ライフサイエンスコーパス: ITAM

1 ITAM multiplicity amplifies TCR signals, but the importa

2 ITAM receptors engage Src-family tyrosine kinases (SFKs)

3 ITAM-bearing proteins are also found in many oncogenic v

4 ITAM-coupled receptors play an essential role in regulat

5 ITAM-expressing cells were resistant to both serum starv

6 ITAM-induced inhibitors abrogated TLR responses by coope

7 ITAM-mediated cross-regulation can either augment or dam

8 ITAMs also have been identified in the cytoplasmic tails

9 a, zetaa, zetab, or zetac) at each of the 10 ITAM locations exhibit a substantial reduction in thymic

10 ular cellular response, they must use the 10 ITAMs found within the CD3 subunits (CD3gammaepsilon, CD

11 ering receptor expressed on myeloid cells 2) ITAM-coupled receptor plays a key role in bone remodelin

12 the adaptor FcepsilonR1gamma to activate an ITAM-signaling cascade.

13 beta-glucan receptor Dectin-1, activates an ITAM-Syk-dependent pathway in dendritic cells, which is

14 ling domains, a proline-rich sequence and an ITAM.

15 IIa (FcgammaRIIa) has been identified as an ITAM-bearing transmembrane receptor responsible for medi

16 Because DC-HIL contains an ITAM-like intracellular sequence, we questioned whether

17 X-activating protein of 12 kDa (DAP12) is an ITAM-bearing transmembrane adaptor protein that integrat

18 FcRgamma is an ITAM-containing adaptor required for CD16 signaling and

19 tyrosine-based activation motif (ITAM) or an ITAM-like domain, namely the collagen receptor complex g

20 Our data demonstrate that an ITAM-dependent pathway involving the Src-family kinase F

21 y express Tim-3 and are activated through an ITAM-containing receptor for IgE (FcepsilonRI), using si

22 lar domain promoting phagocytosis through an ITAM-domain-SFK-Syk-mediated signalling cascade.

23 that alphaIIbbeta3 regulates Syk through an ITAM-independent pathway in mice and provide novel insig

24 the inhibitory motif in FcgammaRIIb with an ITAM (FcgammaRIIb-ITAM) reconstituted ADE capacity to le

25 3Kgamma, to platelet activation by GPCRs and ITAM-coupled receptors.

26 tyrosine-based activation motif (ITAM)- and ITAM-like-mediated signals are severely compromised in F

27 ion between FlnA and Syk regulates ITAM- and ITAM-like-containing receptor signaling and platelet fun

28 se was dependent on activation via MyD88 and ITAM signaling pathways through TLRs and FcRs, respectiv

29 e mass, but Dap12(-/-) mice, lacking another ITAM protein, FcRgamma, were severely osteopetrotic.

30 ells transduced with these molecules bearing ITAM mutations were indistinguishable from untransduced

31 tor tyrosine-based activation motif-bearing (ITAM-bearing) adapter protein (DAP12) interruption of CD

32 mulation, thereby limiting crosstalk between ITAM and RANK/TNFR signaling and allowing fine tuning of

33 s also yield insights into crosstalk between ITAM-coupled receptors and heterologous receptors such a

34 the complexity in signal integration between ITAM- and TLR-mediated signaling.

35 ely how the timing of cellular activation by ITAM-coupled receptors is regulated by ITIM-containing r

36 ator of NF-kappaB) requires costimulation by ITAM-coupled receptors.

37 cross-inhibition of type I IFN signaling by ITAM-coupled beta2 integrins and demonstrate that ITAM s

38 ation, cytokine production was unaffected by ITAM number.

39 eptor gamma-chain, even though the canonical ITAM signaling was not activated by papain.

40 ccurring analog of cholesterol, inhibits CD3 ITAM phosphorylation, a crucial first step in T cell act

41 te development or whether any particular CD3 ITAM motif is sufficient.

42 of the adaptor Vav1 with phosphorylated CD3 ITAMs to mediate the recruitment and activation of the o

43 ne secretion, a high multiplicity of TCR-CD3 ITAMs was required for TCR-driven proliferation.

