Thr phosphatase calcineurin (CN).
90 overy to elucidate the regulatory network of calcineurin (CN)/PP2B, the Ca(2+)-activated phosphatase
91      PPP3R1 is the regulatory subunit of the calcineurin complex.
92                                       Fungal calcineurin complexes are similar to the mammalian compl
93           In eukaryotic microbial pathogens, calcineurin controls essential virulence pathways, such
94  Rcr1, but not Rcr2, is up-regulated via the calcineurin/Crz1 signaling pathway.
95  kinase activation, Ca(2+) mobilization, and calcineurin-dependent activation of NFAT, the master tra
96                           This was caused by calcineurin-dependent dephosphorylation of Orm2, a repre
97  K(+) current to the resting state after the calcineurin-dependent dephosphorylation of TRESK.
98 on of glial Ca(2+) causes hyperactivation of calcineurin-dependent endocytosis and accumulation of ea
99 d that CEFIP overexpression further enhances calcineurin-dependent hypertrophic signal transduction,
100     We earlier reported that the Ca(2+)- and calcineurin-dependent MtRS induces macrophage differenti
101  induction of the IP-10 gene was mediated by calcineurin-dependent NFAT signaling in pancreatic beta-
102   We show that FKBP12 profoundly affects the calcineurin-dependent phosphoproteome, promoting the dep
103 increase of cholinergic synapses and a TAX-6/calcineurin-dependent reduction of GABA synapses.
104                  The TRESK component confers calcineurin-dependent regulation to the heterodimer and
105  the in vivo relevance of HDAC1 and identify calcineurin-dependent serine dephosphorylation as the si
106 in the activated state of TRESK (i.e., after calcineurin-dependent stimulation) than in the resting s
107 al context for this regulation and show that calcineurin dephosphorylates and positively regulates Rg
108 at the calcium-activated protein phosphatase calcineurin dephosphorylates Hoxb13 at serine-204, resul
109 2 mutant that is defective for regulation by calcineurin display increased gene expression in respons
110                                      Whether calcineurin/FKBP12 represents a native physiologically r
111 m/calmodulin-dependent phosphatase 2B (PP2B, calcineurin) focuses and insulates termination of local
112 ggest that leukemia cells are dependent upon calcineurin for immune evasion by restricting the regula
113 disrupts myofibril integrity by activating a Calcineurin-FoxO-MuRF1-proteosome signaling pathway.
114 in anchoring by AKAPs confers specificity to calcineurin function in the cardiac myocyte.
115                   Although WNT signaling and calcineurin have been implicated separately in muscle re
116 uding calcineurin, and inhibition of SOCE or calcineurin impairs antigen-dependent T cell proliferati
117 activating the calcium-activated phosphatase calcineurin in a Ca(2+)/calmodulin-dependent manner, pre
118          We sought to understand the role of calcineurin in ALL and observed that depletion of calcin
119           Our results suggest a key role for calcineurin in cardiac remodeling during long-term hypox
120 iscuss the current knowledge on the roles of calcineurin in eukaryotic microbial pathogens, focusing
121 which is dephosphorylated by the phosphatase calcineurin in MG cells.
122                                          SNO-Calcineurin in mutant led to a significant increase of p
123   However, little is known about the role of calcineurin in promyelinating SCs after birth.
124 stic understanding of the role of endogenous calcineurin in regulating synaptic plasticity and nocice
125    Finally, this paper clarifies the role of calcineurin in Schwann cells and myelination.
126   In contrast, we did find a unique role for calcineurin in SCs after nerve injury.
127 oupling while not stimulating hypertrophy by calcineurin in the normal heart.
128 rast, the mutations of the target residue of calcineurin in TRESK, S264A, and S264E prevented the eff
129 s in a feed-forward loop in which it becomes calcineurin-independent and sustained in T(ex) cells.
130 of TRESK at the regulatory residue S264 in a calcineurin-independent manner.
131 efined may represent novel targets to reduce calcineurin induced nephrotoxicity.
