ライフサイエンスコーパス: SLO

1 SLO development depends on the precisely regulated expre

2 SLO is required for CMT and can accomplish this activity

3 SLO TRM were overrepresented in IL-15-deficient mice, su

4 SLO's translocation activity does not require host cell

5 SLO-1 belongs to a family of channels that are highly co

6 SLO-1 expressed in Xenopus oocytes could be activated by

7 SLO-2 activity in motor neurons depends on Ca(2+) entry

8 SLO-deficient GAS mutants induced less macrophage apopto

9 ctural properties of soybean lipoxygenase-1 (SLO-1).

10 nd/or phagocytosis by the HA capsule and (2) SLO-mediated induction of DC apoptosis by intracellular

11 ine significance (MP-1, 2.51 log min arc(2); SLO, 2.26 log min arc(2); P = 0.06).

12 1 and SLO values (MP-1, 2.94 log min arc(2); SLO, 2.90 log min arc(2); P = 0.88).

13 egree) FA and ICGA, using the Staurenghi 230 SLO Retina Lens and the Heidelberg scanning laser ophtha

14 In the absence of ERG-28, SLO-1 channels undergo aspartic protease DDI-1-dependent

15 In addition to its cytolytic activity, SLO mediates the translocation of GAS NAD-glycohydrolase

16 were apparent as autofluorescent foci on AF-SLO.

17 uorescence scanning laser ophthalmoscopy (AF-SLO) and electroretinography, and the extent of laser-in

18 All SLOs serve to generate immune responses and tolerance.

19 Only prevention of T-cell entry to all SLOs could completely abrogate the onset of aGVHD.

20 tion in both types of cells without altering SLO-1 protein level.

21 central plane of the vitreous humor with an SLO.

22 s no significant difference between MP-1 and SLO values (MP-1, 2.94 log min arc(2); SLO, 2.90 log min

23 BKIP-1 and SLO-1 showed similar expression and subcellular localiza

24 Detailed ERG and SLO analysis supported the histopathologic findings.

25 ich correlated with the amount of NADase and SLO activities in culture supernatant fluids.

26 Production of both NADase and SLO is associated with augmented host cell injury beyond

27 Group IV, OCT exhibited 100% sensitivity and SLO 77% sensitivity for an attenuated RNFLT in patients

28 l relationship between production of SLS and SLO and poor outcomes.

29 ed stG6792 strains secreted abundant SLS and SLO rather than other SDSE emm types, indicating the pot

30 We conclude that both SPN and SLO contribute significantly to S. pyogenes pathogenesis

31 The biological functions of SPN and SLO have been extensively studied using eukaryotic cell

32 showed that increased production of SPN and SLO in epidemic serotype M1 and M89 S. pyogenes strains

33 The mutant strain lacking both SPN and SLO production is severely attenuated in ability to resi

34 luated the relative contributions of SPN and SLO toxins to virulence in mouse models of necrotizing m

35 regulated virulence factors (such as SPN and SLO), and increased virulence in a mouse model of necrot

36 elevation of CXCL10 expression in blood and SLOs was secondary to the induction of CD14(+) CD16(+) m

37 erature, rapidly quenched microspherules and SLOs; (ii) corundum, mullite, and suessite (Fe(3)Si), a

38 OCT and ERG parameters, as well as AO-SLO cone densities, were stable during treatment.

39 n of retinal hard exudates in patients by AO-SLO may help in understanding the pathogenesis and clini

40 ive optics scanning laser ophthalmoscopy (AO-SLO) to examine the characteristics of hard exudates in

41 ive optics scanning laser ophthalmoscopy (AO-SLO).

42 Six eyes had serial AO-SLO imaging.

43 High resolution imaging using AO-SLO enables morphological classification of retinal hard

44 These cells were positioned at SLO entry points for peripheral Ags: the splenic margina

45 ocalized measurement with a widely available SLO of rhodopsin, the most abundant protein in the retin

46 in the human retina with a widely available SLO.

47 Because SLO is the prototype of cholesterol-dependent cytolysins

48 didates by which prion dissemination between SLO may occur.

49 tion of B cells that can recirculate between SLO.

50 proteins from FDC and recirculating between SLO via the blood and lymph mediate the initial propagat

51 ants of SLO and binding domain swaps between SLO and homologous cholesterol-dependent cytolysins reve

52 mined that the big current K(+) channel (BK)/SLO-1 genetically interacts with ether-a-go-go (EAG)/EGL

53 A general caspase inhibitor blocked SLO-induced apoptosis and enhanced macrophage killing of

54 cytolysins revealed that membrane binding by SLO is necessary but not sufficient for CMT, demonstrati

55 o-secretion of SPN but not glycan binding by SLO.

