ライフサイエンスコーパス: NFAT

1 NFAT (the nuclear factor of activated T cells) upregulat

2 NFAT activity is required for ECM stimulation by TGF-bet

3 NFAT proteins are important TCR and Ca(2+)-dependent reg

4 NFAT transcription factors control the proliferation and

5 NFAT was activated by SCF in bone marrow-derived mast ce

6 NFAT-activated gene expression, triggered in response to

7 NFAT-dependent gene expression is essential for the deve

8 We revealed more than 170 NFAT-associated proteins, half of which are involved in

9 eptor-related orphan receptors on the Ca(2+)-NFAT pathway.

10 n sustaining T cell receptor-mediated Ca(2+)-NFAT signaling and effector functions by repressing sarc

11 Rankl expression, in which JNK and/or Ca(2+)/NFAT pathways were involved and therefore were engaged i

12 h cell differentiation by controlling Ca(2+)/NFAT signaling, but its requirement in CD8(+) T cell res

13 ned the ability to flux calcium and activate NFAT-transcription-factor-dependent cytokine production.

14 ucidate the pathway by which G1 can activate NFAT luciferase.

15 contrast, only 3 of 5 were able to activate NFAT (nuclear factor of activated T cells); chimpanzee a

16 utan BILF1 molecules were unable to activate NFAT.

17 ort that the paralog Orai3 fails to activate NFAT.

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

19 tion, rendering it ineffective in activating NFAT.

20 Although NFAT is mostly known for its transcription function in t

21 yte-specific GRK5 overexpression activate an NFAT-reporter in mice basally and after hypertrophic sti

22 Overall, these findings elucidate an NFAT-MAPK signaling paradigm for induction of isletokine

23 and proliferation of cancer stem cells in an NFAT-dependent manner and promotes the development of in

24 uired for NK cell IFN-gamma production in an NFAT-dependent manner, NK cell degranulation/cytotoxicit

25 d that the transcription factors Smad2/3 and NFAT-1 are two critical regulators of this process.

26 equired for TCR-triggered p38 activation and NFAT-dependent expression of proinflammatory cytokines,

27 result in long-lasting calcium activity and NFAT translocation, a measure of full T-cell activation.

28 We demonstrate that calcineurin and NFAT factors are constitutively expressed by primary IEC

29 demonstrate an active involvement of CN- and NFAT-mediated signalling pathway in alpha-syn-mediated d

30 , CsA inhibited integrin-LFA-1-dependent and NFAT-independent adhesion of T cells to the intercellula

31 in CLL, where excess programming by EGR and NFAT with reduced EBF and AP-1 programming imbalances th

32 Further, ACK1 promoted calcium flux and NFAT-AP1 promoter activity and decreased the motility of

33 Although c-fos and NFAT often interact to activate gene expression synergis

34 regulatory T (Treg) cells was increased and NFAT-deficient Tregs were fully protective in GvHD.

35 tor engagement for maximal Ca(2+) influx and NFAT activation.

36 vation of the transcription factors JunB and NFAT.

37 ations driving increased MAPK, NF-kappaB and NFAT activity upon T cell receptor stimulation.

38 lls exhibit hyperactivation of NF-kappaB and NFAT and produce increased levels of IL-2 compared with

39 ed transcriptional activity of NF-kappaB and NFAT, resulting in increased IL-6 and TNF production fol

40 ines and readouts dependent on NF-kappaB and NFAT.

41 ent nuclear translocation of pGFP-NFAT1, and NFAT-dependent but not NFkappaB-dependent gene expressio

42 cription, but interactions between Notch and NFAT are understood poorly.

43 nt for consensus binding motifs for Nr4a and NFAT transcription factors.

44 t7a induced both canonical Wnt signaling and NFAT and Akt non-canonical signaling.

45 pidermal wound healing, LPA induces SOCE and NFAT activation through Orai1 channels and promotes cell

46 ke phenotype involves remodeling of SOCE and NFAT signaling, which together control the expression of

47 trigger store-operated Ca2+ entry (SOCe) and NFAT nuclear accumulation.

