ライフサイエンスコーパス: SOS

1 SOS (Swedish Obese Subjects) is a prospective matched co

2 SOS Env supported virus entry and cell-cell fusion only

3 SOS is freely available to use at sites.google.com/view/

4 SOS-induced levels of DNA polymerase IV (Pol IV) confer

5 SOS-SFC appears possible without any density correction,

6 SOS versus 26.6% of patients with grade 0-1 SOS (P = 0.032).After a median follow-up of 36.9 months,

7 occurred in 16.9% of patients with grade 2-3 SOS versus 26.6% of patients with grade 0-1 SOS (P = 0.0

8 sponse is reduced in patients with grade 2-3 SOS.

9 dditionally, wild mango butter comprises 65% SOS (1, 3-distearoyl-2-oleoyl-glycerol) which indicates

10 In addition, SOS induction could lead to markedly elevated bypass eff

11 t pyocin production during the P. aeruginosa SOS response carries both expected and unexpected costs.

12 A0906, coordinate the Pseudomonas aeruginosa SOS response.

13 Both before and after SOS induction, RecA* largely appears at locations distal

14 When all SOS genes are constitutively expressed and many SOS prot

15 tor that is induced by DNA damage, but in an SOS-independent manner.

16 f RecA, thereby preventing LexA cleavage and SOS induction.

17 LET-23/EGFR and SOS-1, an exchange factor for Ras, are required for G1 j

18 rity fraction of membrane-recruited Grb2 and SOS both exhibit fast kinetics and single exponential dw

19 erentiated kinetic species for both Grb2 and SOS on the LAT assemblies.

20 k, oxidative stress, nitrogen limitation and SOS responses.

21 aphical patterns of the EG in NDVI(max3) and SOS, there are no prevalent trends of vegetation homogen

22 erent major TAGs (PPO-, PSO-, SSO-, POP- and SOS-rich blends) were evaluated.

23 The internal prodrug and SOS concentrations were optimized for their impact on in

24 A positive feedback loop involving RAS and SOS, which leads to bistability and allows for switch-li

25 RasGRP1 and SOS are Ras-specific nucleotide exchange factors that ha

26 e required stress responses (RpoS, RpoE, and SOS, key network hubs), apparently sensing stress.

27 analysis, diabetes status was determined at SOS health examinations until May 22, 2013.

28 The bacterial SOS response is the essential signal for high level prod

29 l V) are expressed late during the bacterial SOS response, it has long been thought that TLS was the

30 mage via its multiple roles in the bacterial SOS response.

31 ng PT, including induction of bacteriophage, SOS response and DNA repair-related genes.

32 rtant to examine outcome differences between SOS and non-SOS hospitals with more contemporary data.

33 nvestigated the possible interaction between SOS and the cellular deoxynucleoside triphosphate (dNTP)

34 iveness of different antibiotics in blocking SOS response and Stx1/2 production, we constructed a rep

35 incorporates an intersubunit disulfide bond (SOS) to covalently link the gp120 and gp41 ectodomain (g

36 The further addition of a disulfide bond (SOS) to link the gp120 and gp41 subunits in the uncleave

37 s Ras/MAPK signaling and interacts with both SOS and Ras in vivo and in vitro.

38 xidant rich and serum free supplement called SOS.

39 ificial disulfide bonds: A501C/T605C (called SOS) and I201C/A433C (called DS).

40 ectivity supercritical fluid chromatography (SOS-SFC) are demonstrated with typical low density mobil

41 optimized selectivity liquid chromatography (SOS-LC) for improved separation of complex mixtures has

42 ns of selected gene promoters of the E. coli SOS DNA repair system to the Photorhabdus luminescens lu

43 ced DNA breaks activate the Escherichia coli SOS DNA-damage response and error-prone DNA polymerases

44 Escherichia coli SOS gene (recA, lexA, dinI and umuC) expression in respo

45 The Escherichia coli SOS system is a well-established model for the cellular

46 ed inhibition of RAS-MAPK pathway components SOS and RAF.

47 The highly evolutionarily conserved SOS-response associated peptidase (SRAP) domain of HMCES

48 ss this requirement and display constitutive SOS expression as well as a spontaneous (SOS) mutator ef

49 strongly suppressive effect on constitutive SOS expression in recA730 strains.

50 In contrast, SOS LASSO uncovers a network spanning all four lobes of

51 proteins may be part of the LexA-controlled SOS response in bacteria.