56 deficient neurotransmitter release caused by SLO-1(gf).

57 of fundus autofluorescence were detected by SLO imaging of any strain.

58 rane binding also promotes pore formation by SLO, demonstrating that pore formation can occur by dist

59 ll membrane cholesterol or pore formation by SLO, yet SLO does form pores during infection via a chol

60 odepside-selective pharmacophore harbored by SLO-1.

61 effect on the release is mainly mediated by SLO-1 activation.

62 ted host cell injury beyond that produced by SLO alone, but the mechanism of enhanced cytotoxicity is

63 egions in muscle cells, and dyb-1(lf) caused SLO-1 mislocalization in both types of cells without alt

64 lter the expression of either the BK channel SLO-1 or the Shaker type potassium channel SHK-1.

65 ed by mutation or blockade of the BK channel SLO-1.

66 ffectors, the calcium-activated K(+) channel SLO-1 and gap junctions, and show that they contribute t

67 nnel SHK-1 and the Ca2+/Cl--gated K+ channel SLO-2 play important roles in controlling the speed of m

68 t is the calcium-activated potassium channel SLO-1.

69 Comparisons of whole-cell and single-channel SLO-2 currents in native neurons and muscle cells betwee

70 ns, mutations that eliminate the BK channel, SLO-1, convey dramatic resistance to intoxication by eth

71 calization of the Ca(2+)-gated K(+) channel, SLO-1, in muscle cells, while ionotropic acetylcholine r

72 The OCT, confocal SLO and ICG fluorescence images were simultaneously pres

73 B- or C-scan OCT images along with confocal SLO views, with and without ICG filtration.

74 t only do stromal cells physically construct SLO architecture but they are essential for regulating h

75 ptosis induced by the pore-forming cytolysin SLO contributes to GAS immune evasion and virulence.

76 mRNA, and hrpu-2(lf) mutants show decreased SLO-2 protein expression.

77 acceleration in the onset of renal disease, SLO germinal center formation, and autoreactive plasma c

78 chemokine receptor profile, thus disrupting SLO homing, while driving migration toward inflammatory

79 BKIP-1, an auxiliary subunit of C. elegans SLO-1, facilitates SLO-1 membrane trafficking and regula

80 serves as an auxiliary subunit of C. elegans SLO-2, a high-conductance K(+) channel gated by membrane

81 rculation, DKO SP thymocytes failed to enter SLOs.

82 The activation of eukaryotic SLO K(+) channels by intracellular cues, mediated by a c

83 ary subunit of C. elegans SLO-1, facilitates SLO-1 membrane trafficking and regulates SLO-1 function

84 d images), examination plus ultra wide-field SLO images, and examination plus wide-field FA.

85 rization (AHP) and the pattern of AP firing; SLO-2 is also important in setting the resting membrane

86 The aggregate data for SLO-1 show how judicious placement of hydrophobic side c

87 from Tfh cells acts as a survival factor for SLO PC in vivo.

88 erol was considered the primary receptor for SLO, SLO's membrane-binding domain also encodes a putati

89 Despite being the only known receptor for SLO, this membrane interaction does not require choleste

90 periments suggest that DYB-1 is required for SLO-1 function in both neurons and muscle cells.

91 MT, demonstrating a specific requirement for SLO in this process.

92 on controls the egress of T and B cells from SLO.

93 APCs isolated from SLO of B cell-depleted EAE monkeys were also less respon

94 promotes mobilization of leukemic cells from SLOs, normalizes the imbalance between CXCR4/CCR7 and S1

95 Consistent with a potential role in guarding SLO pathogen entry points, SLO TRM did not vacate their

96 tion of the Caenorhabditis elegans homologue SLO-2 in motor neurons through electrophysiological anal

97 However, SLO also recognizes host cell membranes via a second mec

98 a sluggish phenotype caused by a hyperactive SLO-2.

99 Tunneling-impaired SLO variants show increased DADs and variations in subst

100 Neutrophils accumulate in SLO over the course of lupus progression, preferentially

101 VHD similar to WT T cells and accumulated in SLO and target organs in similar numbers as WT T cells.

102 ns suggest that the loss of a salt bridge in SLO and a cation-pi interaction are determining factors

103 bset of virus-specific memory CD8 T cells in SLO exhibit phenotypic signatures associated with TRM, i

104 oles for DL ligand-expressing fibroblasts in SLO niches as drivers of multiple Notch-mediated immune

105 ealed that glycan recognition is involved in SLO's pore formation pathway and is an essential step wh

106 if and the rest of domain 4 that are lost in SLO.

