ライフサイエンスコーパス: SLP

1 SLP revealed a decrease in retardance in eyes with axona

2 SLP-2 deficiency was associated with impaired cardiolipi

3 SLP-76 (SH2 domain-containing leukocyte protein of 76 kD

4 SLP-76 (Src homology 2 domain-containing leukocyte phosp

5 SLP-76 co-precipitated alternately tagged SLP-76 in resp

6 SLP-76 ubiquitination is mediated by Ser-376 phosphoryla

7 SLP-76-deficient I-A(b):gp61 cells are unable to rapidly

8 SLP-76-dependent signals are required during the contrac

9 ivation; in these complexes are Nck, SHIP-1, SLP-76, Grb2, and TULA-2 (UBASH3B or STS-1).

10 Stomatin-like protein 2 (SLP-2) is a mostly mitochondrial protein that regulates

11 with mitochondrial Stomatin-like protein 2 (SLP-2), which also binds the mitochondrial lipid cardiol

12 he nasal inferior visual field (SOCT, -0.81; SLP, -0.57).

13 thymic selection by MTS is not rescued by a SLP-76 mutant whose localization is restricted to the cy

14 s its OC cytoskeleton-organizing effect in a SLP-76/Vav3-dependent manner.

15 enous SLP-76 with transgenic expression of a SLP-76 SH2 domain mutant, we demonstrate that the SLP-76

16 bind lymphatic endothelial PDPN and activate SLP-76 signaling to regulate embryonic vascular developm

17 ion and proteasomal degradation of activated SLP-76, which is mediated by Ser-376 phosphorylation, le

18 ntre of LAT-based complexes, and the adapter SLP-76 and actin molecules localize to the periphery.

19 Here, we show that the immune cell adaptor SLP-76 binds directly to SUMO-RanGAP1 of cytoplasmic fib

20 Despite the importance of the immune adaptor SLP-76 in T-cell immunity, it has been unclear whether S

21 s, including the essential signaling adaptor SLP-76, are dephosphorylated in the presence of YopH in

22 Surprisingly, the adaptor SLP-76 localized to the periphery of LAT clusters.

23 a intermediaries including the SLP adaptors, SLP-76 and BLNK (B cell linker).

24 In addition, SLP-2-deficient T cells showed a significant increase in

25 In addition, SLP-76-deficient memory CD4 T cells exhibited reduced st

26 ed vaccination with this carcinoembryonic Ag SLP in mice shows improved T cell responses and simultan

27 Conversely, an SLP-76 mutant unable to bind ADAP (adhesion and degranul

28 of parallel microwires, we have observed an SLP improvement by one order of magnitude; 950 W/g for a

29 ON>6 eyes: OCT (r(2) = 0.52; P < 0.0001) and SLP (r(2) = 0.51; P < 0.01); and in no-ON eyes, OCT (r(2

30 no-ON eyes, OCT (r(2) = 0.21; P < 0.01) and SLP (r(2) = 0.17; P < 0.05).

31 1.6 mm2; 95% CI, 0.8-23.5 mm2; P = .045) and SLP (11.9 vs 23.5 mm2; mean difference, 11.6 mm2; 95% CI

32 tip cells include ESM-1, angiopoietin-2, and SLP-76.

33 rested in cultured OCs deficient in BLNK and SLP-76 double knockout (DKO) phenotypes.

34 Interestingly, co-expression of Cdk2 and SLP-1 does not inhibit Fbw7-gamma degradation, suggestin

35 -gamma degradation, suggesting that Cdk2 and SLP-1 may have opposing functions.

36 asts in the omentum of both conventional and SLP mice.

37 despite normal association between Gads and SLP-76, TCR-mediated formation of SLP-76 microclusters w

38 ion by YopH by targeting PRAM-1/SKAP-HOM and SLP-76/Vav/PLCgamma2 signaling hubs may be critical for

39 heir functions, LAT2/SLP-76 interactions and SLP-76-independent LAT1 functions also mediate a positiv

40 r to disrupt the association between ITK and SLP-76 in live cells.