44 d that whereas a low multiplicity of TCR-CD3 ITAMs was sufficient to engage canonical TCR-induced sig

45 TCR signaling, as phosphorylation of the CD3 ITAMs by CD4-associated Lck is important for CD4(+) T ce

46 relation between the number of wild-type CD3 ITAMs and T cell proliferation, cytokine production was

47 Mice with fewer than seven wild-type CD3 ITAMs developed a lethal, multiorgan autoimmune disease

48 g inhibits phosphorylation of the CD3epsilon ITAM by Fyn and Lck kinases in vitro.

49 eds to result in unbinding of the CD3epsilon ITAM from the membrane to render these tyrosines accessi

50 A subpopulation of CD3epsilon ITAMs was mono-phosphorylated, owing to Lck kinase selec

51 ility is explored through the use of CD3zeta ITAM transgenic mice that express a CD3 zeta-chain with

52 hat T cells expressing 4D5 CARs with CD3zeta ITAM mutations were less prone to apoptosis.

53 iple adaptors permits fine-tuning of NK-cell ITAM responses over the course of an immune response.

54 We conclude that FcRgamma-chain ITAM signaling facilitates IC uptake and is essentially

55 (FcRgamma(-/-)) mice reported FcRgamma-chain ITAM signaling to be responsible for enhancing both IC u

56 work, we studied the role of FcRgamma-chain ITAM signaling using DCs from NOTAM mice that express no

57 e phosphorylation of the GPVI-FcRgamma-chain ITAM, which has 2 YxxL motifs, is independent of actin p

58 e or inhibit BCR signaling through consensus ITAMs and ITIMs; however, the extracellular ligands of t

59 igation of cell-surface receptors containing ITAM, ITIM or ITSM tyrosine phosphorylation motifs to th

60 Notably, only receptors containing ITAMs induced PKCtheta microclusters on their own, expla

61 tyrosine-based activation motif-containing (ITAM-containing) receptors/adaptors, predominantly tyros

62 ssay that it signals through its cytoplasmic ITAM.

63 containing tyrosine phosphatases that dampen ITAM-dependent signals.

64 s revealed that phosphorylation of the DAP12 ITAM was required for normal migration in vitro and asso

65 Strikingly, mice with disrupted DC ITAMs show defective T helper cell priming in vivo and a

66 and stabilization and resulted in defective ITAM receptor-mediated platelet aggregation.

67 th a CAR bearing a phosphorylation-defective ITAM were not activated.

68 mammary cell lines expressing two different ITAM-containing proteins, one encoding a MMTV provirus a

69 her than that for the interaction between dp-ITAM and tSH2 but is close to that for a singly tyrosine

70 receptor tyrosine-based activation motif (dp-ITAM) of the BCR complex.

71 n constant for the binding of tSH2(pm) to dp-ITAM (1.8 microM) is significantly higher than that for

72 ylinositol 3-kinase (PI3K) activation during ITAM-dependent platelet activation.

73 ual phosphotyrosines within FcepsilonRIgamma-ITAMs (immunoreceptor tyrosine-based activation motifs).

74 tif in FcgammaRIIb with an ITAM (FcgammaRIIb-ITAM) reconstituted ADE capacity to levels of the wild t

75 orylated and exposed PRS, that is, the first ITAM tyrosine has to be in the unphosphorylated state.

76 ionally critical residue of CD79B, the first ITAM tyrosine, was mutated.

77 ides what we believe to be a new concept for ITAM regulation of cytokine receptors in different tissu

78 a pathogen and may represent a paradigm for ITAM-coupled receptors sensing self and non-self.

79 dicated that PKC- is absolutely required for ITAM-mediated IFN-gamma secretion, whereas it has no mar

80 Thus, RBP-J imposes a requirement for ITAM-mediated costimulation of RANKL or TNF-alpha-induce

81 t that CD4 recruits Lck proximal to the four ITAMs of the CD3 heterodimers.

82 This first demonstration of a functional ITAM in a nonenveloped virus presents a new mechanism fo

83 mu2 is phosphorylated, contains a functional ITAM, and activates NF-kappaB.

84 of activating FcgammaR, but lack functional ITAM signaling.

85 edictions that short distances between gamma ITAM pairs are required for trans docking.