48 or (CTGF), E-cadherin, SRY-box 7 (SOX7), and NFAT (nuclear factor of activated T cells) kinase dual-s

49 transcription factors phosphorylated SP1 and NFAT were master regulators promoting or inhibiting EMT,

50 otifs and had high co-occupancy of STAT5 and NFAT transcription factors (TFs).

51 at nevertheless enhanced anti-CD3-driven AP1/NFAT transcription and IL-2 production.

52 ed self-association and anti-CD3 induced AP1/NFAT transcription.

53 phatase whose primary targets in T cells are NFAT transcription factors, and inhibition of calcineuri

54 Participants: Participants with benign NFATs ("exposed"; n = 166) and those with no adrenal tum

55 e reciprocal regulatory relationship between NFAT proteins and p53 pathway.

56 No significant associations between NFATs and other outcomes were observed.

57 ary analyses evaluated relationships between NFATs and cortisol physiology.

58 Calcineurin-NFAT (nuclear factor of activated T-cells) signaling was

59 phy through a cross-talk between calcineurin-NFAT and IKK-NFkappaB pathways.

60 we defined the role of VEGF/Flk1-Calcineurin-NFAT signaling cascade in the transcriptional regulation

61 data indicate that inhibition of calcineurin-NFAT drives proliferation of megakaryocyte precursors by

62 To investigate the role of calcineurin-NFAT in megakaryopoiesis, we examined wild-type mice tre

63 s several negative regulators of calcineurin-NFAT, candidates in the pathogenesis of Down syndrome (t

64 onse was associated with reduced calcineurin-NFAT activity.

65 lular senescence, which suggests calcineurin-NFAT signaling as a potential target in preventing PCa.

66 s, followed by activation of the calcineurin-NFAT axis, resulting in IP3R transcription.

67 gnal-transduction via the Ca(2+)/calcineurin/NFAT pathway.

68 protein via Epac-mediated Ca(2+)/calcineurin/NFAT signaling.

69 ckdown repressed hypertrophy and calcineurin/NFAT activity.

70 ted cardiac oxidative stress and calcineurin/NFAT signaling in diabetic mice.

71 ted by [Ca(2+)]i chelator BAPTA, calcineurin/NFAT inhibitor VIVIT, and TRPC6 channel knockdown.

72 associated with Ca(2+) handling, calcineurin/NFAT signaling, insulin signaling, cardiac apoptosis and

73 However, calcineurin/NFAT regulation did not contribute to constitutive expre

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

75 zed protein CEFIP that modulates calcineurin/NFAT signaling in cardiomyocytes, a finding with possibl

76 RF2) activation independently of calcineurin/NFAT inhibition.

77 lets, Ex-4 induced expression of calcineurin/NFAT signaling components as well as target genes for pr

78 omoter activity through PLCgamma/calcineurin/NFAT and MAPK pathways in SaOS-2 and MC3T3-E1 osteoblast

79 ment of STAT5, NF-kappaB, or the calcineurin/NFAT pathways.

80 ates Sox9 expression through the calcineurin/NFAT signaling pathway during tracheal chondrogenesis.

81 and the ensuing induction of the calcineurin/NFAT, FasL/Fas, and caspase signaling cascades promote n

82 lated gene transcription through calcineurin/NFAT (nuclear factor of activated T cells) signaling thr

83 at the suppression of astrocytic calcineurin/NFATs helps to protect synaptic function and plasticity

84 s of the nuclear factor of activated T cell (NFAT) family are essential for antigen-specific T cell a

85 Nuclear factor of activated T cell (NFAT) proteins are activity-dependent transcription fact

86 gulating nuclear factor of activated T cell (NFAT) signaling and LPA-induced keratinocyte cell motili

87 cineurin/nuclear factor of activated T cell (NFAT) signaling.

88 n of the nuclear factor of activated T cell (NFAT) was also reduced in CaV3.1-deficient T cells.