132 uclear calpain 1, by cleaving and activating calcineurin, induces NFIB dephosphorylation.
133 functional driver of ABC DLBCL and highlight calcineurin inhibition as a novel strategy for the treat
134                               We showed that calcineurin inhibition enhances physical interaction bet
135                                     Although calcineurin inhibition increases NMDAR activity in the s
136                         Accordingly, in vivo calcineurin inhibition leads the most self-reactive naiv
137  activated in both DLBCL subtypes, long-term calcineurin inhibition with cyclosporin A or FK506, both
138                           Interestingly, the calcineurin inhibitor (CNI) cyclosporine A (CsA), an imm
139 d the association of optimal-dose mTORi with calcineurin inhibitor (CNI) have excluded hypersensitize
140 d the association of optimal-dose mTORi with Calcineurin Inhibitor (CNI) have excluded hypersensitize
141 ipients with renal dysfunction attributed to calcineurin inhibitor (CNI) nephrotoxicity.
142                           As conversion from calcineurin inhibitor (CNI) to sirolimus (SRL), an mTOR-
143 -1a) cells, which were highly sensitive to a calcineurin inhibitor (CNI), while co-stimulation of TLR
144 kidney (SPK) recipients were randomized to a calcineurin inhibitor (CNI)-based immunosuppressive regi
145 dy sought to examine whether conversion from calcineurin inhibitor (CNI)-based to SRL-based IS was as
146                                            A calcineurin inhibitor (CNI)-free immunosuppressive regim
147 with poor renal response when switching to a calcineurin inhibitor (CNI)-lowered or CNI-free immunosu
148 mbination of mycophenolates (MMF/MPA) with a calcineurin inhibitor (CNI).
149 ) and graft-versus-host disease prophylaxis (calcineurin inhibitor and mycophenolate).
150 ansplant Everolimus De Novo Study With Early Calcineurin Inhibitor Avoidance trial, where de novo HTx
151 tics and concurrent graft function and blood calcineurin inhibitor concentration.
152 clinically available, we recommend to adjust calcineurin inhibitor dose according to whole blood trou
153          If nephrotoxicity is suspected, the calcineurin inhibitor dose should be reduced.
154 nsistently, AMPA receptor antagonist CNQX or calcineurin inhibitor FK506 abolished the S-SCAM overexp
155 to analyze this association exploring median calcineurin inhibitor levels and intrapatient variabilit
156 ment of dnDSA in 69 LT patients who received calcineurin inhibitor monotherapy and were enrolled in t
157 inhibition of cathepsin K, or treatment with calcineurin inhibitor rescued cells from high-glucose tr
158        Treatment with sirolimus, but not the calcineurin inhibitor tacrolimus, at levels routinely ac
159 ive patients were treated with conversion of calcineurin inhibitor to mammalian target of rapamycin i
160                           As conversion from calcineurin inhibitor to sirolimus (SRL), a mechanistic
161 mozygotes were less likely to report topical calcineurin inhibitor use (OR, 0.16; 95% CI, 0.06-0.42),
162 nt included antimetabolite withdrawal (68%), calcineurin inhibitor withdrawal (23%), hydroxychloroqui
163 herapy (steroids, mycophenolate mofetil, and calcineurin inhibitor).
164 4s with the immunosuppressant cyclosporin, a calcineurin inhibitor, robustly inhibited HIV-1 reactiva
165 th the highest remission rates achieved with calcineurin inhibitor-based protocols.
166               alpha2delta-1 is essential for calcineurin inhibitor-induced aberrant activation of pre
167                                              Calcineurin inhibitor-induced neurotoxicity (CIIN) is a
168 ting alpha2delta-1-NMDAR interaction reduces calcineurin inhibitor-induced pain hypersensitivity.
169  neurons or alpha2delta-1 KO also attenuates calcineurin inhibitor-induced pain hypersensitivity.
170 re pain in patients, commonly referred to as calcineurin inhibitor-induced pain syndrome (CIPS).