107 bic residues by site-specific mutagenesis in SLO reduces the reaction rate 10(4)-fold and is accompan

108 suggest that HRPU-2 plays important roles in SLO-2 function by regulating SLO-2 protein expression, a

109 nition, adopts a very different structure in SLO to that of the well-characterized CDC perfringolysin

110 ments of proton-coupled electron transfer in SLO and (ii) sensitivity of ENDOR probes to test, detect

111 e ability of leukemic cells to accumulate in SLOs.

112 y in circulating leukemic cells, but also in SLOs of CLL patients with lymphoadenopathy.

113 s between stromal and hematopoietic cells in SLOs are therefore integral to the normal functioning of

114 on of Ly-6C(-)CD44(hi) gammadelta T cells in SLOs.

115 geting of CXCR3(+) CCR5(+) CD4(+) T cells in SLOs.

116 otoxin alpha knockout (LT) mice deficient in SLOs as recipients.

117 Restricted infection in SLOs by Delta5G also suggests that glycosylation of Env

118 nificantly higher levels of SIV infection in SLOs occurred with a massive accumulation of infiltrated

119 AC387(+) macrophages recently infiltrated in SLOs.

120 sm is responsible for camouflaging prions in SLOs and has broad implications.

121 f T cells from blood, prolonged retention in SLOs, and accumulation in bone marrow, but did not alter

122 s infected distinct CD4(+) T cell subsets in SLOs and the small intestine, respectively (C.

123 1 in a Ca(2)+-dependent manner and increased SLO-1 surface expression.

124 teraction critical for T-cell migration into SLOs.

125 suppressive cells from tertiary tissues into SLOs.

126 veal region, appeared hyper-reflective in IR-SLO and were called peripheral pseudodrusen.

127 ere seen more frequently in color than in IR-SLO images (P < .001).

128 ts, often with a target configuration, in IR-SLO images.

129 his subtype was faintly hyporeflective in IR-SLO imaging.

130 d infrared scanning laser ophthalmoscope (IR-SLO) images of patients with pseudodrusen were evaluated

131 Correlations were made between the IR-SLO, SD-OCT, and AO images.

132 dodrusen were detected more commonly with IR-SLO imaging than in color photography (P = .014) and rib

133 IL-21 enhanced Ig secretion by isolated SLO PC but not bone marrow PC.

134 A double mutant lacking SLO and NADase activity had an intermediate virulence ph

135 ohol dehydrogenase and soybean lipoxygenase (SLO) as compared to Fe(III) metal complexes], and the ge

136 The enzyme soybean lipoxygenase (SLO) has served as a prototype for hydrogen-tunneling re

137 atic tunneling system, soybean lipoxygenase (SLO), it has remained unclear whether the requisite clos

138 ied a double mutant of soybean lipoxygenase (SLO-1, an enzyme previously shown to follow quantum mech

139 hers that produce crucial cytokines maintain SLOs in the adult.

140 r the SLO Fe ion; X-ray diffraction shows Mn-SLO is structurally faithful to the native enzyme.

141 In ctn-1 loss-of-function (lf) mutants, SLO-1 was mislocalized in body-wall muscle but its trans

142 In hrpu-2(lf) mutants, SLO-2-mediated delayed outward currents in neurons are g

143 eurons abolishes the bursts whereas mutating SLO-1 K(+) channel, a potent presynaptic inhibitor of ex

144 transgenic experiments in which the nematode SLO-1 channel was swapped for a mammalian ortholog, huma

145 from the draining lymph node to nondraining SLO is blocked.

146 or trafficking into inflamed tissues but not SLO and that donor T cells may use multiple P-selectin l

147 extracellular DNase Sda1 and streptolysin O (SLO) activity in vivo, whereas subinhibitory CLI concent

148 Two such proteins, streptolysin O (SLO) and NAD(+)-glycohydrolase (NADase), have been shown

149 NADase (SPN) and streptolysin O (SLO) are two toxins that play important roles in pathoge

150 d the pore-forming cytolysin streptolysin O (SLO) as necessary and sufficient for the apoptosis-induc

151 eB cysteine protease and the streptolysin O (SLO) cytolysin, but not SIC, a protein that protects S.