52 mns segments, as is the case in conventional SOS-LC.

53 ing degrees of LexA regulation of other core SOS functions.

54 Our results reveal a shared core SOS network, complemented by varying degrees of LexA reg

55 porter of the global response to DNA damage (SOS) and the TUNEL assay, we show that 3MST-derived H2S

56 100 MPa elicits a RecA-dependent DNA damage (SOS) response in Escherichia coli K-12, despite the fact

57 de bridge between gp120 and gp41 designated "SOS" (A501C/T605C).

58 abbits with B41 SOSIP (gp120-gp41 disulfide [SOS] with an isoleucine-to-proline mutation [IP] in gp41

59 This work identifies DRK/DOS/SOS as the upstream Rac GEF complex required for glial r

60 earliest steps of glial activation, DRK/DOS/SOS function in a partially redundant manner with Crk/Mb

61 ase in urban size could result in an earlier SOS of about 1.3 days and a later EOS of around 2.4 days

62 pool of RecA rapidly nucleates to form early SOS-signaling complexes, maturing into DNA-bound RecA bu

63 f cells where the percentage having elevated SOS expression (91%) nearly equals the percentage with a

64 fied among others by generating time-encoded SOS morse signals and implementing the time domain in tw

65 amage DNA in persisters and that the ensuing SOS response accelerates the development of antibiotic r

66 4N, T50I, V152G, and D153V Ras mutants evade SOS autoinhibition.

67 for S3, 18% for O3, 26% for SOO, and 35% for SOS.

68 exchange and to an increase in affinity for SOS Ras/Rac GEF 1 (SOS1), which appears to be the major

69 tioning therapy as dominant risk factors for SOS after transplant.

70 cA filaments, few (about 1%) are induced for SOS.

71 A polygenic risk score for SOS was trained and selected in 2 separate subsets of UK

72 erstanding of the importance of a functional SOS response for bacterial fitness in the context of a c

73 Further, SOS-inhibited cell division, which causes multi-chromoso

74 9.6%), and 1,3-distearoyl-2-oleoyl-glycerol (SOS) (37.2-31.4%), with SOS being the major component.

75 LAT (linker for activation of T cells)-Grb2-SOS phosphotyrosine-driven phase transition at the membr

76 a nonredundant role for DVL3 in the Shc-Grb2-SOS complex.

77 e examine molecular mobility within LAT:Grb2:SOS assemblies on supported membranes by single-molecule

78 stic timescale, indicating that the LAT:Grb2:SOS assembly has the dynamical structure of a loosely en

79 the SOS substrate, K-Ras, into the LAT:Grb2:SOS protein condensate.

80 report crystal structures of the human HMCES SOS response-associated peptidase (SRAP) domain in compl

81 I discuss how SOS could be addressed, from prophylaxis to diagnosis an

82 s filament extensively and induce impressive SOS responses before returning to a normal appearance.

83 and long-term outcomes were not different in SOS and non-SOS hospitals except that 2-year repeat targ

84 repeat target lesion PCI rates were lower in SOS hospitals for patients with STEMI.

85 nt mortality differences between patients in SOS and non-SOS hospitals.

86 in this work, recA(Q300R), is proficient in SOS induction and repair of UV-induced DNA damage, but i

87 region of the right replichore, resulting in SOS induction and inhibition of cell division.

88 Patients with STEMI in SOS hospitals had significantly lower 2-year repeat targ

89 We propose an additional essential step in SOS/Ras control that is relevant for human cancer as wel

90 cterized the specific activity of individual SOS molecules catalyzing nucleotide exchange in H-Ras.

91 the initiation of GEF activity of individual SOS molecules on microarrays of Ras-functionalized suppo

92 a single-molecule assay in which individual SOS molecules are captured from raw cell lysate using Ra

93 on, DFT-optimized geometries, and B3LYP/INDO-SOS analysis identify three key features underlying the

94 rm filaments with abnormal nucleoids, induce SOS, and fragment their chromosome, revealing replicatio

95 s hypothesized that RecA's ability to induce SOS expression in log-phase cells is repressed because o

96 review of key features of DNA damage-induced SOS mutagenesis leading us to pol V, and reflects on som

97 as instigator for this enigmatic HP-induced SOS response.

98 sses RAS and RAF, MEK, and ERK that inhibits SOS via phosphorylation.

99 column kit and with the classical isocratic SOS-LC algorithm.