86 e also considered within the context of GPVI/ITAM pathways, including Ras/MAPK axis proteins (ie, KSR

87 Highly regulated GPVI/ITAM targets out of context of curated knowledge were al

88 LAP2 as critical inhibitors of platelet (hem)ITAM signaling in the setting of arterial thrombosis and

89 and thrombin generation in response to (hem)ITAM-coupled, but not G protein-coupled, receptor activa

90 tion residue L70, and Y6 of a potential hemi-ITAM motif in BST2's cytoplasmic domain.

91 In contrast, clustering the hemi-ITAM receptor Dectin-1 induced signaling that did not re

92 at inhibitory engagement of the hFcgammaRIIA ITAM either with anti-hFcgammaRII F(ab')2 fragments or i

93 tyrosine 304 (Y304) within the hFcgammaRIIA ITAM, which was required for recruitment of tyrosine kin

94 yrosine-based activation motifs (ITAMs; high ITAM multiplicity) in the complex of the T cell antigen

95 To study how ITAM signaling affects mammary cell transformation, we u

96 Here, we identified ITAM sequences in three mammalian reovirus proteins: mu2

97 To identify ITAM-bearing proteins that mediate signaling via the pla

98 roximity of the Igalpha ITAM, dampen Igalpha ITAM tyrosine phosphorylation.

99 hich are located in proximity of the Igalpha ITAM, dampen Igalpha ITAM tyrosine phosphorylation.

100 In ITAM-activated platelets that were treated with a PI3K i

101 Mechanistically, we show that deficiency in ITAM signaling results in increased pMHCII internalizati

102 particularly under conditions of incomplete ITAM phosphorylation.

103 70, controls the remaining CD45-independent, ITAM-specific NK-cell functions, demonstrating a functio

104 ansduction, with functions beyond inhibiting ITAM-mediated platelet activation.

105 tory function in T lymphocytes by inhibiting ITAM phosphorylation and/or removing cell surface TCR vi

106 tors NFATc1, BLIMP1, and c-FOS by inhibiting ITAM-mediated expression and function of PLCgamma2 and a

107 n, Leishmania shifts Mincle to an inhibitory ITAM (ITAMi) configuration that impairs DC activation.

108 cteristic of previously described inhibitory ITAM (ITAMi) signaling for hFcalphaRI and hFcgammaRIIIA,

109 Recently, the concept of inhibitory ITAM (ITAMi) has emerged as a new means to negatively co

110 dual ITIM-containing receptor that inhibits ITAM-dependent responses in hematopoietic cells.

111 dulating the activity of this novel integrin/ITAM pair might be effective in controlling thrombosis.

112 of DNAX activating protein of 12 kDa and its ITAMs.

113 complex signals through Src family kinases, ITAM domain-containing adaptor proteins, and other kinas

114 mplex and point to regions of high CD4-Lck + ITAM concentrations therein.

115 reduced the BDCA2/FcepsilonR1gamma-mediated ITAM signaling and blocked its inhibition of TLR9-mediat

116 Conversely, TLRs and cytokines modulate ITAM-mediated signaling, by means including activation o

117 ds, as well as in cells expressing monomeric ITAM or hemITAM gamma-chimeras, support model prediction

118 unoreceptor tyrosine-based activating motif (ITAM) phosphorylation.

119 unoreceptor tyrosine-based activating motif (ITAM)-containing adaptor proteins, we used different gen

120 unoreceptor tyrosine-based activation motif (ITAM) adaptor protein Fc receptor gamma-chain, even thou

121 unoreceptor tyrosine-based activation motif (ITAM) and G-protein-coupled receptors, increased adhesio

122 tion of an immune tyrosine activation motif (ITAM) and hemITAM, respectively.

123 unoreceptor tyrosine-based activation motif (ITAM) and the nonreceptor tyrosine kinase Syk.

124 f the immunotyrosine-based activation motif (ITAM) bearing activating receptors.

125 unoreceptor tyrosine-based activation motif (ITAM) cascade in platelets.

126 unoreceptor tyrosine-based activation motif (ITAM) in the Draper intracellular domain.

127 unoreceptor tyrosine-based activation motif (ITAM) in the FcRgamma signaling adaptor.

128 unoreceptor tyrosine-based activation motif (ITAM) monophosphorylation.