41 or (TCR)-induced association between ITK and SLP-76, recruitment and transphosphorylation of ITK, act

42 y limiting the communication between LAT and SLP-76 and preventing the dynamic formation of SLP-76-si

43 sitively-charged residues and favors LAT and SLP-76 phosphosites that are surrounded by negatively-ch

44 zeta chain and the scaffold proteins LAT and SLP-76.

45 The sequence features in ZAP-70, LAT, and SLP-76 that underlie electrostatic selectivity likely co

46 Comparison of SLP-76(-/-) LAT1(-/-) and SLP-76(-/-) mast cells revealed that some functions of L

47 OCT and SLP revealed different aspects of RNFL changes associate

48 etween the defect size measured with OCT and SLP was found (r = 0.89; P < .001).

49 Threshold perimetry, OCT, and SLP were used to prospectively study eyes with papillede

50 l and genetic interaction between Parkin and SLP-2 and the compensatory potential of SLP-2 suggest a

51 s showed a genetic interaction of Parkin and SLP-2, and further, tissue-specific or global overexpres

52 Both splenectomized and SLP mice were protected against lethal ehrlichial challe

53 m 1980 to 2013, using the identified SST and SLP patterns from the previous spring.

54 t Jurkat T cells compared with wild-type and SLP-76-reconstituted Jurkat T cells.

55 Transmission electron microscopy showed anti-SLP-76 cytoplasmic labeling of the majority of NPCs in a

56 e N-terminal domain of Fbw7-gamma as well as SLP-1.

57 Because SLP-76 is also important for integrin activation and sig

58 he canonical membrane complex formed between SLP-76 and linker for activation of T cells (LAT) family

59 We demonstrate that both SLPs localize to mitochondrial membranes.

60 owed RNFL thinning by OCT (7/17 eyes) and by SLP (14/16 eyes) in contrast to optic neuritis (by OCT,

61 ic neuritis (by OCT, 0/12, P = 0.006; and by SLP, 1/12, P = 0.0004).

62 reduction of the RNFL thickness assessed by SLP.

63 The RNFL by SLP was reduced in at least one quadrant in 1 eye with p

64 Average RNFL by SLP was slightly increased for papilledema and optic neu

65 We show that CD30, CD79b, SLP-76, DEC205, IL-5Ralpha, STAT5, and Thy1 are induced

66 However, conventional SLP-2-deficient T cells had a posttranscriptional defect

67 ith abnormal field regions had corresponding SLP sectors thinner (P = 0.003) than for sectors with no

68 imers stabilize SLP-76 microclusters, couple SLP-76 to the force-generating systems responsible for m

69 Conversely, measured amplitude-dependent SLP profiles of all studied constructs conform to no pre

70 Through its protein-binding domains, SLP-76 serves as a platform for the assembly of multiple

71 LP-76, indicates that SLP-76 is the dominant SLP family member in the resorptive process.

72 ivo is inhibited approximately 40% in either SLP-76(-/-) or DKO mice.

73 ently, deletion of the SAM region eliminated SLP-76 co-precipitation of itself, concurrent with a los

74 Combining regulated deletion of endogenous SLP-76 with transgenic expression of a SLP-76 SH2 domain

75 have extended a method developed to estimate SLP from the inherently non-adiabatic measurements, wher

76 all estimates was selected as the estimated SLP.

77 We also find SLP-76 is phosphorylated in a Syk-dependent manner.

78 ely to result in distinct functions, and for SLP sequences, distinctive and possibly functionally sig

79 Using T-cells depleted for SLP-76, ADAP, or Pyk2, or expressing Pyk2 kinase-inactiv

80 Our findings demonstrate a dominant role for SLP-76-dependent TCR signals in regulating turnover and

81 llele reveals a dose-sensitive threshold for SLP-76 in the balance of immunity and immune dysregulati

82 Furthermore, SLP-76 facilitated the association of negative regulator

83 selected for validation studies: PLC2, G6f, SLP-76, and Dok-2.

84 plexes were distinct from canonical LAT-GADs-SLP-76 complexes.

85 AT-GRB2-SKAP1 complexes relative to LAT-GADs-SLP-76 complexes.

86 odel in which bivalent recruitment of a GADS/SLP-76 complex is required for costimulation by CD6.

