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 SLP-8348 was previously shown to enhance LPS-induced act

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

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

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

13 m probiotic Lactobacillus kefiri CIDCA 8348 (SLP-8348) is recognized by Mincle (macrophage inducible

14 ycosylation pattern of three SLPs, SLP-8348, SLP-8321, and SLP-5818, and explore how these patterns i

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

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

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

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

27 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

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

29 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

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

31 ndritic cells; we now show that SLP-8321 and SLP-5818 have a similar effect regardless of the differe

32 ttern of three SLPs, SLP-8348, SLP-8321, and SLP-5818, and explore how these patterns impact their re

33 lation signals were detected in SLP-8348 and SLP-8321, but SLP-5818 was observed to have two sites ca

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

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

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

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

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

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

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

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

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

46 OCT and SLP revealed different aspects of RNFL changes associate

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

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

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

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

51 results indicate that the presence of PR and SLP in cell culture media may significantly impact in vi

52 We show for the first time that PR and SLP themselves suppress expression of differentiation-sp

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

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

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

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

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

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

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

60 We demonstrate that both SLPs localize to mitochondrial membranes.

61 were detected in SLP-8348 and SLP-8321, but SLP-5818 was observed to have two sites carrying complex

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

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

64 reduction of the RNFL thickness assessed by SLP.

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

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

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

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

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

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

71 demonstrate that the Caulobacter crescentus SLP readily crystallizes into sheets in vitro via a calc

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

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

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

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

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

77 all estimates was selected as the estimated SLP.

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 resveratrol, and naringin in the fruit from SLP.

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

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

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

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

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

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

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

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

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

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

93 No N-glycosylation signals were detected in SLP-8348 and SLP-8321, but SLP-5818 was observed to have

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

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

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

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

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

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

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

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

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

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

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

114 the immunomodulatory effect of the L. kefiri SLPs on antigen-presenting cells.

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

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

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

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

119 localization of three adaptor proteins, LAT, SLP-76, and Grb2.

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

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

122 Although serum lipids (SLPs) and phenol red (PR) are ubiquitous components of c

123 These surface lipoproteins (SLPs) fulfill critical roles in immune evasion and nutri

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

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

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

127 ulting in larger variance of calculated mean SLP values.

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

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

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

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

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

133 nisms of binding and in the discovery of new SLPs.

134 elaborate on the structures of some notable SLPs required for binding target molecules in hosts and

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

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

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

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

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

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

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

142 30 wk after LCMV infection in the absence of SLP-76.

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

144 ealed that the immunostimulatory activity of SLP-8321 depends on its recognition by Mincle, whereas S

145 3-3 binding, resulting in the attenuation of SLP-76 activation and downstream signaling; however, the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

160 plasma membrane recruitment and function of SLP-76.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

180 Removal of SLP increased expression of K1, K10 and K2 in 2D and 3D

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

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

183 30 is identified as a ubiquitination site of SLP-76.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 ocal longshore winds induced by the positive SLP anomalies caused strong offshore Ekman transport alo

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

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

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

215 d with an unusually high sea level pressure (SLP) pattern over the NE Pacific.

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

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

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

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

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

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

222 n imaging, and tracking the S-layer protein (SLP) from C. crescentus, we show that 2D protein self-as

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 S-layer (glyco)-proteins (SLPs) form a nanostructured envelope that covers the sur

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

227 S-layer proteins (SLPs) regulate their extracellular self-assembly by crys

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

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

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

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

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

233 This review will focus on representative SLPs that gram-negative bacteria use to overcome host in

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

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

236 -molecule tracking whereby randomly secreted SLP monomers diffuse on the lipopolysaccharide (LPS) out

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

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

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

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

241 yze the glycosylation pattern of three SLPs, SLP-8348, SLP-8321, and SLP-5818, and explore how these

242 -driven phase separation of LAT, Grb2, Sos1, SLP-76, Nck, and WASP.

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

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

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

246 5 in the absence of H1-4 sufficed to support SLP-76 self-association with smaller microclusters that

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

263 ow-derived dendritic cells; we now show that SLP-8321 and SLP-5818 have a similar effect regardless o

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

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

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

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

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

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

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

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

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

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

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

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

276 6 SH2 domain mutant, we demonstrate that the SLP-76 SH2 domain is required for peripheral T cell acti

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

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

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

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

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

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

283 n of both the potential application of these SLPs as new adjuvants and the protein glycosylation mech

284 e analyze the glycosylation pattern of three SLPs, SLP-8348, SLP-8321, and SLP-5818, and explore how

285 ajor component in the O-glycans of the three SLPs; however, some differences in the length of hexose

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

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

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

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

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

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

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 epends on its recognition by Mincle, whereas SLP-5818's effects are dependent on SignR3 (murine ortho

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

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

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

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.