ライフサイエンスコーパス: AICD

1 AICD binds to the transcriptional coactivator Fe65, and

2 AICD in CD4 T helper (Th) cells, including Th1 and Th2 e

3 AICD is initiated by Ag re-engagement of the TCR and is

4 AICD is stabilized by Fe65, interacts with the transcrip

5 AICD occurred rapidly and was mediated primarily by Fas-

6 AICD of gamma delta T cells, therefore, provides an expl

7 AICD of T cells in tumor immunotherapy can be counterpro

8 AICD transgenic mice show activation of glycogen synthas

9 AICD was diminished, albeit not eliminated, by p53 small

10 AICD) as well as Abeta by stimulating gamma-secretase-me

11 AICD, activation-induced cell death; APC, antigen-presen

12 ST4 as functional kinase of FOXO1 in a 27OHC AICD-driven, hormetic pathway providing insight for ther

13 an activity-dependent manner to form Abeta, AICD, and secreted APPbeta.

14 We addressed AICD actions at synapses, per se, combining in vivo AICD

15 we investigated whether VIP and PACAP affect AICD in mature peripheral T cells and T cell hybridomas.

16 f Gadd45beta protected significantly against AICD, whereas IEX-1 and Bcl-x(L) were much less effectiv

17 ine-induced production of IL-4 and IL-13 and AICD of CD4(+) T cells.

18 timately yielding lower amounts of Abeta and AICD (APP intracellular domain).

19 cells neither affects Abeta40, Abeta42, and AICD production, nor intramembrane processing of Notch a

20 lgi traffic greatly impairs APP cleavage and AICD-dependent nuclear signaling, whereas blocking exocy

21 ligation of Fas induced Th17 cell death; and AICD was completely absent in Th17 cells differentiated

22 ation of Fas, FasL, and TRAIL expression and AICD directly in purified Th cells.

23 elicit a potent block of FasL expression and AICD.

24 nd promoted Fas ligand (FasL) expression and AICD.

25 tabilization of the AICD peptide by FE65 and AICD-mediated transcription were also retained at Abeta4

26 We examined whether proliferation and AICD are necessary for apoptotic cell death in sepsis us

27 f the generation of sAPPalpha, sAPPbeta, and AICD.

28 indings indicate that Fas-mediated apoptosis/AICD plays a major role in the spontaneous remission aft

29 on of the oxygen sensing pathway via the APP/AICD cleavage cascade.

30 The APP/AICD system regulates neuronogenesis and neurite length

31 s related to increased levels within the APP/AICD system.

32 a c) prevented Bcl-2 induction and augmented AICD.

33 tify one mechanism by which TGF-beta1 blocks AICD to allow the clonal expansion of effector T cells a

34 VIP/PACAP-mediated inhibition of both AICD and FasL expression is mediated through the specifi

35 ponents, PS1 fragments hyperaccumulated, but AICD levels were not elevated.

36 termine whether this process was mediated by AICD associated with IFN-gamma or with Fas-Fas ligand in

37 tial agonist TCR signaling pattern and cause AICD on Ag-activated, cycling T cells.

38 diminishes but does not ablate murine B cell AICD, indicating that activation-induced cytosine deamin

39 In CD4+ T cells, AICD is mediated by the Fas pathway and is enhanced by I

40 cell apoptosis that is distinct from classic AICD.

41 Unlike classic AICD, this type of T cell apoptosis pathway requires eng

42 ns because of activation-induced cell death (AICD) after initial proliferation.

43 resistant to activation-induced cell death (AICD) and expressed a unique set of cell-surface markers

44 that undergo activation-induced cell death (AICD) and fail to up-regulate c-Myc expression after B c

45 Activation-induced cell death (AICD) and programmed cell death prevent the untoward sid

46 Fas-mediated activation-induced cell death (AICD) as this process has been identified as an importan

47 Activation-induced cell death (AICD) as well as programmed cell death (PCD) serve to co

48 the so-called activation-induced cell death (AICD) essential for immune tolerance regulation.

49 /TNF-mediated activation-induced cell death (AICD) fits nicely with the original and recent descripti

50 The Ag-induced cell death (AICD) in T cells is a main mechanism for maintaining per

51 of apoptosis/activation-induced cell death (AICD) in the spontaneous recovery from acute disease.