152 Streptolysin O (SLO) is a cholesterol-dependent cytolysin produced by th

153 holesterol-binding cytotoxin streptolysin O (SLO) prevented internalization of GAS into lysosomes.

154 of streptolysin S (SLS) and streptolysin O (SLO) production between clinically dominant stG6792 stra

155 ion with the bacterial toxin streptolysin O (SLO) requires endocytosis via a novel pathway that remov

156 lesterol-dependent cytolysin Streptolysin O (SLO) to translocate the NAD(+) -glycohydrolase (SPN) int

157 lesterol-dependent cytolysin Streptolysin O (SLO) to translocate the NAD(+) glycohydrolase SPN into h

158 al member of the CDC family, streptolysin O (SLO), a virulence factor from Streptococcus pyogenes.

159 , perfringolysin O (PFO) and streptolysin O (SLO), were found to exhibit strikingly different binding

160 rge amounts of the cytotoxin streptolysin O (SLO).

161 -glycohydrolase (NADase) and streptolysin O (SLO).

162 S. pyogenes NADase (SPN) and streptolysin O (SLO).

163 actor IFS and the cytolysin (streptolysin O [SLO]), were more abundant in the mutant strain, which co

164 ences may explain the differing abilities of SLO and PFO to efficiently penetrate target cell membran

165 inant GAS NADase in yeast, in the absence of SLO, induced growth arrest, depletion of NAD+ and ATP, a

166 ntrations induced expression and activity of SLO, DNase, and Streptococcus pyogenes cell envelope pro

167 e provided evidence that the augmentation of SLO-mediated cytotoxicity by NADase is a consequence of

168 This SPN-mediated membrane binding of SLO correlates with SPN translocation, and requires SPN'

169 y without pore formation, but the details of SLO's interaction with the membrane preceding SPN transl

170 This disruption of SLO-homing capacity in response to respective chemokines

171 portant role in regulating the expression of SLO-2 (a homolog of mammalian Slo2) in Caenorhabditis el

172 a demonstrating the functional importance of SLO fibroblasts during Notch-mediated lineage specificat

173 type caused by a gain-of-function isoform of SLO-1 in Caenorhabditis elegans, we isolated multiple lo

174 xpressing a gain-of-function (gf) isoform of SLO-1.

175 t manner, through the proper localization of SLO-1 channels.

176 is required for subcellular localization of SLO-1, the Caenorhabditis elegans BK channel alpha-subun

177 103 can partially compensate for the loss of SLO-1 function.

178 nsable for both formation and maintenance of SLO microarchitecture; their expression of lymphotoxin a

179 ings and the postsynaptic mislocalization of SLO-1, we observed an increase in muscle excitability do

180 Analysis of binding domain mutants of SLO and binding domain swaps between SLO and homologous

181 lesterol from host membranes and mutation of SLO's cholesterol recognition motif abolished pore forma

182 rate, and single-channel open probability of SLO-2.

183 d with significantly increased production of SLO and NADase.

184 c activity associated with GAS production of SLO.

185 his loop conferred the binding properties of SLO to PFO and vice versa.

186 fted the conductance-voltage relationship of SLO-1 in a Ca(2)+-dependent manner and increased SLO-1 s

187 BKIP-1 may serve as an auxiliary subunit of SLO-2.

188 embrane protein, promotes the trafficking of SLO-1 BK channels from the ER to the plasma membrane by

189 s generated and maintained in the absence of SLOs.

190 could respond to challenge in the absence of SLOs.

191 allenge infection in the complete absence of SLOs.

192 study illustrates that, upon colonization of SLOs, the sialylation status of prions changes by host S

193 The wide geographic distribution of SLOs is consistent with multiple impactors.

194 Despite a lack of SLOs, intrapulmonary allografts in splenectomized LT mic

195 Thus, we demonstrate redundancy of SLOs at different anatomical sites in aGVHD initiation.

196 atants for erythrocytes but had no effect on SLO-mediated poration of synthetic cholesterol-rich lipo

197 abundant TAG of olive oils were ECN 48, OOO, SLO+POO, ECN 46 and LOO/PLO.

198 ra wide-field scanning laser ophthalmoscope (SLO) imaging and angiography.

199 quired with a scanning laser ophthalmoscope (SLO) were constructed from the measured OCT data, which

200 the maze in a scanning laser ophthalmoscope (SLO).

201 n situ with a scanning laser ophthalmoscope (SLO).