129 unoreceptor tyrosine-based activation motif (ITAM) of all CD3 chains upon TCR stimulation.

130 unoreceptor tyrosine-based activation motif (ITAM) or an ITAM-like domain, namely the collagen recept

131 unoreceptor tyrosine-based activation motif (ITAM) phosphorylated tyrosine residue at position 204 in

132 ream of the immunotyrosine activation motif (ITAM) platelet collagen receptor GPVI.

133 unoreceptor tyrosine-based activation motif (ITAM) proteins and B cell receptor (BCR) signaling by PA

134 unoreceptor tyrosine-based activation motif (ITAM) signaling and thereby regulates diverse functions,

135 unoreceptor tyrosine-based activation motif (ITAM) signaling motif of LMP2A.

136 et immunoreceptor tyrosine activation motif (ITAM) signaling, but not GPCR signaling, is critical for

137 unoreceptor tyrosine-based activation motif (ITAM) signaling.

138 unoreceptor tyrosine-based activation motif (ITAM) signalling modules of CD79B and CD79A were detecte

139 unoreceptor tyrosine-based activation motif (ITAM), the activating collagen receptor glycoprotein (GP

140 unoreceptor tyrosine-based activation motif (ITAM), which signals through Src family tyrosine kinases

141 unoreceptor tyrosine-based activation motif (ITAM)- and ITAM-like-mediated signals are severely compr

142 unoreceptor tyrosine-based activation motif (ITAM)-containing adapters, which trigger both cytotoxicy

143 unoreceptor tyrosine-based activation motif (ITAM)-containing adaptors (DAP12 and FcRgamma) and Vav f

144 unoreceptor tyrosine-based activation motif (ITAM)-containing proteins have recently been demonstrate

145 unoreceptor tyrosine-based activation motif (ITAM)-containing receptors in almost all hematopoietic c

146 unoreceptor tyrosine-based activation motif (ITAM)-coupled CD16.

147 unoreceptor tyrosine-based activation motif (ITAM)-coupled receptors glycoprotein (GP)VI or C-type le

148 unoreceptor tyrosine-based activation motif (ITAM)-coupled receptors is cross-regulation of heterolog

149 unoreceptor tyrosine-based activation motif (ITAM)-dependent pathway.

150 o the immunoreceptor-based activation motif (ITAM)-like sequence within the cytoplasmic domain of CEA

151 unoreceptor tyrosine-based activation motif (ITAM)-linked receptors.

152 unoreceptor tyrosine-based activation motif (ITAM)-specific NK-cell functions and processes such as d

153 unoreceptor tyrosine-based activation motif (ITAM).

154 unoreceptor tyrosine-based activation motif (ITAM).

155 unoreceptor tyrosine-based activation motif (ITAM).

156 unoreceptor tyrosine-based activation motif (ITAM).

157 unoreceptor tyrosine-based activation motif (ITAM).

158 unoreceptor tyrosine-based activation motif (ITAM).

159 unoreceptor tyrosine-based activation motif (ITAM): a short peptide sequence in the cytoplasmic tails

160 unoreceptor-Tyrosine-based-Activation-Motif (ITAM) that initiates TCR signalling by recruiting protei

161 unoreceptor tyrosine-based activation motif [ITAM] and FcgammaRIIb with an immunoreceptor tyrosine-ba

162 noreceptor tyrosine-based activation motifs (ITAM) in both these receptors.

163 noreceptor tyrosine-based activation motifs (ITAMs) and those that contain immunoreceptor tyrosine-ba

164 noreceptor tyrosine-based activation motifs (ITAMs) are signaling domains located within the cytoplas

165 noreceptor tyrosine-based activation motifs (ITAMs) have recently been shown to cooperate with specif

166 noreceptor tyrosine-based activation motifs (ITAMs) in their intracellular domains.

167 noreceptor tyrosine-based activation motifs (ITAMs) initiates the macrophage antimicrobial response.

168 noreceptor tyrosine-based activation motifs (ITAMs) is to regulate signaling by heterologous receptor

169 noreceptor tyrosine-based activation motifs (ITAMs) on T-cell receptors.