100 HMCES mediates Alt-EJ through its SOS-response-associated-peptidase domain (SRAPd), a func

101 opying damaged DNA as part of the well known SOS regulon.

102 enables characterization of the full-length SOS protein, which has not previously been studied in re

103 genes are constitutively expressed and many SOS proteins are stabilized by the removal of ClpXP, mic

104 The rise-and-fall shape of the measured SOS activation time distribution and the long mean time

105 gSOS was strongly correlated with measured SOS (r2 = 23.2%, 95% CI 22.7% to 23.7%).

106 r, leading to expression of the 30(+)-member SOS regulon.

107 eport the mechanism by which ezrin modulates SOS activity and thereby Ras activation.

108 oved mutant chromosomes due to the mutagenic SOS response and possible recombination of the new allel

109 m outcomes were not different in SOS and non-SOS hospitals except that 2-year repeat target lesion PC

110 mine outcome differences between SOS and non-SOS hospitals with more contemporary data.

111 differences between patients in SOS and non-SOS hospitals.

112 merase transcription occur in the absence of SOS induction by exogenous agents and indicate that cell

113 The expected allosteric activation of SOS by Ras-guanosine triphosphate (GTP) was conspicuousl

114 nine nucleotide exchange factor) activity of SOS is activated indicates that kinetic stabilization fr

115 ezrin also is important for the activity of SOS itself.

116 nd membrane interactions, govern activity of SOS.

117 , and D153V deregulate the autoactivation of SOS to populate their active form.

118 We report two cases of SOS investigated by 18F-fluorodeoxyglucose positron emis

119 Control of SOS depends largely on the RecA protein.

120 echanism responsible for the deregulation of SOS autoactivation, where I24N, T50I, V152G, and D153V R

121 a hydrophobic pocket in the CDC25 domain of SOS adjacent to the Switch II region of Ras.

122 ogy (DH)/pleckstrin homology (PH) domains of SOS, bringing GDP-Ras to the proximity of the allosteric

123 site is blocked by autoinhibitory domains of SOS.

124 se of the potentially detrimental effects of SOS mutagenesis.

125 ution of CTX prophage in the essentiality of SOS response master regulator LexA, which is otherwise n

126 The expression of SOS genes is under the control of LexA, a global transcr

127 Conclusion: Frequencies of SOS and DILI after inotuzumab ozogamicin treatment were

128 Frequency of SOS among patients who received InO was 5 of 328 (1.5%),

129 tic cell transplantation (HCT); frequency of SOS in those previously exposed to InO was 21 of 79 (27%

130 mal liver have a relatively low frequency of SOS, but a relatively high frequency of DILI.

131 aded into liposomes containing a gradient of SOS, resulting in highly stable SOS-drug complexes being

132 Z-ring inhibition occurred independently of SOS, SlmA-mediated nucleoid occlusion, and MinCDE protei

133 and severe cell filamentation, indicative of SOS induction.

134 less (SOS):Ras complex, increase the rate of SOS-catalyzed nucleotide exchange in vitro, and modulate

135 omain limits Grb2-independent recruitment of SOS to the membrane through binding of Ras.GTP in the SO

136 s to the proximity of the allosteric site of SOS.

137 Next to the classical use of SOS for faster baseline separation of all solutes in a m

138 activation of Ras and highlight a pocket on SOS that may be exploited to modulate Ras signaling.

139 The only SOS gene required (of 19 tested) for the cell length phe

140 The report of an operational SOS response in presumed symbiotic and parasitic bacteri

141 e relative energy difference between the OSS/SOS and OOS/OSO isomers due to their different beta valu

142 (TD) computations, within the sum-overstate (SOS) perturbational approach, expose that the prevailing

143 ecially with older and more infirm patients, SOS remains an important area for clinicians.

144 s DNA damage, we deleted the only Lula/phi80 SOS-controlled gene, dinL.

145 d oleic acid) and triglyceride profile (POP, SOS and POS) to cocoa butter.

146 ctor not only detaches LexA from its primary SOS role, but also fine-tunes gene expression from the M

147 bacter crescentus, cells lacking the primary SOS-regulated inhibitor, sidA, can often still delay div

148 agreement with RasGRP allosterically priming SOS, exponential ERK activation is severely decreased by

149 ron microscope images revealed dense prodrug-SOS complex in the aqueous core of the immunoliposomes.