202 laris using a scanning laser ophthalmoscope (SLO).

203 he Rodenstock scanning laser ophthalmoscope (SLO; Rodenstock GmbH, Munich, Germany) in persons with a

204 (IR) confocal scanning laser ophthalmoscopy (SLO) and eye-tracked spectral-domain optical coherence t

205 (SD-OCT) and scanning laser ophthalmoscopy (SLO) every other month and histological, biochemical, an

206 h, wide-field scanning laser ophthalmoscopy (SLO), and investigated the effect of rhodopsin bleaching

207 blin, CA) and scanning laser ophthalmoscopy (SLO; Heidelberg Retinal Tomograph; Heidelberg Engineerin

208 e of isogenic mutants deficient in HA and/or SLO, we determined that GAS inhibits DC maturation throu

209 s through blocking monoclonal antibodies, or SLO ablation, did not alter aGVHD pathophysiology.

210 In addition, mutants lacking either SPN or SLO are significantly attenuated in the bacteremia and s

211 mperature, siliceous scoria-like objects, or SLOs, that match the spherules geochemically.

212 of CXCR4, but not secondary lymphoid organ (SLO)-homing CCR7.

213 ast-like cells of secondary lymphoid organs (SLO) are important for tissue architecture.

214 Secondary lymphoid organs (SLO) provide the structural framework for coconcentratio

215 most nondraining secondary lymphoid organs (SLO), including the spleen, by a previously underdetermi

216 er they populated secondary lymphoid organs (SLO).

217 ailed analysis of secondary lymphoid organs (SLO).

218 iate zones within secondary lymphoid organs (SLO).

219 g and egress from secondary lymphoid organs (SLO).

220 CD4(+) T cells in secondary lymphoid organs (SLOs) and within the lamina propria of the small intesti

221 nd that different secondary lymphoid organs (SLOs) imprint distinct homing receptor phenotypes on evo

222 relationship with secondary lymphoid organs (SLOs) in allograft airway rejection.

223 Secondary lymphoid organs (SLOs) include lymph nodes, spleen, Peyer's patches, and

224 nd the underlying secondary lymphoid organs (SLOs) needs to be established to prime adaptive immune r

225 Secondary lymphoid organs (SLOs) promote primary immune responses by recruiting nai

226 pheral tissues to secondary lymphoid organs (SLOs) through the afferent lymph.

227 te between blood, secondary lymphoid organs (SLOs), and lymph in the steady state.

228 Secondary lymphoid organs (SLOs), including lymph nodes, Peyer's patches, and the s

229 cell migration to secondary lymphoid organs (SLOs), reduced in vivo proliferation within these organs

230 autoreactivity in secondary lymphoid organs (SLOs), we characterized the localization and cell-cell c

231 irculation and in secondary lymphoid organs (SLOs).

232 in the spleen and secondary lymphoid organs (SLOs).

233 te efficiently to secondary lymphoid organs (SLOs).

234 h colonization of secondary lymphoid organs (SLOs).

235 , and the spleen (secondary lymphoid organs [SLO]) but barely on terminally mature bone marrow PC.

236 The retina was imaged with an Optos P200C SLO by its reflectance of 532 and 633 nm light, and its

237 role in guarding SLO pathogen entry points, SLO TRM did not vacate their position in response to per

238 The spleen is the primordial SLO, and evolved concurrently with Ig/TCR:pMHC-based ada

239 n at intraretinal hyperreflective foci on PS-SLO and PS-OCT images, and by the presence of hyper-AF o

240 -sensitive scanning laser ophthalmoscope (PS-SLO), and the degree of polarization uniformity was calc

241 Purified recombinant SLO bound NADase in vitro, supporting a specific, physic

242 tes SLO-1 membrane trafficking and regulates SLO-1 function in neurons and muscle cells.

243 ortant roles in SLO-2 function by regulating SLO-2 protein expression, and that SLO-2 is likely among

244 endocytosis via a novel pathway that removes SLO-containing pores from the plasma membrane.

245 SPN's membrane localization also requires SLO, suggesting a co-dependent, cholesterol-insensitive

246 Analysis of carbohydrate-binding site SLO mutants and carbohydrate-defective cell lines reveal

247 was considered the primary receptor for SLO, SLO's membrane-binding domain also encodes a putative ca

248 nd regulates the expression of the Slowpoke (SLO) BK potassium channel.