171 cate that alpha2delta-1-bound NMDARs mediate calcineurin inhibitor-induced tonic activation of presyn
172 Altogether, these results might suggest that calcineurin inhibitor-induced tubular SNAI1 protein cyto
173 ly evident in biopsy specimens obtained from calcineurin inhibitor-treated patients, which might be b
174 c anti-inflammatory drug Tacrolimus (TAC), a calcineurin inhibitor.
175 28-CD80/86 costimulatory pathway, allows for calcineurin-inhibitor free immunosuppressive therapy in
176 ors probably reduced skin cancer compared to calcineurin inhibitors (12 trials, 2225 participants, RR
177 and safety of belatacept when converted from calcineurin inhibitors (CNI) in HLA-sensitized (HS) kidn
178 and safety of belatacept when converted from calcineurin inhibitors (CNI) in HLA-sensitized kidney tr
179 such as polyomavirus-associated nephropathy, calcineurin inhibitors (CNI), and genetic factors.
180                         The long-term use of calcineurin inhibitors (CNIs) after liver transplantatio
181                                              Calcineurin inhibitors (CNIs) are among the most effecti
182                     Maintenance steroids and calcineurin inhibitors (CNIs) at discharge were associat
183 pressive regimen mostly relies on converting calcineurin inhibitors (CNIs) into EVL.
184  been partially attributed to treatment with calcineurin inhibitors (CNIs).
185 mplementation of this strategy to avoid both calcineurin inhibitors and corticosteroids at this time.
186 mitigate early rejection risk while limiting calcineurin inhibitors and corticosteroids.
187 rity and responsiveness to topical steroids, calcineurin inhibitors and step-up treatment.
188 es are limited by toxicities associated with calcineurin inhibitors and steroids.
189                            Nephrotoxicity of calcineurin inhibitors and uncontrolled effector functio
190                     The antitumor effects of calcineurin inhibitors are associated with the reduced e
191 e development of CIPS.SIGNIFICANCE STATEMENT Calcineurin inhibitors are immunosuppressants used to pr
192 an HEart transplant De-novo stUdy with earLy calcineurin inhibitors avoidancE trial was a prospective
193 an HEart transplant De-novo stUdy with earLy calcineurin inhibitors avoidancE trial was the first ran
194     Until measurement of unbound fraction of calcineurin inhibitors becomes clinically available, we
195  understanding the association between early calcineurin inhibitors exposure post-liver transplantati
196                    Likewise, alternatives to calcineurin inhibitors have been investigated as a strat
197                                              Calcineurin inhibitors have shown evidence to promote ca
198                                              Calcineurin inhibitors induce nephrotoxicity through poo
199                                       Use of calcineurin inhibitors is associated with HTN.
200                                      Topical calcineurin inhibitors may be used in steroid-dependent/
201 atacept, induction agents, and withdrawal of calcineurin inhibitors or corticosteroids).
202                                              Calcineurin inhibitors successfully control rejection of
203                           CKD was related to calcineurin inhibitors toxicity in 38 (84.4%) cases.
204                          Antimetabolites +/- calcineurin inhibitors were held or reduced.
205 ical corticosteroids with or without topical calcineurin inhibitors where inadvisable for topical cor
206 th either topical corticosteroids or topical calcineurin inhibitors) in mild AD cases or the preventi
207 r monoclonal antibodies, 28% did not receive calcineurin inhibitors, and 36% did not receive steroids
208 opical corticosteroids, vitamin D analogues, calcineurin inhibitors, and keratolytics.
209 sted of plasma exchanges (PE), high doses of calcineurin inhibitors, and steroids.
210   For decades, GVHD prophylaxis has included calcineurin inhibitors, despite their incomplete efficac
211 llograft rejection without using steroids or calcineurin inhibitors, enriches for naive cells suscept
212 egimes (azathioprine, mycophenolate mofetil, calcineurin inhibitors, mammalian target of rapamycin [m
213 equired the use of topical steroids, topical calcineurin inhibitors, or other medications within the
214                                              Calcineurin inhibitors, such as tacrolimus (FK506) and c
215 g all patients that had discontinued topical calcineurin inhibitors, those with the rs1898671 single-
216 rapidly released Gal-3, which was blocked by calcineurin inhibitors.