87 nd the function of this domain, we generated SLP-76 knockin mice with the SAM domain deleted.

88 a high-molecular-weight S-layer protein (HMW SLP) and its low-molecular-weight partner protein (LMW S

89 Cwp13 cleaves SlpA in the HMW SLP domain, which we suggest may reflect a role in cleav

90 Overall, we have identified SLP-76 as a direct regulator of nuclear pore function in

91 TSS resulting from the appearance of ARP in SLP are associated with low peripapillary choroidal thic

92 ively studied, the role of the SAM domain in SLP-76 function is not known.

93 areas except for the central visual field in SLP.

94 n SLP-76 by HPK1, a function that is lost in SLP-76 SH2 domain mutant T cells.

95 n by CXCL12 is a common mediator response in SLP-76-, ADAP-, and Pyk2-regulated cell adhesion involvi

96 een the wires, showing a decreasing trend in SLP with increasing wire separation.

97 ules critical for NK cytotoxicity, including SLP-76, PLCgamma2, and Vav1.

98 mily members, a novel LAT family-independent SLP-76-dependent signaling pathway was identified.

99 ression of ITK-SYK fusion requires an intact SLP-76 function and significantly induces IL-2 secretion

100 es of proximal signaling complexes involving SLP-76 were formed.

101 imal ITAM-mediated signaling, each involving SLP-76 and contributing to optimal NK-cell function.

102 omain-containing leukocyte protein of 76 kD (SLP-76) is recruited to microclusters at the plasma memb

103 ntaining leukocyte phosphoprotein of 76 kDa (SLP-76) has been constitutively targeted to the membrane

104 main-containing leukocyte protein of 76 kDa (SLP-76) is an essential mediator of signaling from the T

105 main-containing leukocyte protein of 76 kDa (SLP-76) is critical for multiple aspects of T cell devel

106 main-containing leukocyte protein of 76 kDa (SLP-76) is critical for proximal TCR-generated signaling

107 ntaining leukocyte phosphoprotein of 76 kDa (SLP-76) nucleates a signaling complex critical for T-cel

108 ntaining leukocyte phosphoprotein of 76 kDa (SLP-76) plays a crucial role in T cell activation by lin

109 main-containing leukocyte protein of 76 kDa (SLP-76) to reduce MC density in Nef-expressing and HIV-1

110 domain-containing phosphoprotein of 76 kDa (SLP-76) with MHC:peptide tetramers to study the requirem

111 main containing leukocyte protein of 76 kDa (SLP-76), an adaptor protein that nucleates the proximal

112 main-containing leukocyte protein of 76 kDa (SLP-76), for example, cause an arrest of T cell positive

113 -domain-containing phosphoprotein of 76 kDa (SLP-76), to analyze signaling mechanisms for memory CD4

114 main-containing leukocyte protein of 76 kDa (SLP-76)-deficient Jurkat T cells compared with wild-type

115 leukocyte phosphoprotein of 76 kilodaltons (SLP-76) is a cytosolic adaptor protein essential for thy

116 s cytoskeletal organization of those lacking SLP-76 is delayed, thus modestly reducing bone resorptio

117 The origin of the large SLP and relevant heating mechanisms are discussed.

118 The large SLP is attributed to the rectangular hysteresis loop res

119 The largest SLP is obtained when the wires are aligned along the dir

120 rosine kinase, ZAP-70, and the adaptors LAT, SLP-76, and Nck.

121 each other for many of their functions, LAT2/SLP-76 interactions and SLP-76-independent LAT1 function

122 ve the greatest similarity: Shewanella-like (SLP), Rhizobiales-like (RLPH), and ApaH-like (ALPH) phos

123 ts low-molecular-weight partner protein (LMW SLP).

124 Administration of low SLP doses in the slow-release vehicle IFA prevented the

125 tant with a decrease in the levels of mature SLPs in the cell wall.

126 ulting in larger variance of calculated mean SLP values.

127 time a role for the SAM domain in mediating SLP-76 self-association for T-cell function.