249 r dynamics simulations of the fully solvated SLO model using ENDOR-derived restraints give additional

250 Yet preventing T-cell entry to specific SLOs through blocking monoclonal antibodies, or SLO abla

251 All imaging was performed using a Spectralis SLO+OCT device (Heidelberg Engineering, Heidelberg, Germ

252 We found that isogenic mutants lacking SPN, SLO, and both toxins are equally impaired in ability to

253 ive membrane binding; in the absence of SPN, SLO's binding is characteristically cholesterol-dependen

254 (gf) isoform of the BK channel alpha-subunit SLO-1.

255 Surprisingly, SLO requires the coexpression and membrane localization

256 subjects, MP-1 BCEA values were larger than SLO by 0.25 log min arc(2), though the difference was sm

257 egulating SLO-2 protein expression, and that SLO-2 is likely among a restricted set of proteins regul

258 We find that SLO-2 is the primary K(+) channel conducting delayed out

259 enotype, consistent with the hypothesis that SLO evokes a protective innate immune response.

260 Parabiosis revealed that SLO CD69(+) memory CD8 T cells do not circulate, definin

261 nt to initiate autoimmunity, indicating that SLOs are a primary site for maintaining peripheral toler

262 These data show that SLOs are dispensable for the maintenance of immunologic

263 uce Mn(2+) as a spin-probe surrogate for the SLO Fe ion; X-ray diffraction shows Mn-SLO is structural

264 DYSC and uncover non-canonical roles for the SLO potassium channel at Drosophila synapses.

265 difference was found in BCEA values from the SLO and MP-1 in control subjects and patients with diabe

266 Video images from the SLO showing the fingers and maze on the retina during th

267 a less immunostimulatory environment in the SLO reflected by reduced expression of MHC class II, CD4

268 ins with different missense mutations in the SLO-1 channel.

269 works transport small antigens deep into the SLO parenchyma.

270 ting three-dimensional representation of the SLO active site ground state contains a reactive (a) con

271 on stability was recorded monocularly on the SLO and the MP-1 in counterbalanced order while particip

272 ke it a useful and viable alternative to the SLO in the assessment of fixation.

273 A strain with the SLO-1 missense mutation T381I in the RCK1 domain was hig

274 stence of resident gammadelta T cells in the SLOs of specific pathogen-free mice.

275 Thus, SLO-2 is functionally coupled with CaV1 and regulates ne

276 P-1 is a novel auxiliary subunit critical to SLO-1 function in vivo.

277 xtend the range of tissue resident memory to SLO.

278 ions, distinct subsets of DCs can migrate to SLOs via afferent lymph.

279 correlates with impaired Treg recruitment to SLOs and, conversely, promotion of Tregs into these tiss

280 Diminished Treg trafficking to SLOs is sufficient to initiate autoimmunity, indicating

281 ed through modulation of Treg trafficking to SLOs, a process that can be controlled by adjusting KLF2

282 stream of DCs from peripheral regions toward SLOs under normal conditions.

283 The pore-forming toxin SLO was directly visualized entering cells within caveol

284 to the surface of epithelial cells in vitro, SLO forms pores in the cell membrane and delivers NADase

285 mation pathway and is an essential step when SLO is secreted by non-adherent bacteria, as occurs duri

286 :CXCL13 positive feedback loop without which SLO cannot properly form.

287 ody-wall muscle cells, CTN-1 coclusters with SLO-1 at regions of dense bodies, which are Z-disk analo

288 DYB-1 colocalized with SLO-1 at presynaptic sites in neurons and dense body reg

289 n assays indicate that BKIP-1 interacts with SLO-2 carboxyl terminal.

290 tonin-stimulated feeding by interfering with SLO-1 signaling in the nervous system.

291 hown that expression of NADase together with SLO dramatically enhanced the lytic activity of GAS cult

292 ty tests were performed after treatment with SLO to ensure that the cells have intact membranes, are

293 sustained CCR7 expression on T cells within SLO, limiting their release into the circulation.

294 e dynamics and priming of lymphocytes within SLO even in the absence of significant concentration gra

295 aling blockade sequesters lymphocytes within SLO, resulting in lymphopenia in the blood and lymph.

296 s for regulating immune cell function within SLOs.

297 f CCR7 to mount host immune responses within SLOs during gastrointestinal Yersinia pseudotuberculosis

298 us tissue occurs in a delayed manner without SLO in association with intrapulmonary lymphoid neogenes

299 ble of mounting alloimmune responses without SLOs.

300 ne cholesterol or pore formation by SLO, yet SLO does form pores during infection via a cholesterol-d