52 Fas-mediated activation-induced cell death (AICD) in vivo.

53 occur through activation-induced cell death (AICD) in which engagement of the Ag receptors by cognate

54 Activation-induced cell death (AICD) is a major mechanism for peripheral T cell toleran

55 Activation-induced cell death (AICD) is a naturally occurring process regulating the re

56 Activation-induced cell death (AICD) is a process that regulates the size and the durat

57 that mediate activation induced cell death (AICD) of allo-antigen-responsive murine CD4+ T cells, re

58 ively enhance activation-induced cell death (AICD) of anti-recipient T cells within transplant donor

59 tudy was that activation-induced cell death (AICD) of CD4(+) T cells is involved in the immune inflam

60 Activation-induced cell death (AICD) of lymphocytes is an important mechanism of self-t

61 mers to cause activation-induced cell death (AICD) of previously activated CD8 T cells in an Ag-speci

62 asL-dependent activation-induced cell death (AICD) of T cells is believed to be a major contributor t

63 Activation-induced cell death (AICD) of T cells is one of the major mechanisms of perip

64 e TCR induces activation-induced cell death (AICD) of T cells that have been previously stimulated.

65 f VIP against activation-induced cell death (AICD) of Th2 effectors.

66 (anergy) and activation-induced cell death (AICD) or apoptosis through death receptor (Fas) signalin

67 Activation-induced cell death (AICD) plays an essential role in the contraction of acti

68 Activation-induced cell death (AICD) plays an important role in peripheral T-cell toler

69 -dependent, activation-induced T cell death (AICD) plays an important role in peripheral tolerance.

70 ells leads to activation-induced cell death (AICD) resulting in the downregulation of immune response

71 s to the high activation-induced cell death (AICD) susceptibility of replicating blasts.

72 resistant to activation-induced cell death (AICD) than normal T cells, a significant proportion of C

73 ntiation or activation-induced T cell death (AICD) through apoptosis.

74 s can undergo activation-induced cell death (AICD) upon stimulation of the T cell receptor-CD3 comple

75 This activation-induced cell death (AICD), a common mechanism for elimination of activated T

76 cytes induces activation-induced cell death (AICD), and also triggers apoptosis of target cells durin

77 IL-2-mediated activation-induced cell death (AICD), and the cytokine TGFbeta.

78 non, known as activation-induced cell death (AICD), plays a pivotal role in the removal of Ag-reactiv

79 also known as activation-induced cell death (AICD), plays an important role in the control of immune

80 corticoids on activation-induced cell death (AICD), the effects of dexamethasone and anti-CD3 stimula

81 apoptosis, or activation-induced cell death (AICD), upon T-cell receptor ligation.

82 T cells from activation-induced cell death (AICD), we transfected the T cell hybridoma A1.1, which i

83 of T cells to activation-induced cell death (AICD), which increases during the rapid in vitro expansi

84 cess known as activation-induced cell death (AICD), which requires the transcriptional induction of F

85 is as well as activation-induced cell death (AICD).

86 cells die is activation-induced cell death (AICD).

87 pression, and activation-induced cell death (AICD).

88 resistant to activation-induced cell death (AICD).

89 s is known as activation-induced cell death (AICD).

90 and survival, activation-induced cell death (AICD).

91 ) expression and antigen-induced cell death (AICD).

92 deficient in activation-induced cell death (AICD).

93 Fas-mediated activation-induced cell death (AICD).

94 that control activation-induced cell death (AICD).

95 b Ag-mediated activation-induced cell death (AICD).

96 tope-specific activation-induced cell death (AICD).

97 into the molecular mechanism(s) of defective AICD in autoimmune arthritis.

98 rIL-2 could completely restore the defective AICD in IL-4-deficient T cells.

99 damage is a likely trigger for p53-dependent AICD because susceptible lymphoblasts expressed signific

100 this phenomenon can arise from differential AICD susceptibility of T helper subsets, and asymmetries

101 e formation of the APP intracellular domain (AICD) and amyloid beta that is crucially involved in the

102 es to generate the APP intracellular domain (AICD) and Notch intracellular domain (NICD), respectivel

103 arate domains, the APP intracellular domain (AICD) and the soluble secreted APP.