150 S allosteric site, thus aberrantly promoting SOS autoactivation, resulting in the population of activ

151 X-ray crystallography of Ras:SOS:Ras in complex with these molecules reveals that the

152 ied ligands that bound reversibly to the Ras:SOS complex in two distinct sites, but these compounds w

153 stabilizing or covalently modifying the Ras:SOS complex to prevent the reloading of Ras with GTP.

154 y of three fragment binding sites on the Ras:SOS complex.

155 anine nucleotide exchange factors (RasGEFs), SOS and RasGRP, activate Ras and the downstream RAF-MEK-

156 able and that the enhancement requires RecA, SOS induction, an opportunity to recover from treatment,

157 re three independent mechanisms that repress SOS expression in log-phase cells.

158 cells lacking aPLs fail to initiate a robust SOS response after DNA damage, indicating that the membr

159 ch substitution-oriented fragment screening (SOS) because it focuses on the identification of novel s

160 urban areas starts earlier (start of season, SOS) and ends later (end of season, EOS), resulting in a

161 The Salt Overly Sensitive (SOS) pathway in Arabidopsis (Arabidopsis thaliana) funct

162 Salt Overly Sensitive (SOS)2, a member of the SnRK3 subfamily, is a critical me

163 The SALT-OVERLY-SENSITIVE (SOS) pathway in Arabidopsis (Arabidopsis thaliana) funct

164 The Seattle Obesity Study series (SOS I and II) yielded the study sample (n = 1636).

165 then introduce the sparse-overlapping-sets (SOS) LASSO-a whole-brain multivariate approach that expl

166 respectively) and the GEF son of sevenless (SOS) (mammalian homolog, mSOS) are required for efficien

167 nucleotide exchange factor Son of Sevenless (SOS) catalyzes the activation of RAS by converting it fr

168 tide exchange factor (GEF) Son of Sevenless (SOS) is a key Ras activator that is autoinhibited in the

169 Son of Sevenless (SOS) is a Ras guanine nucleotide exchange factor.

170 Ras by the exchange factor Son of Sevenless (SOS) is an important hub for signal transduction.

171 tor-bound protein 2 (Grb2):Son of Sevenless (SOS) networks, derived from the T-cell receptor signalin

172 tide exchange factor (GEF) Son of Sevenless (SOS) plays a critical role in signal transduction by act

173 tor-bound protein 2 (Grb2):son of sevenless (SOS) protein condensation on the surface of giant unilam

174 ion of these G proteins is Son of sevenless (SOS), which catalyzes the nucleotide exchange on Ras.

175 a unique pocket on the Ras:Son of Sevenless (SOS):Ras complex, increase the rate of SOS-catalyzed nuc

176 r receptor-bound-2 (Grb2), son-of-sevenless (SOS), and the tumor suppressor DAB2.

177 proteases return the high levels of several SOS proteins to homeostasis.

178 n response to Ras-activating cell signaling, SOS autoinhibition is released and is followed by accele

179 hospitals with and without surgery on-site (SOS), but one earlier study found differences in target

180 ons and on the adjacent southern open slope (SOS) between October 2005 and October 2006.

181 this gap by presenting Simple OLGA & SONIA (SOS), a web-based interface where users with no coding s

182 heel quantitative ultrasound speed of sound (SOS)-a heritable risk factor for osteoporotic fracture-c

183 Spheres-on-sphere (SOS) silica particles are prepared in a one-pot scalable

184 cing the relative probability of spontaneous SOS activation in the absence of receptor triggering.

185 ive SOS expression as well as a spontaneous (SOS) mutator effect.

186 n vegetation greenness (NDVI(max3)), spring (SOS) and autumn phenology (EOS) during 1982-2015.

187 gradient of SOS, resulting in highly stable SOS-drug complexes being formed inside the liposome.

188 Here, we identify SosA as the staphylococcal SOS-induced cell division inhibitor.

189 ns in combinations with the sum-over-states (SOS) formalism revealed that the enhancement is due to t

190 quinolones, antibiotics that elicit a strong SOS response.

191 19 controls from the Swedish Obese Subjects (SOS) cohort.

192 The Swedish Obese Subjects (SOS) is a prospective matched cohort study conducted at

193 spective, controlled Swedish Obese Subjects (SOS) study and participants in the SOS reference study (

194 ND PARTICIPANTS: The Swedish Obese Subjects (SOS) study is an ongoing, nonrandomized, prospective, co

195 e recruited from the Swedish Obese Subjects (SOS) study, which was a matched (nonrandomized) prospect

196 vention trial of the Swedish Obese Subjects (SOS) study.