128 overed a pattern of ancestral mitochondrial (SLP and RLPH) or archaeal (ALPH) gene entry into eukaryo

129 strate a novel role for the adaptor molecule SLP-76 in regulating HIV-1 infection in T cells with the

130 g complex nucleated by the adaptor molecules SLP-76 and LAT1 is required for activation through this

131 ure (SLP) anomalies over Hawaii and negative SLP anomalies over the Atlantic and North America.

132 These findings identify ACK1 as a novel SLP-76-associated protein-tyrosine kinase that modulates

133 tent with these genetic findings, we observe SLP-76-dependent platelet aggregate formation on the sur

134 RanGAP1 bound to the N-terminal lysine 56 of SLP-76 where the interaction was needed for optimal RanG

135 We found that ablation of SLP-76 expression after T cell priming did not inhibit g

136 ific CD4(+) memory T cells in the absence of SLP-76 and normal levels of homeostatic division.

137 central memory phenotype, but the absence of SLP-76 during memory homeostasis substantially alters th

138 se in homeostatic turnover in the absence of SLP-76 is a cell-intrinsic process.

139 30 wk after LCMV infection in the absence of SLP-76.

140 To determine the mechanism of action of SLP-2, we generated T cell-specific SLP-2-deficient mice

141 3-3 binding, resulting in the attenuation of SLP-76 activation and downstream signaling; however, the

142 hanistically, SHP-1 modulated the binding of SLP-76 to ADAP by dephosphorylation of the YDGI tyrosine

143 Comparison of SLP-76(-/-) LAT1(-/-) and SLP-76(-/-) mast cells reveale

144 Direct in vivo deletion of SLP-76 in polyclonal memory CD4 T cells likewise led to

145 CR ligation and abrogated by the deletion of SLP-76 SAM domain (DeltaSAM) or mutation of Tyr-113, Tyr

146 We used temporally mediated deletion of SLP-76 to interrupt tonic and activating TCR signals aft

147 dependent pathway involved the SH2 domain of SLP-76 and adhesion and degranulation-promoting adaptor

148 inal-located tyrosines and the SH2 domain of SLP-76 are required for downstream signaling and slow le

149 lysis revealed that the N-terminal domain of SLP-76 was important for regulating HIV-1 infection.

150 the function of the C-terminal SH2 domain of SLP-76.

151 nase Bruton tyrosine kinase is downstream of SLP-76 and, together with ADAP, regulates PI3Kgamma (pho

152 Importantly, induced expression of SLP-2 corrected for these mitochondrial alterations caus

153 in a mouse strain with reduced expression of SLP-76 (twp mice).

154 ses suggested that Nef prevents formation of SLP-76 MCs at the level of the upstream adaptor protein,

155 n Gads and SLP-76, TCR-mediated formation of SLP-76 microclusters was impaired by the deletion of the

156 P-76 and preventing the dynamic formation of SLP-76-signaling MCs.

157 plasma membrane recruitment and function of SLP-76.

158 study underscores both the immunogenicity of SLP vaccination, for inducing T cell as well as B cell r

159 high-affinity alpha4beta1 is independent of SLP-76, ADAP, and Pyk2, the strength of alpha4beta1-VCAM

160 nctions of LAT1 could occur independently of SLP-76.

161 er mechanistic studies revealed that lack of SLP-76 impaired virus release, but did not affect viral

162 Thus, fixed localization of SLP-76 reveals differential requirements for the subcell

163 sults reveal a novel regulation mechanism of SLP-76 by ubiquitination and proteasomal degradation of

164 gamma) activation due to a Y145F mutation of SLP-76 were also defective in their suppressive function

165 Overexpression of SLP-1 inhibits the degradation of Fbw7-gamma, suggesting

166 bw7-gamma is stabilized by overexpression of SLP-1, c-Myc protein abundance decreases, suggesting tha

167 tissue-specific or global overexpression of SLP-2 transgenes rescued parkin mutant phenotypes, in pa

168 on-receptor 2) as a novel binding partner of SLP-76.

169 membrane localization and phosphorylation of SLP-76 in LAT1(-/-) mast cells.