89 bitor of nuclear factor of activated T cell (NFAT)-calcineurin association-6 (INCA6) prevented IKs re

90 und that nuclear factor of activated T-cell (NFAT) activity is profoundly attenuated if Ca(2+) cleara

91 cineurin/nuclear factor of activated T-cell (NFAT) pathway.

92 urin/nuclear factor of the activated T-cell (NFAT) signaling pathway, and a previously unidentified N

93 redicted nuclear factor of activated T-cell (NFAT) transcription factors as potential regulators for

94 tion of nuclear factor of activated T cells (NFAT) and subsequent IL-2 induction.

95 tion of nuclear factor of activated T cells (NFAT) and the PI3K-AKT kinase-mTOR nutrient-sensing path

96 tion of nuclear factor of activated T cells (NFAT) and Treg proliferation.

97 tive of nuclear factor of activated T cells (NFAT) as a real-time T cell activation indicator.

98 of the nuclear factor of activated T cells (NFAT) because GRK5 causes enhancement of NFAT-mediated h

99 nsitive nuclear factor of activated T cells (NFAT) c1 transcription factor, as an OC signature gene,

100 ineurin/nuclear factor of activated T cells (NFAT) control and is upregulated by calcineurin inhibito

101 nd the nuclear factors of activated T cells (NFAT) family of transcription factors as likely mediator

102 of the nuclear factor of activated T cells (NFAT) family of transcription factors, shows increased e

103 The nuclear factor of activated T cells (NFAT) family proteins are transcription factors that reg

104 ineurin-nuclear factor of activated T cells (NFAT) inhibitor, cyclosporin A (CsA), suggesting that NF

105 ling to nuclear factor of activated T cells (NFAT) luciferase.

106 induced nuclear factor of activated T cells (NFAT) nuclear accumulation was abrogated by either antio

107 cause nuclear factor for activated T cells (NFAT) nuclear translocation in VSMCs.

108 ineurin-nuclear factor of activated T cells (NFAT) pathway modulates the physiology of numerous cell

109 factor nuclear factor of activated T cells (NFAT) plays an important role numerous signaling and the

110 sis for nuclear factor of activated T cells (NFAT) showed that PLCG1-mutated cases exhibited strong N

111 ediated nuclear factor of activated T cells (NFAT) signaling, long-term potentiation, and responsiven

112 ineurin/nuclear factor of activated T cells (NFAT) signaling.

113 ed with nuclear factor of activated T cells (NFAT) transcription factor activity and was sensitive to

114 of the nuclear factor of activated T cells (NFAT) was down-regulated progressively in accordance to

115 tion of nuclear factor of activated T cells (NFAT), a CnAbeta-regulated transcription factor, decreas

116 Nuclear factor of activated T cells (NFAT), a known actor in AF-associated remodeling, was fo

117 atenin, nuclear factor of activated T cells (NFAT), and major signaling molecules, resulted in signif

118 factors nuclear factor of activated T cells (NFAT), nuclear factor kappaB (NF-kappaB), and activator

119 cluding nuclear factor of activated T cells (NFAT), which control T cell function and differentiation

120 os- and nuclear factor of activated T cells (NFAT)-dependent genes.

121 ion via nuclear factor of activated T cells (NFAT).

122 of the nuclear factor of activated T cells (NFAT).

123 ity of nuclear factor for activated T cells (NFAT; by approximately 49%).

124 hibited nuclear factor of activated T-cells (NFAT) activity.

125 ith the nuclear factor of activated T-cells (NFAT) and is required for the recruitment of NFAT to the

126 Nuclear factors of activated T-cells (NFAT) are transcription factors that regulate osteoclast

127 ineurin/nuclear factor of activated T-cells (NFAT) pathway and the production of interleukin 8 trigge

128 ineurin/nuclear factor of activated T-cells (NFAT) pathways.