197 in the aqueous core with sucroseoctasulfate (SOS).

198 Sinusoidal obstruction syndrome (SOS) is a potentially fatal liver injury that mainly occ

199 Grade 2-3 sinusoidal obstruction syndrome (SOS) was present in 124 patients (38.4%), grade 2-3 stea

200 also called sinusoidal obstruction syndrome (SOS), is a potentially life-threatening complication of

201 Sinusoidal obstruction syndrome (SOS), previously called veno-occlusive disease (VOD) can

202 sinusoids (sinusoidal obstruction syndrome; SOS).

203 catalysis for sustainable organic syntheses (SOS), highlighting key advances and representative examp

204 sistent with other methods-illustrating that SOS LASSO can detect both widely distributed and localiz

205 Single-molecule kinetic traces revealed that SOS samples a broad distribution of turnover rates throu

206 The SOS change exerted more subtle, context-dependent effect

207 The SOS DNA repair regulon is induced at cytotoxic levels of

208 The SOS particles exhibit solid-core porous-shell properties

209 The SOS response is an essential process for responding to D

210 L10b has an enhanced ability to activate the SOS pathway while EsCBL10a has a function not performed

211 ors can block Stx1 production even after the SOS response is fully induced.

212 oacetic acids, and unregulated DBPs, and the SOS genotoxicity followed the breakthrough of dissolved

213 fertility was analyzed in wild type and the SOS pathway mutants grown in saline conditions.

214 This network is known as the SOS response and aids in bacterial survival by regulatin

215 tely 4-fold higher than those induced by the SOS response severely impede its growth.

216 and in vitro approaches to characterize the SOS transcriptional response to DNA damage in the Patesc

217 ze regulatory networks by characterizing the SOS meta-regulon in the human gut microbiome.

218 lation, was ascertained by crosschecking the SOS database with the Swedish National Patient Register

219 In Escherichia coli, after DNA damage, the SOS response increases the transcription (and protein le

220 transcription factor, DriD, that drives the SOS-independent transcription of didA following DNA dama

221 rminus following Pol IV induction during the SOS DNA damage response.

222 mbda CI repressor, is inactivated during the SOS response to DNA damage, and this regulation ensures

223 that when produced at high levels during the SOS response, RecN interferes with nucleoid partitioning

224 products, which are up-regulated during the SOS response, were previously shown to bind to the alpha

225 ormation of a RecA-ssDNA filament during the SOS response.

226 In an unperturbed environment, the SOS-off mutant is impaired for stable colonization relat

227 entally define a novel binding motif for the SOS transcriptional repressor LexA, and we use this moti

228 biliary infiltration in 5.6%.The higher the SOS grade the lower the pathological response: TRG 1-2 o

229 physiological environment and highlights the SOS response as a possible mechanism that contributes to

230 e membrane through binding of Ras.GTP in the SOS allosteric binding site.

231 In the SOS cohort, E167K carriers had higher alanine aminotrans

232 In the SOS cohort, patients with the chromosome 9p21.3 rs133304

233 In the SOS reference cohort, the median duration of follow-up w

234 Subjects (SOS) study and participants in the SOS reference study (reference cohort), a random sample

235 t bundles and plays an important role in the SOS response.

236 ry and 1803 controls given usual care in the SOS study (Swedish Obese Subjects).

237 ncentrations of ciprofloxacin did induce the SOS response, but not when the cells were exposed to rif

238 olecules in Escherichia coli and induced the SOS response to DNA damage in E. coli.

239 DNA damage induces the SOS response that in bacteria inhibits cell division whi

240 astic process, which temporarily induces the SOS response, and is followed by DNA repair, maintaining

241 ollowing DNA damage in bacteria involves the SOS response where cleavage of the transcriptional repre

242 e show, however, that NL trimers lacking the SOS and/or IP change can be affinity purified in amounts

243 that described for other inhibitors like the SOS response protein SulA or the moonlighting enzyme Opg

244 tran sulfate sodium (DSS) colitis model, the SOS-off colonization defect persisted but was not exacer

245 In contrast, in a germ-free model, the SOS-off mutant colonized with efficiency equal to that s

246 We conclude that the major effect of the SOS and IP changes is to substantially increase trimer s

247 The antigenicity of the SOS Env was similar to that of the unmodified Env, excep

248 nd determine the relative composition of the SOS network in a natural setting.

249 o characterize the conserved elements of the SOS regulatory network in Patescibacteria.