217 nosuppressive agents were antimetabolites or calcineurin inhibitors.
218 nteract with immunosuppressive drugs such as calcineurin inhibitors.
219  The Ca(2+)/calmodulin-dependent phosphatase calcineurin is a key regulator of cardiac myocyte hypert
220 ous Ca(2+) /calmodulin-dependent phosphatase calcineurin is a key regulator of pathological cardiac h
221                                              Calcineurin is a phosphatase whose primary targets in T
222                                              Calcineurin is an essential Ca(2+)-dependent phosphatase
223                                              Calcineurin is cleaved and activated by calpain protease
224                                              Calcineurin is cleaved and thereby activated by calpain
225                                              Calcineurin is important for fungal virulence and a pote
226                                              Calcineurin is known to be critical in cardiac hypertrop
227             Together, our data indicate that calcineurin is not essential for myelination but has a n
228                                              Calcineurin is targeted to diverse intracellular compart
229 onstrate a previously unknown specificity of calcineurin isoforms as well as the broader impact of al
230 n cue-induced reinstatement, suggesting that calcineurin may be a potential therapeutic target for re
231 the nucleus 3 d after crush, suggesting that calcineurin may regulate autophagy in SCs via TFEB activ
232 rom endoplasmic reticulum stores, leading to calcineurin-mediated dephosphorylation and activation of
233 ut mediated by an increased calcium flux and calcineurin-mediated dephosphorylation of NFAT.
234 ssed at P0, and combined Foxc2 deletion with calcineurin-Nfat inhibition disrupted early Prox1(hi) en
235 ricytes in APOE4-mediated CAA and highlights calcineurin-NFAT signaling as a therapeutic target in CA
236 as inositol phosphate-mediated signaling and calcineurin-NFAT signaling cascade as important biologic
237 ricytes of APOE4 carriers, and inhibition of calcineurin-NFAT signaling reduces APOE4-associated CAA
238  and its knockdown repressed hypertrophy and calcineurin/NFAT activity.
239 neage where it mediates proper regulation of calcineurin/NFAT signaling and COX-2 expression.
240  juvenile islets, Ex-4 induced expression of calcineurin/NFAT signaling components as well as target
241 -regulation of NFAT-c2, reflecting increased calcineurin/NFAT signaling in myocyte hypertrophy.
242 K and those associated with Ca(2+) handling, calcineurin/NFAT signaling, insulin signaling, cardiac a
243  mechanistic investigation revealed impaired calcineurin/NFATc1 activation and decreased COX-2 expres
244 l experiments revealed that dysregulation of calcineurin-nuclear factor of activated T cells (NFAT) s
245 w that the mitogenic effect of Ex-4 requires calcineurin/nuclear factor of activated T cells (NFAT) s
246                                              Calcineurin/nuclear factor of activated T cells (Nfat) s
247 eted by Cdks during the cell cycle, and that calcineurin opposes Fus3 to activate Rga2 and decrease C
248  structural responses to NPY or CRF required calcineurin or CaMKII, respectively.
249 t groups, older age, less physical activity, calcineurin or mammalian target of rapamycin inhibitor-b
250                              Mutants lacking calcineurin, or its client CrzA, displayed normal alkali
251 by decreased intracellular Ca(2+) levels via calcineurin, p38 mitogen-activated protein kinase (MAPK)
252 rate that calcium-mediated activation of the calcineurin pathway acts as a rheostat to shape both the
253 cells enhanced downstream factors in the BCR-calcineurin pathway, including a nuclear factor of activ
254 osphorylation in the brain through the RCAN1-calcineurin pathway.
255 ds on the NFI phosphorylation state and that calcineurin phosphatase dephosphorylates and activates N
256  the IDR results in CR defects and abolishes calcineurin phosphatase localization to the CR.