129 ineurin-nuclear factor of activated T-cells (NFAT) signaling in regulating pathological cardiac hyper

130 mation, nuclear factor of activated T-cells (NFAT) transcription, and interleukin-2 production in Jur

131 in (Cn)-nuclear factor of activated T-cells (NFAT)-mediated hypertrophic signaling, which was reliant

132 fector, nuclear factor of activated T-cells (NFAT).

133 ERK) or nuclear factor of activated T-cells (NFAT).

134 tion of nuclear factor of activated T cells (NFATs) in mDA neurons.

135 endent (nuclear factor of activated T cells, NFAT) VAV1 effector pathways.

136 AD through a mechanism involving aberrant CN/NFAT signaling and impaired glutamate transport.

137 Blockade of the astrocytic CN/NFAT pathway in rats using adeno-associated virus (AAV)

138 The blockade of astrocytic CN/NFAT signaling in a common mouse model of AD, using aden

139 However, the impact of astrocytic CN/NFAT signaling on neural function/recovery after acute i

140 Lastly, the CN/NFAT-signaling inhibitor INCA-6 was shown to reduce TNFa

141 s Nox2 and Nox4, indicating that the CnAbeta/NFAT pathway modulates Nox.

142 These data reveal that the CnAbeta/NFAT pathway regulates Nox and plays an important role i

143 Many of these elements contain composite NFAT/AP-1 sites, which typically support cooperative bin

144 We identified critical NFAT binding motifs in the AQP5 promoter that are involv

145 1 show increased proliferation and decreased NFAT activation compared with euploid controls.

146 itive to inhibition of calcineurin-dependent NFAT activation.

147 0 gene was mediated by calcineurin-dependent NFAT signaling in pancreatic beta-cells in response to o

148 mphoid-biased HSCs through calcium-dependent NFAT signaling, providing molecular insights into the ba

149 pon activation, calcineurin dephosphorylates NFAT family transcription factors, triggering their nucl

150 ry peptide revealed that FOXP3 downregulates NFAT-driven promoter activity of CD40L and IL-17.

151 identify a crucial role for RIPK3-PGAM5-Drp1/NFAT signalling in NKT cell activation, and further sugg

152 signaling, play no role in activating either NFAT protein.

153 cineurin (CN)-dependent transcription factor NFAT (Nuclear Factor of Activated T cells) mediates dele

154 ndent activation of the transcription factor NFAT (Nuclear Factor of Activated T cells) selectively,

155 act physically with the transcription factor NFAT (nuclear factor of activated T-cells) that binds to

156 ive complex between the transcription factor NFAT and FOXP3, a lineage specification factor for Tregs

157 we demonstrate that the transcription factor NFAT controls the program of T cell exhaustion.

158 pical LXVP motif in the transcription factor NFAT, and assessed stability of the mutant Drp1-CaN comp

159 m and activation of the transcription factor NFAT.

160 te the Ca(2+)-dependent transcription factor NFAT.

161 dent on calcium and the transcription factor NFAT.

162 pathways, complexes of transcription factors NFAT and AP-1 promote effector T cell differentiation.

163 Activation induced the transcription factors NFAT and AP-1 which created thousands of new DNase I-hyp

164 ed calcium biosensor Twitch1 and fluorescent NFAT.

165 plasmic-nuclear translocation of fluorescent NFAT, indicative of calcium-dependent activation of the

166 -regulated Ca(2+) homeostasis is crucial for NFAT-mediated transcriptional control required for induc

167 ogether, these studies show a clear role for NFAT-signaling in TNFalpha-induced retinal leukostasis,

168 ere enriched for consensus binding sites for NFAT and Nr4a family members, indicating that chronic st

169 FOXP3/NFAT interaction is required to repress expression of IL

170 hort synthetic peptide able to inhibit FOXP3/NFAT interaction impaired suppressor activity of convent

171 Inhibition of FOXP3/NFAT interaction upregulated CD40L expression on effecto

172 Specific inhibition of FOXP3/NFAT interaction with this inhibitory peptide revealed t

173 se activity and increased transcription from NFAT or NF-kappaB response element reporters, respective

174 of cytotoxic T lymphocyte effector functions.NFAT nuclear translocation has been shown to be required

175 d STIM deletion impairs calcium homeostasis, NFAT activation, and growth of smooth muscle.