104 ence suggests that APP intracellular domain (AICD) could regulate synapse function, but the underlyin

105 recursor protein (APP) intracellular domain (AICD) downregulates Wiskott-Aldrich syndrome protein (WA

106 o test whether the APP intracellular domain (AICD) functions analogously, we investigated how APP and

107 reasoned that the APP intracellular domain (AICD) has a role analogous to the NICD.

108 anscriptionally active intracellular domain (AICD) in response to 27-hydroxycholesterol (27OHC), an o

109 that releases the APP intracellular domain (AICD) in the cytoplasm.

110 recursor protein (APP) intracellular domain (AICD) is insensitive to low concentrations of GSIs and i

111 recursor protein (APP) intracellular domain (AICD) results in nuclear translocation and signaling thr

112 vages that release its intracellular domain (AICD) to the nucleus.

113 Generation of the APP intracellular domain (AICD) was further not inhibited in a cell-free assay at

114 cing Abeta and the APP intracellular domain (AICD), referred to as gamma and epsilon, respectively.

115 es memory, and the APP intracellular domain (AICD), which has been implicated in the regulation of ge

116 liberation of the APP intracellular domain (AICD).

117 expression of the APP intracellular domain (AICD).

118 well as a cytoplasmic intracellular domain (AICD).

119 loid precursor protein intracellular domain (AICD).

120 ) peptides, and an APP intracellular domain (AICD).

121 that also produces APP intracellular domain (AICD).

122 cellular fragment [APP intracellular domain (AICD)] that forms a transcriptively active complex.

123 interaction with Fe65 and thus downregulate AICD-mediated signaling.

124 ted kinase (ERK) pathway is activated during AICD.

125 nted the induction of FasL expression during AICD and inhibited AICD.

126 ERK pathway inhibited FasL expression during AICD, whereas activation of the ERK pathway with a const

127 nduction of Nur77 and FasL expression during AICD.

128 T cell thresholds for IL-2 signaling during AICD.

129 e and that only membrane-tethered AICD (i.e. AICD coupled to a transmembrane region) and not free AIC

130 tigen, sensitizes T cells to undergo "early" AICD resulting in tolerance.

131 tracellular domain (AID, or called elsewhere AICD).

132 etaPP intracellular domain (AID or elsewhere AICD) is indeed phosphorylated by JNK1.

133 e demonstrating direct binding of endogenous AICD to the EGFR promoter.

134 Here, we show that endogenous AICD in primary neurons is detectable only during a shor

135 We conclude that endogenous AICD undergoes tight temporal regulation during the diff

136 genic expression of Cyclon markedly enhanced AICD through increased expression of Fas whose expressio

137 f anti-apoptotic Bcl-2 or Bcl-xL facilitates AICD in T cells, whereas upregulation of Bcl-xL promotes

138 s potential role in AD pathogenesis, we find AICD levels to be elevated in brains from AD patients.

139 factor required for potentiating T cells for AICD.

140 isms by which IL-2 prepares CD8+ T cells for AICD.

141 77, which has been shown to be essential for AICD.

142 ce that IL-2 prepares CD8+ T lymphocytes for AICD by at least two mechanisms: 1) by up-regulating a p

143 stinct TCR signaling pattern is required for AICD by TCR partial agonist ligands.

144 strates that the ERK pathway is required for AICD of T cells and appears to regulate the induction of

145 We now demonstrate a functional role for AICD in regulating phosphoinositide-mediated calcium sig

146 We provide a new physiological role for AICD, which becomes pathological upon AICD increase in m

147 This inhibitory effect is specific for AICD through suppressing NFAT1-regulated FasL expression

148 APP metabolites (APP intracellular fragment (AICD) and Abeta) and Tau on the nucleus has emerged as a

149 pled to a transmembrane region) and not free AICD (i.e. soluble AICD) is a potent transactivator of t

150 IRS1, but not IRS2, protects A1.1 cells from AICD by diminishing FasL transcription through a pathway

151 cted Mart-1(27-35)-reactive primary CTL from AICD without impairing their functional capability.