170 noreceptor tyrosine-based activation motifs (ITAMs), is a critical factor regulating myeloid-cell act

171 noreceptor tyrosine-based activation motifs (ITAMs), little is known about the ITAM requirements for

172 noreceptor tyrosine-based activation motifs (ITAMs), such as Fc receptor common gamma (FcRgamma) and

173 noreceptor tyrosine-based activation motifs (ITAMs).

174 on of CD3 immune tyrosine activation motifs (ITAMs).

175 noreceptor tyrosine-based activation motifs (ITAMs).

176 ssociated immune receptor activation motifs (ITAMs).

177 noreceptor tyrosine-based activation motifs (ITAMs; high ITAM multiplicity) in the complex of the T c

178 primarily by two amino acid sequence motifs, ITAMs (immunoreceptor tyrosine-based activation motifs)

179 A mutant virus lacking the mu2 ITAM activates NF-kappaB less efficiently and induces lo

180 Moreover, both the mu2 ITAM and Syk are required for maximal mu2 activation of

181 ired for reovirus-induced apoptosis, the mu2 ITAM is advantageous for viral spread and enhances viral

182 hat the cell type-specific effect of the mu2 ITAM on viral spread reflects the cell type-specific eff

183 appaB is not required for apoptosis, the mu2 ITAM stimulates cellular defense mechanisms and diminish

184 tories and this recruitment requires the mu2 ITAM.

185 Notably, the consequences of these mu2 ITAM effects are cell type specific.

186 ergent property, so that removal of multiple ITAMs, sequential phosphorylation, or differential affin

187 The purpose of multiple ITAMs, their sequential phosphorylation, and the differe

188 echanism, and find no evidence that multiple ITAMs modulate a switchlike response but do find that th

189 otein function, we suggest that the multiple ITAMs on the TCR function mainly to amplify subsequent s

190 various combinations of wild-type and mutant ITAMs in TCR-CD3 complexes.

191 These data reveal a novel ITAM-mediated inhibitory signaling pathway in DCs trigge

192 f platelet GPVI-collagen interactions and of ITAM receptor CLEC-2 pathways.

193 lished model of ITIM-mediated attenuation of ITAM-driven activation.

194 ating FcgammaRs, hampering the dissection of ITAM-dependent and independent FcgammaR functions in FcR

195 Simultaneous engagement of ITAM-coupled beta2 integrins or Dectin-1 with TLR4 did n

196 anism of c-MYC regulation was independent of ITAM/BCR activity.

197 Integration of ITAM signaling into signaling networks through cross-tal

198 sted the effects of simultaneous ligation of ITAM-associated receptors and TLR4 on TLR4-induced Jak-S

199 We show that high-avidity ligation of ITAM-coupled beta2 integrins and FcgammaRs in macrophage

200 Preligation of ITAM-coupled beta2 integrins and FcgammaRs inhibited pro

201 ood, the initial mechanism and regulation of ITAM phosphorylation remains unknown.

202 mbrane proteins that mimic the activation of ITAMs, murid herpesvirus-4 perturbs B cell signaling usi

203 Ag engagement causes phosphorylation of ITAMs on the TCR; these motifs recruit kinases and adapt

204 infection, the impact of CD45 deficiency on ITAM signaling differs depending on the downstream funct

205 as all the CD3 subunits possess at least one ITAM, the CD3 epsilon subunit also contains a proline-ri

206 GPVI or genetic deletion of Clec2, the only ITAM receptors expressed on mouse platelets, significant

207 ntain activating or inhibitory ITIM, ITSM or ITAM motifs; for example, inhibition of the macrophage S

208 Our findings may be generalizable to other ITAM and Jak-STAT signaling pathways and may help explai

209 lls, downstream kinase SYK can phosphorylate ITAM sequences independently of SFK, allowing it to comp

210 ced binding of mutated Syk to phosphorylated ITAM due to this increased phosphorylation.

211 he binding of Syk to tyrosine-phosphorylated ITAM subunits of immunoreceptors, such as FcepsilonRI on

212 inated by the multiplicity of phosphorylated ITAMs in TCR-CD3.

213 s, in vivo, Zap70 is bound to phosphorylated ITAMs in resting T cells.

214 a cytosolic kinase, binds to phosphorylated ITAMs with differential affinities.