176 To determine if there is an alteration in NFAT after TBI, we examined NFATc3 and c4 levels at 6 h,

177 TIM1-mediated control of Ca(2+) clearance in NFAT induction during T-cell activation.

178 antitumor activity were largely preserved in NFAT-deficient effector T cells.

179 tivation of transcription factors, including NFAT and Egr2/3.

180 ored the specific contribution of individual NFAT factors in donor T cells in animal models of GvHD a

181 tudy was to determine the role of individual NFAT isoforms in TNFalpha-induced retinal leukostasis.

182 transfected with siRNA targeting individual NFAT isoforms were treated with TNFalpha, and qRT-PCR wa

183 We found that LMW-FGF-2 induced NFAT and Ets1 binding to conserved cis-elements in the p

184 uate KCa3.1 as a modulator of Ca(2+)-induced NFAT-dependent osteoclast differentiation in inflammator

185 iency resulted in defective TCR/CD28-induced NFAT translocation to the nucleus in CD8(+) T cells.

186 ive Ca(2+) homeostasis prevents PDGF-induced NFAT activation in both contractile and proliferating SM

187 hat mTOR and CHEK1 kinase activity influence NFAT's transcriptional potency.

188 on and migration significantly by inhibiting NFAT/STAT3.

189 cific signal transduction pathways involving NFAT or C/EBPbeta transcription factors.

190 Although IL-33 induces AP-1 and NF-kappaB, NFAT signaling has not been described in ILC2s.

191 e inducible transcription factors NF-kappaB, NFAT, and AP-1.

192 c cellular transcription factors (NF-kappaB, NFAT, and STAT5), and that inhibition of Hsp90 greatly r

193 s (</=50 nmol/L) were associated with larger NFAT size and higher prevalence of type 2 diabetes.

194 mentary to this, GRK5 null mice exhibit less NFAT transcriptional activity after transverse aortic co

195 s nuclear factor of activated T lymphocytes (NFAT) and NF-kappaB.

196 ribe a new and pivotal role of SLAT-mediated NFAT activation in CD8(+) T cells, providing new insight

197 pression of LZTFL1 enhanced the TCR-mediated NFAT signaling, suggesting that LZTFL1 is an important r

198 unity, Martinez et al. report that monomeric NFAT binding in the absence of a transcriptional partner

199 Most NFAT protein resides in the cytoplasm because of extensi

200 Transcriptome analysis identifies a MYC-NFAT axis important for osteoclastogenesis.

201 the importance of an I-BET151-inhibited MYC-NFAT axis in osteoclastogenesis, and suggest targeting e

202 ) Jurkat cells displayed defective NFkappaB, NFAT, and MAPK activities owing to attenuated surface ex

203 In this study, we report a nonredundant NFAT-dependent role for lipid-derived leukotrienes (LTs)

204 During delayed export, nuclear NFAT constituted a short-term imprint of transient TCR s

205 AKT, pGSK-3beta, and nuclear accumulation of NFAT.

206 ar targets that compromise the activation of NFAT and NF-kappaB transcription factors and ultimately

207 found no evidence that DeltaNT activation of NFAT is dependent on Galphaq/11-mediated or beta-arresti

208 (including TGFalpha shedding, activation of NFAT luciferase, and beta-arrestin recruitment) but redu

209 Activation of NFAT requires dephosphorylation by the calcium-dependent

210 ion, and calcineurin-dependent activation of NFAT, the master transcription factor regulating IL-2 ex

211 ardioprotective effect through activation of NFAT/NFkappaB, downregulation of Bnip3, and inhibition o

212 ation of SPPL3 in a screen for activators of NFAT, a transcription factor that controls lymphocyte de

213 oth Ndfip1 and IL-2 requires the activity of NFAT and Erk.

214 ession of IL-2 by modulating the activity of NFAT.