152 subsets were capable of protecting CTL from AICD, and a major role for soluble factors in this prote

153 e CTLs, interestingly, could be rescued from AICD by the JNK inhibitor, SP600125.

154 ned whether these CTLs could be rescued from AICD.

155 ll clones proliferated and were rescued from AICD.

156 a marked accumulation of the APP-CTF gamma (AICD) fragment and a concomitant reduction in levels of

157 We previously generated AICD-overexpressing transgenic mice that showed abnormal

158 nvestigate its functional role, we generated AICD transgenic mice, and found that AICD causes signifi

159 Cells lacking APP (and hence AICD) exhibited similar calcium signaling deficits, and-

160 CD, Abeta, and Tau reach the nucleus and how AICD and Abeta control protein expression at the transcr

161 Here we discuss (i) how AICD, Abeta, and Tau reach the nucleus and how AICD and

162 However, AICD as well as Fas-mediated apoptosis of PKC-theta(-/-)

163 ical role of other ICDs, especially APP ICD (AICD), in regulating gene expression remains controversi

164 The impaired AICD in PGIA might be ascribed to an aberrant expression

165 This impaired AICD correlates with the failure to induce degradation o

166 In vitro studies have implicated AICD in cell signaling and transcriptional regulation, b

167 length Bid protein significantly declines in AICD-susceptible replicating blasts, whereas Bid mRNA do

168 1 gene, leading to a significant decrease in AICD but not of any other APP cleavage products.

169 This defect in AICD in PGIA may lead to the accumulation of autoreactiv

170 A defect in AICD may result in autoimmunity.

171 leading to nonapoptotic, caspase-independent AICD were identified, one contingent upon Fas ligation a

172 ence of soluble Fas ligand (sFasL) to induce AICD in alloreactive cells.

173 ulation of the T-cell receptor (TCR) induced AICD, as a result of activating the DNA damage response

174 endent pathway act independently in inducing AICD.

175 or Fas, even though both molecules influence AICD and the transient immune deficiency seen in the LCM

176 Evidence for p53-influenced AICD during this route of T cell-independent clonal expa

177 of FasL expression during AICD and inhibited AICD.

178 g IL-2, IL-2R alpha, or IL-2R beta inhibited AICD.

179 r alpha2beta1 integrin specifically inhibits AICD by inhibiting Fas-L expression in activated Jurkat

180 ion with APP constructs containing an intact AICD, but not by constructs lacking this domain.

181 Mechanistically, AICD has been largely attributed to the interaction of F

182 f the key cell surface proteins that mediate AICD in CD4(+) and CD8(+) T cells.

183 as, FasL and TRAIL and promoted Fas-mediated AICD of CD4(+) T cells.

184 ffect on NF-kappaB activity, in TCR-mediated AICD with implications in peripheral tolerance, T-cell h

185 d Do11.10 as cellular models of TCR-mediated AICD, we have demonstrated that the proapoptotic protein

186 PS/gamma-secretase-generated APP metabolite AICD in gene transcription and in EGFR-mediated tumorige

187 rovides a mechanism by which the activity of AICD might be modulated by extracellular stimuli.

188 h the inhibition of FasL and the decrease of AICD induced by TGF-beta1, providing that 4-hydroxytamox

189 opment, which is related to dysregulation of AICD.

190 IL-4-mediated enhancement of AICD and cellular FLIP degradation requires a Janus kina

191 ve Notch intracellular domain, expression of AICD did not activate transcription.

192 totic pathways as a mechanism for failure of AICD in leukemic LGLs.

193 hE by APP does not require the generation of AICD or amyloid beta peptide.

194 in-1/2-deficient cells lacking generation of AICD.

195 ypoxic response, involving the generation of AICD.

196 amined TCR signaling during the induction of AICD by anti-CD3 fos, a non-FcR-binding anti-CD3 mAb.

197 asL pathway is critical for the induction of AICD in T cells, and moreover this pathway can be negati

198 tion of Lck is required for the induction of AICD.

199 that the alpha2beta1-mediated inhibition of AICD and Fas-L expression required the focal adhesion ki

200 Furthermore, inhibition of AICD in wild-type T cells causes a defect in Th2 develop

201 al study demonstrates that the inhibition of AICD is achieved through the inhibition of activation-in

202 Closer inspection of AICD signaling showed that stabilization of the AICD pep

203 s to CTL significantly reducing the level of AICD.