170 Ser-376 phosphorylation of SLP-76 mediates 14-3-3 binding, resulting in the attenua

171 that the recruitment and phosphorylation of SLP-76 were preserved in LAT1(-/-) mast cells and that S

172 and SLP-2 and the compensatory potential of SLP-2 suggest a functional epistatic relationship to Par

173 ory CD8 T cells generated in the presence of SLP-76 and then acutely deprived of TCR-mediated signals

174 aling that simple quantitative reductions of SLP-76 were sufficient to trigger immune dysregulation.

175 eins, and the central proline-rich region of SLP-76 have been well studied and are known to be import

176 omain to the polyproline-rich (PR) region of SLP-76.

177 an important negative feedback regulation of SLP-76 by HPK1 (hematopoietic progenitor kinase 1; MAP4K

178 ationship to Parkin and a protective role of SLP-2 in neurons.

179 We further confirmed the role of SLP-76 in HIV-1 infection by small interfering RNA-media

180 In keeping with a central role of SLP-76/Vav3 association in osteoclastic resorption, retr

181 30 is identified as a ubiquitination site of SLP-76.

182 The N terminus of SLP-76, which contains three tyrosines that serve as doc

183 astic resorption, retroviral transduction of SLP-76, in which the Vav binding site is disrupted (3YF)

184 Mutations in the tyrosines of SLP-76 result in graded defects in TCR-induced signals d

185 Loss of Lys-30 ubiquitination of SLP-76 results in enhanced anti-CD3 antibody-induced ERK

186 ed criterion was used to generate a value of SLP, and the mean from all estimates was selected as the

187 ell receptor (TCR) triggers the assembly of "SLP-76 microclusters," which mediate signals required fo

188 phorylation of a negative regulatory site on SLP-76 by HPK1, a function that is lost in SLP-76 SH2 do

189 e rescued by retroviral transduction of only SLP-76, indicates that SLP-76 is the dominant SLP family

190 the SAM domain is indispensable for optimal SLP-76 signaling.

191 SP innate Eomes(+) thymocytes in itk(-/-) or SLP-76(Y145F) mice are dependent on gammadelta T cells f

192 Y cells with a stable knockdown of Parkin or SLP-2, as well as induced pluripotent stem cell-derived

193 s like those seen in animals lacking PDPN or SLP-76.

194 ; however, they were not essential for other SLP-76-dependent events, including phosphorylation of AK

195 riggering from the generation of p-LAT and p-SLP nanoclusters driving TCR signal amplification and di

196 , we identified a novel interaction partner, SLP-1, which binds the N-terminal domain of Fbw7-gamma.

197 n of ITK with two of its signaling partners, SLP-76 and LAT.

198 an adapter with potential binding partners: SLP-76, VASP, and SKAP-HOM.

199 ed spleen, lymph nodes, and Peyer's patches (SLP mice).

200 togenes expressing the LCMV gp61-80 peptide, SLP-76-deficient I-A(b):gp61(+) cells exhibit reduced di

201 Synthetic long peptides (SLP) are a promising vaccine modality to induce therapeu

202 prospectively performed automated perimetry, SLP, and high definition OCT (HD-OCT) of the RNFL in 25

203 Here, we report that phosphorylated SLP-76 is ubiquitinated and targeted for proteasomal deg

204 K-SYK expression in SYF cells phosphorylates SLP-76 in the absence of SRC family kinases.

205 e tomography (OCT) and slitlamp photography (SLP) with fluorescein staining.

206 s acquired using scanning laser polarimetry (SLP) and optical coherence tomography (OCT) in patients

207 mography (CSLT), scanning laser polarimetry (SLP) and photographic imaging of the optic nerve head (O

208 ypothesized that scanning laser polarimetry (SLP) compared with OCT might reveal the status of axon i

209 Scanning laser polarimetry (SLP) results can be affected by an atypical retardation

210 Scanning laser polarimetry (SLP) reveals abnormal retardance of birefringence in loc

211 omography (OCT), scanning laser polarimetry (SLP), and visual evoked potentials.

212 graphy (OCT) and scanning laser polarimetry (SLP).