250 se growth in the absence of induction of the SOS regulon by external agents that damage DNA.

251 time-resolved, simultaneous read-out of the SOS response (recAP-cfp) and Stx1 production (stx1::yfp)

252 Induction of the SOS response by the genotoxic antibiotic ciprofloxacin c

253 ter gene analyses indicated induction of the SOS response for some of the derivatives, suggesting int

254 terial pathogenesis, and yet the role of the SOS response in nonpathogenic organisms and in physiolog

255 modification, and we confirm binding of the SOS response transcriptional repressor to sites in the p

256 Induction of the SOS response, a cellular system triggered by DNA damage

257 The induction of the SOS response, the appearance of RecA foci, the appearanc

258 nal repressor LexA is a key component of the SOS response, the main mechanism for the regulation of D

259 ymerase, one that was induced as part of the SOS response, we actually rediscovered DNA polymerase II

260 ally delayed with respect to the peak of the SOS response.

261 esion synthesis as a primary function of the SOS response.

262 ge tail-like particles upon induction of the SOS response.

263 on DNA replication for the generation of the SOS signal, ssDNA.

264 The primary end point of the SOS study (total mortality) was published in 2007.

265 phase separation drives localization of the SOS substrate, K-Ras, into the LAT:Grb2:SOS protein cond

266 derlying mechanism involved a priming of the SOS-dependent amplification loop of RAS activation.

267 lkyldT lesions and revealed the roles of the SOS-induced DNA polymerases in bypassing these lesions i

268 ds to a novel mechanism of inhibition of the SOS-mediated interaction between Ras and Raf and is effe

269 er, once the trimers have been purified, the SOS and IP changes have only subtle impacts on thermosta

270 Recently, the SOS response has been shown to play an important role in

271 erichia coli strain, MP1, we showed that the SOS response plays a vital role during colonization of t

272 site inhibits Z-ring formation and that the SOS system, SlmA, and MinC are not required for this inh

273 ionally, genotoxicity was measured using the SOS-Chromotest (detects DNA-damaging agents).

274 revealed that CS induced SCVs emerge via the SOS response DNA mutagenic repair system.

275 dly evolve resistance to antibiotics via the SOS response, a state of high-activity DNA repair and mu

276 ion tolerance events (i) only occur when the SOS response is fully induced and (ii) are executed in c

277 tail improved the efficiency with which the SOS Env supported virus infection in a reducing environm

278 ey are capable of forming a complex with the SOS allosteric site, thus aberrantly promoting SOS autoa

279 Without the SOS and IP changes, proteolytically cleaved trimers tend

280 phase, the expression patterns of all three SOS polymerases change during the transition from log ph

281 only monomeric Grb2 is capable of binding to SOS and upregulating MAP kinase signalling and that the

282 and autoimmune diseases but, in contrast to SOS, its regulatory mechanisms are poorly understood.

283 1.74-4.56, P < .001, Gray test) with all VOD/SOS events.

284 27 patients treated with Defibrotide for VOD/SOS diagnosis, where detailed data were available for fi

285 ide in patients with established hepatic VOD/SOS and advanced MOF.

286 hown promising efficacy treating hepatic VOD/SOS with MOF in phase 2 studies.

287 Untreated hepatic VOD/SOS with multi-organ failure (MOF) is associated with >8

288 large UK transplant center reporting on VOD/SOS in consecutive HSCT adult patients (n = 530), transp

289 Defibrotide for the treatment of severe VOD/SOS in adults regardless of time of onset.

290 disease/sinusoidal obstruction syndrome (VOD/SOS) is a serious complication post allogeneic hematopoi

291 redictions and experiments exploring whether SOS functions as a RacGEF or adaptor in Rac-p38 activati

292 While SOS-induced DNA polymerases play redundant roles in bypa

293 lone induces analog Ras-ERK activation while SOS and RasGRP cooperate to establish bimodal ERK activa

294 l-2-oleoyl-glycerol (SOS) (37.2-31.4%), with SOS being the major component.

295 a population where the number of cells with SOS expression more closely equaled the number of RecA f

296 atography (HPLC) for the columns packed with SOS-particles.

297 ion in which electron transfer together with SOS induce ROS, which activate the sigma-S (sigma(S)) ge

298 binding to a second Ras-binding site within SOS.

299 mpare outcomes in hospitals with and without SOS for all patients and for patients with and without S

300 We found that, without SOS induction, all alpha-dN lesions except alpha-dA stro