215 Sustained association of NFAT and p300 histone acetyltransferase with the IP-10 g

216 Finally, our dataset of NFAT-associated proteins provides a good basis to furthe

217 nuclear entry, but not dephosphorylation, of NFAT proteins.

218 ls (NFAT) because GRK5 causes enhancement of NFAT-mediated hypertrophic gene transcription.

219 xit of Ets-1 precedes rapid nuclear entry of NFAT and Ets-1 deficiency results in impaired nuclear en

220 rget of rapamycin-1 (mTOR) and expression of NFAT and Myc transcription factors, abrogating the energ

221 nase independent manner, is a facilitator of NFAT activity and part of a DNA-binding complex responsi

222 LP region with the corresponding fragment of NFAT transcription factor, perfectly matching the previo

223 Thus, specific inhibition of NFAT opens an avenue for an advanced therapy of GvHD mai

224 Our results suggest that inhibition of NFAT/FOXP3 interaction might improve antitumor immunothe

225 The mechanism of NFAT activation by Ca(2+) has been determined.

226 receptors or a constitutive active mutant of NFAT.

227 ntify as yet unknown interaction partners of NFAT, we purified biotin-tagged NFATc1/alphaA, NFATc1/be

228 hannels drastically decreased recruitment of NFAT and histone modifications within key gene loci invo

229 NFAT) and is required for the recruitment of NFAT to the IL-2 promoter.

230 mechanisms involving negative regulation of NFAT activity in cardiomyocytes and reduction of periost

231 ied by cardiac fibrosis and up-regulation of NFAT-c2, reflecting increased calcineurin/NFAT signaling

232 In leukocytes, Ca(2+) regulation of NFAT-dependent gene expression oftentimes involves the a

233 ein components of noncoding RNA repressor of NFAT complex (NRON), which serves as a cytoplasmic trap

234 icle we demonstrate a major positive role of NFAT family members in Tfh differentiation.

235 In CRT-/- MEFs, TGF-beta stimulation of NFAT nuclear translocation and reporter activity is impa

236 nes by facilitating nuclear translocation of NFAT and dephosphorylation of dynamin-related protein 1

237 alcineurin, whereas nuclear translocation of NFAT is associated with increased death from CRC.

238 theta, and impaired nuclear translocation of NFAT, AP-1, and NF-kappaB.

239 alpha, which caused nuclear translocation of NFAT.

240 rease in ICa, T and nuclear translocation of NFAT.

241 und preferentially in the direct vicinity of NFAT-binding motifs and in a distinct orientation to the

242 EGR1, dictates the gene regulatory action of NFATs.

243 ciated with an increase in the activities of NFATs 1 and 4 in the hippocampus at 7 d after injury.

244 e effects of traumatic brain injury (TBI) on NFAT are currently unknown.

245 We identify the ORAI1/NFAT calcium signaling pathway as an essential regulator

246 ves as a cytoplasmic trap for phosphorylated NFAT proteins.

247 We experimentally validated the predicted NFAT/Sp1 signaling axis for each phenotype response.

248 Expression of TAK1DeltaN also promoted NFAT (nuclear factor of activated T-cells) transcription

249 Similarly, VEGF promoted NFAT activation and subsequent Adamts-1 induction in aor

250 ity of proinflammatory RCAN1-target proteins NFAT and NF-kappaB.

251 endent control of Ca(2+) clearance regulates NFAT activity during T-cell activation.

252 ts indicate that AS differentially regulates NFAT pathway through PML and p53 and reveal an intricate

253 Ts are key suppressors of OA, and regulating NFATs or their transcriptional targets in chondrocytes m

254 P expression, suggesting that Wnt7a requires NFAT signaling to exert this function.

255 nchronized VSMC showed 39-fold higher Rgs16 (NFAT (nuclear factor of activated T-cells) target; MAPK

256 Direct evidence showing NFAT activation initiates primary tumor formation in viv

257 LPA induced significant NFAT activation as monitored by nuclear translocation of

258 lated in PDE3B(-/-)mice WAT, including smad, NFAT, NFkB, and MAP kinases.

