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 were apparent as autofluorescent foci on AF-SLO.

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

17 All SLOs serve to generate immune responses and tolerance.

18 lly serve this function and are found in all SLOs except spleen.

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 btype is established using gap junctions and SLO BK potassium channels to repress a calcium-activated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

40 Six eyes had serial AO-SLO imaging.

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

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

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

44 in the human retina with a widely available SLO.

45 didates by which prion dissemination between SLO may occur.

46 tion of B cells that can recirculate between SLO.

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

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

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

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

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

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

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

54 eferential lysis of uninfected host cells by SLO, and therefore modulate the effectiveness of SLOPE.

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

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

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

58 odepside-selective pharmacophore harbored by SLO-1.

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

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

61 tified the Caenorhabditis elegans BK channel SLO-1 as a molecular target of the Mel receptor PCDR-1-.

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

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

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

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

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

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

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

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

70 Likewise, depletion of clustered SLO-1 channels in the sarcolemma and neurons leads to et

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

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

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

74 s mechanistic insight into how NSY-7 couples SLO BK potassium channels to transactivation of sox-2 ex

75 in the maintenance of AWC asymmetry, couples SLO BK potassium channels to transactivation of sox-2 ex

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

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

78 etween DF SLO and en face OCT and between DF SLO and CFP for grader 1 was 0.89 and 0.95, respectively

79 aluation of the area of the nevus between DF SLO and en face OCT and between DF SLO and CFP for grade

80 pa values in reproducibility analysis for DF SLO, en face OCT, and CFP were 0.8, 0.71, and 0.67, resp

81 Multimodal imaging, including DF SLO, OCT, and CFP, was performed in 24 patients (24 eyes

82 Using DF SLO in 17 patients (70.8%) and 7 patients (29.2%), nevus

83 Using DF SLO, each nevus was characterized according to the inten

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

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

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

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

88 rculation, DKO SP thymocytes failed to enter SLOs.

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

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

91 Dark-field SLO demonstrated excellent potential for identifying cho

92 Dark-field SLO showed the highest area under the receiver operating

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

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

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

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

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

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

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

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

101 crystallography and EPR spectroscopy on four SLO variants (wild-type (WT) enzyme, DM, and the two par

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

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

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

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

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

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

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

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

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

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

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

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

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

115 C. elegans, loss of function in SLO-1, the BK channel ortholog, confers profound ethanol

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

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

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

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

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

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

122 e ability of leukemic cells to accumulate in SLOs.

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

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

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

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

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

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

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

130 AC387(+) macrophages recently infiltrated in SLOs.

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

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

133 1 in a Ca(2)+-dependent manner and increased SLO-1 surface expression.

134 teraction critical for T-cell migration into SLOs.

135 suppressive cells from tertiary tissues into SLOs.

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

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

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

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

140 s Infrared Scanning Laser Ophthalmoscope (IR-SLO) and Optical Coherence Tomography (OCT) could help i

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

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

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

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

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

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

147 Soybean lipoxygenase (SLO) has served as a prototype for understanding the mol

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

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

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

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

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

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

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

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

156 -channel open probability (P(o)) of neuronal SLO-2 is ~50% lower in scyl-1 knockout mutant than wild

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

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

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

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

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

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

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

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

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

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

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

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

169 We demonstrate that streptolysin O (SLO)-induced glutathione efflux from host cellular store

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

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

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

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

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

175 Here, we show that depletion of SLO-1 channels clustered at the active zones with no cha

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

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

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

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

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

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

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

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

184 103 can partially compensate for the loss of SLO-1 function.

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

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

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

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

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

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

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

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

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

194 s generated and maintained in the absence of SLOs.

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

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

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

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

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

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

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

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

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

204 laris using a scanning laser ophthalmoscope (SLO).

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

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

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

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

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

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

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

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

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

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

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

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

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

218 er they populated secondary lymphoid organs (SLO).

219 ailed analysis of secondary lymphoid organs (SLO).

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

221 Secondary lymphoid organs (SLOs) are important initiators and regulators of immunit

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

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

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

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

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 h colonization of secondary lymphoid organs (SLOs).

232 irculation and in secondary lymphoid organs (SLOs).

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

234 te efficiently to secondary lymphoid organs (SLOs).

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

236 By contrast, reduction in the overall SLO-1 channel level by over 70% causes only moderate eth

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

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

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

240 ADR-1 promotes SLO-2 function not by editing the transcripts of slo-2 b

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

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

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

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

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

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

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

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

249 e show that the function of C. elegans Slo2 (SLO-2) depends on adr-1, a gene important to RNA editing

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

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

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

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

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

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

256 ecently published QM/MM-derived ground-state SLO-substrate complexes for WT and DM, together with the

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

258 Surprisingly, SLO requires the coexpression and membrane localization

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

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

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

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

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

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

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

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

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

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

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

270 and recruit circulating lymphocytes into the SLO parenchyma, where they encounter cognate antigen.

271 works transport small antigens deep into the SLO parenchyma.

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

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

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

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

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

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

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

279 xtend the range of tissue resident memory to SLO.

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

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

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

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

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

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

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

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

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

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

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

291 SCYL-1 physically interacts with SLO-2 in neurons.

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

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

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

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