213 Specific loss power (SLP) generated by magnetic nanoparticles is estimated fr

214 mount of heat, with the specific loss power (SLP) reaching a value as high as 521 W/g for an AC field

215 es is stronger for SOCT than for the present SLP.

216 Ts), as well as positive sea level pressure (SLP) anomalies over Hawaii and negative SLP anomalies ov

217 rface temperature (SST), sea level pressure (SLP), freshwater input, ice cover], and PCs 1-2 of 36 bi

218 g independent records of sea-level pressure (SLP), SST, and SAT, this study investigates northeast (N

219 ted, namely stomatin, paraslipin (previously SLP-2) and flotillin.

220 ion or platelets lacking the adapter protein SLP-76 into TP mice had no significant effect on vascula

221 The adaptor protein SLP-76 is recruited to the phosphorylated CD6 cytoplasmi

222 ires an interaction with the adaptor protein SLP-76.

223 by a specific region of the adaptor protein, SLP-76.

224 These included the adaptor proteins SLP-76, Nck-1, Grb2, and Grb2-related adaptor downstream

225 nstrate that export of the S-layer proteins (SLPs) and an additional cell wall protein (CwpV) is depe

226 t and low-molecular-weight S-layer proteins (SLPs).

227 ogous genes encoding stomatin-like proteins (SLPs; AtSLP1 and AtSLP2) that are phylogenetically relat

228 oject to the superior lateral protocerebrum (SLP) and convey taste information to mushroom body learn

229 field deficits show no significant recovery, SLP can be an early marker for axonal injury, which may

230 In NAION eyes, quadrants with reduced SLP had corresponding visual field loss that did not rec

231 r memory CD4 T cells; however, the resultant SLP-76-deficient memory CD4 T cells could not produce re

232 SAP, SLP, and OCT outcomes were compared between the control

233 We compared sector SLP RNFL thickness with corresponding visual field value

234 ith superior field loss, had inferior sector SLP reduction.

235 We hypothesize initial sector SLP RNFL abnormalities will correlate with long-term reg

236 At presentation, 12 eyes had superior sector SLP reduction, 11 of which had inferior field loss.

237 ction of SLP-2, we generated T cell-specific SLP-2-deficient mice.

238 r data indicate that SKAP55 dimers stabilize SLP-76 microclusters, couple SLP-76 to the force-generat

239 AP55 Src homology 3 (SH3) domains stabilized SLP-76 microclusters and promoted T cell adhesion via th

240 5 in the absence of H1-4 sufficed to support SLP-76 self-association with smaller microclusters that

241 Although LAT2 supported SLP-76 phosphorylation and recruitment to the plasma mem

242 The SYK-SLP-76 signaling pathway is required in blood cells to r

243 SLP-76 co-precipitated alternately tagged SLP-76 in response to anti-CD3 ligation.

244 Mice bearing membrane-targeted SLP-76 (MTS) have a partial T-cell lymphopenia and impai

245 Membrane-targeted SLP-76 (MTS) supports ITAM signaling in platelets and fr

246 At its N terminus, SLP-76 has three key tyrosines (Tyr-113, Tyr-128, and Ty

247 that employed during TCR signaling and that SLP-76 relocalization corresponds to SLP-76-dependent in

248 e preserved in LAT1(-/-) mast cells and that SLP-76(-/-) and LAT1(-/-) mast cells harbored distinct f

249 downstream of integrins in T cells and that SLP-76-deficient T cells fail to support adhesion to int

250 In this study, we demonstrate that SLP-76 (SH2 domain-containing leukocyte phosphoprotein o

251 These findings demonstrate that SLP-76 relocalizes to integrin-initiated signaling compl

252 We report here that SLP-76 also mediates signaling downstream of integrins i

253 Moreover, we show here that SLP-76 is critical for ITK-SYK activation and is particu

254 transduction of only SLP-76, indicates that SLP-76 is the dominant SLP family member in the resorpti

255 omplex I and supercomplexes, indicating that SLP affects the assembly and/or stability of these compl