259 function, is up-regulated in KGM-H via SOCE/NFAT-dependent gene expression.

260 on COX-2 expression are mediated by specific NFAT sites within the COX-2 promoter as confirmed by sit

261 ed that PLCG1-mutated cases exhibited strong NFAT nuclear immunostaining.

262 teins provides a good basis to further study NFAT's diverse functions and how these are modulated due

263 transcription function in the immune system, NFAT also has essential functions even in the central ne

264 mor formation in vivo and supports targeting NFAT signaling in anti-tumor therapy.

265 abilizing cytokine conditions by sensing TCR/NFAT activation, which facilitates the interaction betwe

266 sues with NFATc1 activation, indicating that NFAT oncogenic effects depend on cell types and tissue c

267 Our data show that NFAT promotes T cell anergy and exhaustion by binding at

268 omatin immunoprecipitation data suggest that NFAT proteins likely directly participate in regulation

269 ibitor, cyclosporin A (CsA), suggesting that NFAT controls BCATc expression.

270 Furthermore, these findings indicate that NFATs are key suppressors of OA, and regulating NFATs or

271 rise and thereby its ability to activate the NFAT pathway.

272 Although the NFAT proteins have been extensively investigated in the

273 the astrocyte-specific promoter Gfa2 and the NFAT inhibitory peptide VIVIT reduced signs of glutamate

274 the astrocyte-specific promoter Gfa2 and the NFAT-inhibitory peptide VIVIT prevented the injury-relat

275 voked c-fos activation without impacting the NFAT pathway or Orai1 activity.

276 However, inhibiting the NFAT pathway impaired Wnt7a's ability to inhibit MMP exp

277 Mutagenesis of the NFAT and CRE binding sites, respectively, inhibited the

278 In T cells, members of the NFAT family of transcription factors not only are respon

279 ultimately promote functional binding of the NFAT or C/EBPbeta transcription factors, respectively, t

280 to amino acids within the SP-3 motif of the NFAT regulatory domain.

281 h bound to type 1 IFN promoters and that the NFAT binding site in IFN promoters was required for IRF7

282 xpression and cell proliferation through the NFAT pathway.

283 P response element (CRE) contiguous with the NFAT binding site in the FGF-23 promoter.

284 led Tfr and Tfh cell differentiation through NFAT-mediated IRF4, BATF, and Bcl-6 transcription-factor

285 ai1 was able to couple local Ca(2+) entry to NFAT activation, identifying the N-terminal domain of Or

286 ributes to SCF-induced signaling, leading to NFAT activation, which, together with NF-kappaB and Egr1

287 icited increased downstream signaling toward NFAT activation, and inhibition of this pathway resulted

288 ecause Tregs remain capable of translocating NFAT even in the presence of high CNI levels.

289 ted protein phosphatase calcineurin triggers NFAT migration into the nucleus.

290 ypothesis that nonfunctional adrenal tumors (NFATs) increase risk for cardiometabolic outcomes compar

291 In some cell types, NFAT can be activated by Ca(2+) nanodomains near open st

292 aling pathway, and a previously unidentified NFAT binding site is identified within the mouse Sox9 pr

293 decreases Nox2 and Nox4 expression, whereas NFAT overexpression increases Nox2 and Nox4, indicating

294 in lymph nodes and tumors to show that while NFAT nuclear import was fast (t(1/2 max) approximately 1

295 is unclear whether and how tissue cells with NFAT activation change the local environment for tumor i

296 calcium-dependent signals and competes with NFAT proteins for binding to protein components of nonco

297 udies suggest that GRK5 acts in concert with NFAT to increase hypertrophic gene transcription in the

298 lls and their responses correlated well with NFAT translocation to the nucleus, validating the biolog

299 Conclusion: Participants with NFATs had a significantly higher risk for diabetes than

300 Results: Participants with NFATs had significantly higher risk for incident composi