215 yrosine kinase Zap70 binds to phosphorylated ITAMs, is subsequently activated, and then propagates do

216 ntriguingly, Lck sequentially phosphorylates ITAMs and ZAP-70, a cytosolic kinase, binds to phosphory

217 Platelet ITAM signaling plays a key role for the maintenance of v

218 is closely related to that of the 2 platelet ITAM receptors: glycoprotein (GP)VI and FcgammaRIIa.

219 on the physiological importance of platelet ITAM signaling as well as the molecular mechanisms facil

220 Thus, CLEC-2, unlike platelet ITAM receptors, is not regulated by proteolysis and can

221 ath, whereas the second lies in a predicted "ITAM motif" in the C-terminal domain of CD37 and counter

222 ossess an unexpected bifurcation of proximal ITAM-mediated signaling, each involving SLP-76 and contr

223 wo consensus ITIMs in addition to a putative ITAM sequence in its cytoplasmic domain.

224 Mechanistically, the Csk-recruiting ITAM of CD3epsilon reduced CAR-T cytokine production whe

225 e interaction between FlnA and Syk regulates ITAM- and ITAM-like-containing receptor signaling and pl

226 dent migration through a mechanism requiring ITAM-mediated Syk and Akt activation and inducing membra

227 thrombocytes which signals through the same ITAM-based signalling pathway as mammalian GPVI, providi

228 he SH2(Nck) domain has to bind to the second ITAM tyrosine in the phosphorylated state.

229 is is homologous to the well-established SFK-ITAM-Syk-signaling pathway used in vertebrate adaptive i

230 rticle, we show that mice utilizing a single ITAM sequence (gamma, epsilon, delta, zetaa, zetab, or z

231 ain is a homodimer subunit that contains six ITAMs (12 sites) and exhibits a number of properties tha

232 Whereas the six ITAMs of CD3zetazeta are key determinants of T cell deve

233 er, it remains unclear whether each specific ITAM sequence of the individual subunit (gammaepsilondel

234 tion of both inhibitory ITIM and stimulatory ITAM signaling, the events that regulate receptor phosph

235 Membrane-targeted SLP-76 (MTS) supports ITAM signaling in platelets and from the pre-TCR.

236 our findings indicate that RBP-J suppresses ITAM-mediated costimulation, thereby limiting crosstalk

237 es require Gi-type G proteins as well as TCR ITAM domains and the ZAP70 tyrosine kinase, thus indicat

238 he physiological importance of this high TCR ITAM number is unclear.

239 Most TCR ITAMs (6 of 10) are contributed by the CD3zeta subunits.

240 Here we demonstrate that ITAM multiplicity is important for the development of in

241 coupled beta2 integrins and demonstrate that ITAM signaling qualitatively modulates macrophage respon

242 r own, explaining previous observations that ITAM-coupled receptors promote stronger activating signa

243 Previous studies have shown that ITAM tyrosines engage in structure-inducing interactions

244 Together, the data suggest that ITAM sequence diversity is required for optimal TCR sign

245 Thus, our results suggest that ITAM-containing receptors can respond to exposed ligands

246 on motifs (ITAMs), little is known about the ITAM requirements for iNKT cell selection and expansion.

247 or for interferon-gamma (IFN-gammaR) and the ITAM adaptor Fcgamma as an example, we found that IFN-ga

248 k reveals that the SH2 domain of Syk and the ITAM tyrosine residues and transmembrane domain of DAP12

249 he presence of nearby basic residues and the ITAM tyrosines.

250 involving the Src-family kinase Fgr and the ITAM-containing adaptor proteins DAP12 and FcRgamma is i

251 itching the cytoplasmic tails containing the ITAM/ITIM motifs, leaving the remainder of the receptor

252 pt that unexpectedly, Th1 cells employed the ITAM-bearing protein DAP12, which was not known to be ex

253 sphorylated by Src family PTKs, enabling the ITAM to recruit activated Syk family kinases Inside-out

254 within the inflammatory cells involving the ITAM domain-containing protein Draper-I (a member of the

255 ling pathways widely used in leukocytes: the ITAM pathway and the Jak-STAT pathway.