257 epsilon The effect of PKC is not mediated by calcineurin phosphatase, which is known to evoke the cal
258   These results suggest that, in addition to calcineurin, PKC regulates TRESK by changing the phospho
259 , and the control of Brg1 phosphorylation by calcineurin, PKCbeta1, and p38 regulates the transition
260             Male mice lacking sperm-specific calcineurin (PP2B), a calcium regulated phosphatase, in
261 s based on an isoform-specific mechanism for calcineurin protein-protein interaction and localization
262  A2M gene network that includes regulator of calcineurin (RCAN1), an inhibitor of calcineurin, a well
263                 We here report that SOCE and calcineurin regulate cell cycle entry of quiescent T cel
264                                              Calcineurin regulates Dig2 and Rod1/Art4 to inhibit mati
265         Furthermore, we show that the enzyme calcineurin regulates Kv2.1 ion channel clustering statu
266                                   The enzyme calcineurin regulates Kv2.1 ion channel declustering.
267 ort (including the alpha4 nAChR subunit, the calcineurin regulator RCAN3, and KIF1C of the kinesin fa
268 , mechanistic target of rapamycin (mTOR) and calcineurin, respectively.
269                        We also show that the calcineurin-responsive transcription factor Crz1 undergo
270  by the protein phosphatases PP-1 and PP-2B (calcineurin) reverses this effect.
271 n (FDA)-approved compound Tacrolimus, blocks calcineurin's activity toward those proteins and protect
272 ors against the upstream protein phosphatase calcineurin should be effective for prevention/treatment
273 intracellular compartmentation of Ca(2+) and calcineurin signal transduction.
274 ene delivery in the mouse were used to study calcineurin signaling after transverse aortic constricti
275                                          The calcineurin signaling cascade is one of the major pathwa
276 lin-1 Type III has been proposed to activate calcineurin signaling in immature SCs to initiate differ
277                CNI103 specifically inhibited calcineurin signaling in vitro and in vivo and exhibited
278                                              Calcineurin signaling is a key pathway underlying fibrob
279  cross-talk between NFI and the CAST/calpain/calcineurin signaling pathway in MG cells.
280 he mechanisms conferring this selectivity in calcineurin signaling should reveal new strategies for t
281  N-methyl-D-aspartate receptors coupled with calcineurin signaling, induces t-LTD which is sensitive
282 pression of the receptor TGF-betaRII through calcineurin signaling.
283 chy governing alkaline tolerance circumvents calcineurin signalling.
284                                 Targeting of calcineurin 'signalosomes' may provide a rationale for i
285 ficial effect, whereas overexpression of the calcineurin splice variant calcineurin Abeta1 results in
286 eractivation, which leads to Hsp90-dependent calcineurin stabilization and thereby increased azole re
287 l antifungal target, but compounds targeting calcineurin, such as FK506, are immunosuppressive.
288 relaxation, promotes nuclear localization of calcineurin target Nfatc3, and/or affects expression of
289                                              Calcineurin, the conserved Ca(2+)/calmodulin-activated p
290 indicating that NFI activity is regulated by calcineurin, these results provide a foundation for furt
291 ls must exist to permit catalytically active calcineurin to function during epididymal sperm maturati
292 which signals danger via TRPV4, calcium, and calcineurin to initiate allergic sensitization.
293 tory cross-talk between the ESCRT machinery, calcineurin/TORC2 signaling, and the EGAD pathway import
294  the Ca(2+)/calmodulin-dependent phosphatase calcineurin toward nuclear factor of activated T-cells (
295                           Here we found that calcineurin was recruited to the T cell antigen receptor
296                       Calreticulin activates calcineurin, which dephosphorylates and induces the nucl
297 Ca(2+) influx resulting in the activation of calcineurin, which in turn activates TFEB, the master re
298 w that TPC-released Ca(2+) rapidly activates calcineurin, which in turn dephosphorylates and activate
299 he functional interaction between FKBP12 and calcineurin, with low doses of the Food and Drug Adminis
300 ich triggers a calcium flux signaled through calcineurin within club cells of the bronchioles, inciti

 
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