204 Furthermore, the mechanism of AICD prevention in primary CTL included blockade of JNK

205 The molecular mechanisms of AICD are well-investigated, yet the possibility of regul

206 el, (ii) post-translational modifications of AICD, Abeta, and Tau, and (iii) what these three molecul

207 ur study demonstrates that the modulation of AICD of tumor-infiltrating CD4(+) T cells using HDACIs c

208 uclear p65/RelA correlated with the onset of AICD, suggesting that p65/RelA target genes may maintain

209 During this transient rise, a portion of AICD localizes to the nucleus.

210 Thus, prevention of AICD may be critical to achieve more successful clinical

211 NDeltaE, we observed enhanced production of AICD or NICD, respectively, in cells expressing NCT-ER.

212 itional cofactors that promote production of AICD, NICD, and A beta.

213 The regulation of AICD by IL-4 is poorly understood.

214 the mechanisms involved in the regulation of AICD by transforming growth factor beta1 (TGF-beta1).

215 apy and in further studies for regulation of AICD in CTLs.

216 We report a critical physiological role of AICD in controlling GluN2B-containing NMDA receptors (NM

217 he mechanism of Fe65-mediated stimulation of AICD formation appears to be through enhanced production

218 Intriguingly, Fe65 stimulation of AICD production appears to be inversely related to patho

219 We propose that the timing of AICD, and thus the length of the effector phase, are reg

220 in FasL, the beneficial effect of HDACIs on AICD of infiltrating CD4(+) T cells is not seen, confirm

221 leavage by gamma-secretase, namely, APPct or AICD, has been shown to form a multimeric complex with t

222 ot require proliferation, TCR engagement, or AICD.

223 ade in enhancing proliferation or preventing AICD.

224 EndoU gene disruption prevents AICD and normalizes c-Myc expression.

225 IL-4, IL-7, and IL-15, which do not promote AICD, did not influence FasL or gamma c expression.

226 such that low, but not high, doses promoted AICD transactivation of microtubule associated serine/th

227 of Bcl-xL, and knockdown of Bcl-xL promoted AICD.

228 These data suggest that IL-4 promotes AICD via an IL-2-dependent mechanism.

229 heral alloreactive CD4+ T cells by promoting AICD, which is presumably a key mechanism for its immuno

230 ted deletion of a Cyclon allele show reduced AICD and expression of Fas, indicating a critical role o

231 estigated, yet the possibility of regulating AICD for cancer therapy remains to be explored.

232 rane region) and not free AICD (i.e. soluble AICD) is a potent transactivator of transcription.

233 on as the Fe65 isoforms profoundly stimulate AICD production and simultaneously decrease Abeta42 prod

234 TCR-AICD occurs from a late G1 phase cell-cycle check point

235 alled TCR-activation-induced cell death (TCR-AICD).

236 We conclude that TCR-AICD occurs from a late G1 cell-cycle checkpoint that is

237 Here we show that T cells undergoing TCR-AICD induce the p53-related gene p73, another mediator o

238 dispensable and that only membrane-tethered AICD (i.e. AICD coupled to a transmembrane region) and n

239 Membrane-tethered AICD recruits Fe65 and mediates the activation of bound

240 s GrB as a new significant player in Th1/Th2 AICD and characterizes two mechanisms for the protective

241 In this study, we demonstrate that AICD in lpr and gld CD4(+) and CD8(+) T cells occurs pre

242 The in vivo findings that AICD can contribute to AD pathology independently of Abe

243 nerated AICD transgenic mice, and found that AICD causes significant biologic changes in vivo.

244 This study indicates that AICD is involved in the apoptosis of CD4(+) T cells duri

245 In this study, we report that AICD in IL-4-deficient T cells is significantly reduced

246 We further show that AICD increase in mature neurons, as reported in AD, alte

247 Importantly, we show that AICD mediates transcriptional regulation of EGFR.

248 We further show that AICD, together with Fe65 and Tip60, interacts with the L

249 Our data suggest that AICD is biologically relevant, causes significant altera

250 The AICD binds to the Wasf1 promoter, negatively regulates i

251 The AICD in these CTLs is neither caspase dependent nor is i

252 e therefore generated a plasmid encoding the AICD sequence and studied the subcellular localization o

253 ine previously found to be important for the AICD of T cells, did not affect Th17 cell apoptosis.