256 ane and cytoplasmic domain, inclusive of the ITAM (immunoreceptor tyrosine-based activation motif) in

257 uces shedding of GPVI and proteolysis of the ITAM domain in FcgammaRIIa.

258 RIIa facilitates DENV entry by virtue of the ITAM motif, whereas the swapped version FcgammaRIIa-ITIM

259 Activation of either of the ITAM receptors induces shedding of GPVI and proteolysis

260 Mutation of the ITAM tyrosines of Jedi-1 and MEGF10 prevented engulfment

261 ng-dependent tyrosine phosphorylation of the ITAM-bearing platelet Fc receptor, FcgammaRIIa, as well

262 d turnover, and had impaired function of the ITAM-containing activating NK cell receptors.

263 IL, but not when the tyrosine residue of the ITAM-like sequence was mutated to phenylalanine.

264 in platelets, an essential component of the ITAM-signaling cascade.

265 Specifically, mu2 and muNS recruit the ITAM-signaling intermediate Syk to cytoplasmic viral fac

266 inimizes membrane association, rendering the ITAM motif more accessible to binding partners.

267 induction of migration by LMP2A required the ITAM signaling domain of LMP2A and activation of the Syk

268 and activation of Akt by LMP2A required the ITAM signaling domain of LMP2A.

269 n of beta2 integrins that are coupled to the ITAM-containing adaptors DAP12 and FcRgamma.

270 Lat(-/-) mice have reduced responses to the ITAM-coupled receptor NK1.1.

271 el antithrombotic agents directed toward the ITAM signaling pathway.

272 mmaRs elicit intracellular signaling via the ITAM domain of the associated FcRgamma-chain.

273 TARM1 associated with the ITAM adaptor FcRgamma but not with DAP10 or DAP12.

274 is and receptors that can associate with the ITAM-containing DAP12 adaptor.

275 Within the ITAM pathway, distinct signaling intermediates are varia

276 d by phosphorylation of the tyrosines in the ITAMs by Src family kinases (SFKs).

277 to the TCR-CD3 complex to phosphorylate the ITAMs, initiate intracellular signaling, and drive CD4(+

278 embedded within MHC molecules (pMHC) to the ITAMs of the associated CD3gammaepsilon, CD3deltaepsilon

279 Identification of these ITAM-containing receptors and their ligands remains a hi

280 ss a CD3 zeta-chain with zero, one, or three ITAMs and an MHC class II (DO11.10)- or MHC class I (H-Y

281 show that MMTV suppresses apoptosis through ITAM-mediated Src tyrosine kinase signaling.

282 l events in signaling by hemITAM relative to ITAM receptors.

283 ught to play redundant roles in transmitting ITAM signals in NK cells.

284 soluble Dectin-1 and Dectin-2 and triggered ITAM signaling of corresponding CLR reporter cells.

285 complex, but deletion or mutation of the two ITAM motifs did not.

286 The molecular mechanisms underlying ITAM signaling in platelets continue to be refined.

287 PVI and tumor cell-expressed galectin-3 uses ITAM-signaling components in platelets and favors the ex

288 from mice and patients deficient in various ITAM signaling pathways, we show here that OSCAR costimu

289 e activation triggers osteoclastogenesis via ITAM-based calcium signaling pathways, skewing osteoclas

290 onic BCR signals maintain anergy in part via ITAM monophosphorylation-directed activation of an inhib

291 important finding since these receptors via ITAM contribute to intracellular signaling.

292 ped virus presents a new mechanism for viral ITAM-mediated signaling with likely organ-specific conse

293 We investigated mechanisms by which ITAM-associated receptors inhibit type I IFN (IFN-alpha/

294 This review describes mechanisms by which ITAM-associated receptors modulate signaling by Toll-lik

295 nt of nonhematopoietic cell cancers in which ITAM-mediated signaling plays a role.

296 While ITAMs mobilize activating tyrosine kinases and their con

297 many activating NK cell receptors pair with ITAM-bearing adaptors, we recently reported that NKp80 s

298 Moreover, transfusion of platelets without ITAM receptor function or platelets lacking the adapter

299 hat a full complement of functional CD3 zeta ITAMs is required for effective iNKT cell development.

300 third (YF5,6), or all three (YF1-6) CD3 zeta ITAMs.