256 Based on these results, we propose that SLP-2 organizes the mitochondrial membrane compartmental

257 Signaling studies revealed that SLP-76 associated with viral negative regulatory factor

258 We show that SLP reductions and related atmospheric forcing led to ce

259 ing Pyk2 kinase-inactive forms, we show that SLP-76 and ADAP stimulate chemokine-activated, alpha4bet

260 In this study, we show that SLP-76 self-associates in response to T-cell receptor li

261 We also showed that SLP-76 plays a critical role in cell-to-cell transmissio

262 gulatory factor and F-actin, suggesting that SLP-76 mediates the formation of a signaling complex tha

263 The SLP-76 phosphotyrosine-containing sequence, pY(173)IDR,

264 The SLP-76 pY(173) motif competes with the autoinhibited con

265 YopH inactivated PRAM-1/SKAP-HOM and the SLP-76/Vav/PLCgamma2 signal transduction axes, leading t

266 Furthermore, the SLP-76-mediated induction of IL-2 and CD69 could be furt

267 B cells as a source of IgM production in the SLP mice.

268 its effects via intermediaries including the SLP adaptors, SLP-76 and BLNK (B cell linker).

269 We discovered that one of the SLP contains a linear Ab epitope in combination with a C

270 the results show a linear dependence of the SLP with AMF frequency, as anticipated by current models

271 ACK1 induced phosphorylation of the SLP-76 N-terminal tyrosines (3Y) dependent on the SAM do

272 e peptide that represents the portion of the SLP-76 PR region that interacts with the ITK SH3 domain

273 During the acute phase, the SLP-derived sector correlated with presentation (r = 0.5

274 6 SH2 domain mutant, we demonstrate that the SLP-76 SH2 domain is required for peripheral T cell acti

275 d amount of confounding light getting to the SLP light detectors.

276 e Src kinase, Lck, and binding of Itk to the SLP-76/LAT adapter complex.

277 e Src kinase, Lck, and binding of Itk to the SLP-76/LAT adapter complex.

278 le RNFL measurements were obtained using the SLP and OCT.

279 While the SLP-76-RanGAP1 (K56E) mutant had no effect on proximal s

280 a third or subsequent vaccinations with the SLP when formulated in saline.

281 mulation of the cytoplasmic precursor of the SLPs SlpA and other cell wall proteins was observed in c

282 Thus, SLP-76 and ADAP are involved in E-selectin-mediated inte

283 ty analysis confirmed the binding of ACK1 to SLP-76.

284 on OCT might be an attractive alternative to SLP because OCT provides an objective and 3-dimensional

285 nd that SLP-76 relocalization corresponds to SLP-76-dependent integrin function in T cells.

286 tivated T cells (LAT), that couples ZAP70 to SLP-76.

287 Thus, we asked whether these two SLP proteins regulate OC function.

288 ex shows an elongated molecule, with the two SLPs arranged 'end-to-end' interacting with each other t

289 study we examine a mouse in which wild-type SLP-76 is replaced with a mutant constitutively targeted

290 of Lcp2 that reduced the amount of wild-type SLP-76 protein by ~90%, disrupting immunogenic and toler

291 in 32 sectors (11.25 degrees each) by using SLP with variable cornea compensation (GDxVCC; Laser Dia

292 different vaccine formulations in mice using SLP derived from carcinoembryonic Ag.

293 mokine-stimulated associations between Vav1, SLP-76, and ADAP facilitate Rac1 activation and alpha4be

294 T-cell immunity, it has been unclear whether SLP-76 directly self-associates to form higher order oli

295 ntifying platelets as the cell type in which SLP-76 signaling is required to regulate lymphatic vascu

296 We propose that while SLP-76 and LAT1 depend on each other for many of their f

297 -actin-rich structures that colocalized with SLP-76 and the Rac1 exchange factor, phospho-Vav1.

298 ten healthy subjects were investigated with SLP and spectral domain OCT.

299 rsus 63.73 +/- 6.58; p = 0.03) obtained with SLP compared with healthy individuals.

300 stimulation in the association of Vav1 with SLP-76, Pyk2, and ADAP was observed.

301 cause of the MTS phenotype, we expressed WT SLP-76 along with the MTS followed by deletion of the WT