254 s pathway can be negatively regulated in the AICD-resistant clones by signals that are generated from

255 Of interest, the AICD has been implicated in transcriptional regulation,

256 both Fas and TNFR death pathways mediate the AICD of 2C cells.

257 omain directly functions in the nucleus, the AICD acts indirectly by activating Fe65.

258 r, we find that nuclear translocation of the AICD may be dispensable and that only membrane-tethered

259 D signaling showed that stabilization of the AICD peptide by FE65 and AICD-mediated transcription wer

260 egulates the transcriptional activity of the AICD-Fe65 complex.

261 /FasL pathway is essential in regulating the AICD of Th17 cells.

262 We further show that the AICD effect is mediated through the Fas/CD95-FasL signal

263 We also show that the AICD in TCReng CD4 T cells is a death receptor-independe

264 Our findings indicate that the AICD regulates phosphoinositide-mediated calcium signali

265 location by gamma-cleavage together with the AICD.

266 ion of gamma-secretase activity (and thereby AICD production) attenuated calcium signaling in a dose-

267 Therefore, AICD may be impaired in CD4+ T cells derived from mutant

268 Thus, AICD could contribute to AD synaptic failure.

269 Thus, AICD of Th17 cells occurs via the Fas pathway, but is in

270 ermined the responses of human CTCL cells to AICD and their cytotoxic to Fas(+) target T cells in vit

271 ntial susceptibility of Th1 and Th2 cells to AICD is not known.

272 The resistance of Th17 cells to AICD reveals a novel mechanism to explain the high patho

273 he sensitivity of Stat1-deficient T cells to AICD.

274 the susceptibility of CD4+ T lymphocytes to AICD, and for the survival of resting CD4+ T cells in pe

275 oth bystander cytotoxicity and resistance to AICD are likely to contribute to the loss of cytotoxic a

276 than Th1 cells, and Th17 cell resistance to AICD is due to the high levels of c-Fas-associated death

277 ay in part contribute to their resistance to AICD.

278 g cells did not abrogate their resistance to AICD.

279 CTCL cells expressing Fas were resistant to AICD following activation by CD3 monoclonal antibody (mA

280 -expressing cells were markedly resistant to AICD, while the A1.1 IRS2-expressing cells were not.

281 Stat1 transcription factor are resistant to AICD.

282 relatively, but not completely, resistant to AICD.

283 T cells become sensitive to AICD after activation by antigen and IL-2.

284 and caused the cells to become sensitive to AICD.

285 nique Th subset, but their susceptibility to AICD and the underlying molecular mechanisms have not be

286 We conclude that Th2 susceptibility to AICD is important for stabilizing the two polarized arms

287 gamma delta T cells are more susceptible to AICD and that the Fas-FasL pathways of apoptosis is invo

288 to activation as well as less susceptible to AICD compared with higher-avidity clones.

289 cells were significantly less susceptible to AICD than Th1 cells, and Th17 cell resistance to AICD is

290 Our data offer novel insights toward AICD in TCReng CD4 T cells and identify several potentia

291 ansgenic mice inhabit the spleen but undergo AICD after auto-Ag encounter.

292 27-35) epitope-specific primary CTLs undergo AICD upon the very first secondary encounter of the cogn

293 l-based primary stimulation protocol undergo AICD following their first secondary encounter of the co

294 ce, which develop arthritis, fail to undergo AICD.

295 action of TCReng CD4 T cells from undergoing AICD without affecting their effector function.

296 -gamma receptor 1 (IFN-gammaR1-/-) underwent AICD similar to wild-type cells.

297 ptor signalling inhibits macroautophagy upon AICD induction.

298 le for AICD, which becomes pathological upon AICD increase in mature neurons.

299 Thus, upon AICD induction regulation of macroautophagy, rather than

300 , combining in vivo AICD expression, ex vivo AICD delivery or APP knock-down by in utero electroporat

301 tions at synapses, per se, combining in vivo AICD expression, ex vivo AICD delivery or APP knock-down