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 accelerated inactivation of meizothrombin 1000-fold,

3 SOS bound HCII with K(D) 1.45 +/- 0.30 mm, and this bind

4 SOS bound to two sites on thrombin, with dissociation co

5 SOS induction following topoisomerase I complex accumula

6 SOS is inactive unless Ras is bound to an allosteric sit

7 SOS' feedback loop leads to hysteresis in the dose-respo

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

9 SOS-SFC appears possible without any density correction,

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

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

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

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

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

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

16 A0906, coordinate the Pseudomonas aeruginosa SOS response.

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

18 ds to DNA damage by coordinately inducing an SOS regulon and inhibiting the master regulator CtrA.

19 Escherichia coli dinD is an SOS gene up-regulated in response to DNA damage.

20 N. gonorrhoeae was thought to lack an SOS system, although NG1427 shows amino acid sequence si

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

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

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

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

25 The IraD and SOS regulatory pathways appear to act synergistically to

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

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

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

29 Two molecules, RasGRP and SOS, catalyze Ras activation in lymphocytes.

30 vels of guanine exchange factors, RasGRP and SOS, within T cells have been shown to represent a key d

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

32 resistance, conjugational recombination, and SOS induction to recA(-) cells.

33 with RecA in double-strand-break repair and SOS induction, and RuvABC Holliday-junction resolvase.

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

35 in the absence of Fis and the other assessed SOS induction as a readout of increased DNA cleavage.

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

37 protein plays a principal role in bacterial SOS response to DNA damage.

38 s Rad6 and Rad18 comparable to the bacterial SOS response, controlling damage-induced transcriptional

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

40 n more complex role of DinI in the bacterial SOS response.

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

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

43 Meizothrombin(des-fragment 1), binding SOS with K(D) = 1600 +/- 300 microm, and thrombin were i

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

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

46 ction resolvase to survive rapid growth, but SOS induction, although elevated, is not required.

47 ombin generation in plasma was suppressed by SOS, both in HCII-dependent and -independent processes.

48 deleterious transcriptional response called SOS, which is initiated by RecA protein filaments formed

49 xidant rich and serum free supplement called SOS.

50 ediated DNA damage activates the V. cholerae SOS response, which in turn likely accounts for ParE's i

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

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

53 pacing between the two half-sites of E. coli SOS boxes is invariant.

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

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

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

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

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

59 ent on RecBCD for its high SOS constitutive [SOS(Con)] expression.

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

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

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

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

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

65 100 MPa elicits a RecA-dependent DNA damage (SOS) response in Escherichia coli K-12, despite the fact

66 The potentially deleterious SOS response, which is normally triggered by the appeara

67 The RecA-dependent SOS response and the RapI-PhrI cell sensory system activ

68 Genotoxic stress induces the RecA-dependent SOS response in many bacteria.

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

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

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

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

73 ion-induced bone marrow suppression elicited SOS from a subtoxic dose of Mct, whereas infusion of bon

74 The eubacterial SOS system is a paradigm of cellular DNA damage and repa

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

76 are converted into double-strand breaks for SOS induction by the RecBCD pathway.

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

78 k reversal function of RuvAB is required for SOS induction by the covalent complex formed by topoisom

79 d50 homolog) in recA4142 strains caused full SOS(Con) expression in an ruvAB-, recBCD-, recJ-, and xo

80 9.6%), and 1,3-distearoyl-2-oleoyl-glycerol (SOS) (37.2-31.4%), with SOS being the major component.

81 g patterns of ERK cascade transducers (GRB2, SOS, B-Raf, MEK, and ERK) at the EGR-1 locus resemble bo

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

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

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

85 atible with a model solely depending on HCII.SOS but fit an equilibrium linkage model employing T.SOS

86 mutant, was dependent on RecBCD for its high SOS constitutive [SOS(Con)] expression.

87 switches to the lytic pathway when the host SOS system is induced.

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

89 esolvable, as evidenced by single hyperbolic SOS concentration dependences of the inactivation rate (

90 y of stress responses previously implicated: SOS/DinB and RpoS, and of sigma(32), which was postulate

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

92 Thus, the principal role of RecA* in SOS mutagenesis is to transfer RecA-ATP to pol V, and th

93 may have evolved as a DNA damage response in SOS-deficient bacteria.

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

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

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

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

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

99 micking RecA filament structures that induce SOS and the suppressor alleles mimic RecA filament at en

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

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

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

103 Indeed, selected compounds inhibit SOS-mediated nucleotide exchange and prevent Ras activat

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

105 h corecruitment of IR signaling cascade (IR, SOS, Grb2, B-Raf, MEK, and ERK) to this gene.

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

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

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

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

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

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

112 ecQ, implying that neither recombination nor SOS induction causes hyper-TLD in recB cells, and RecQ i

113 approximately 8-fold higher than the normal SOS-induced levels, failed to impede growth of the dnaN1

114 Sucrose octasulfate (SOS) accelerated thrombin inactivation by HCII but not A

115 f APLP1 in complex with sucrose octasulfate (SOS).

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

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

118 We showed previously that the activity of SOS at the membrane increases with the density of PIP(2)

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

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

121 nd membrane interactions, govern activity of SOS.

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

123 Control of SOS depends largely on the RecA protein.

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

125 (DH) and Pleckstrin homology (PH) domains of SOS (the DH-PH unit) block allosteric Ras binding.

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

127 site is blocked by autoinhibitory domains of SOS.

128 se of the potentially detrimental effects of SOS mutagenesis.

129 ressor alleles mimic RecA filament at end of SOS.

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

131 SOS nearly eradicates histologic features of SOS.

132 ion of membrane-bound Ras by mutant forms of SOS that contain mutations in the histone and the PH dom

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

134 and severe cell filamentation, indicative of SOS induction.

135 A low level of SOS-dependent switching occurs without an overt stimulus

136 % of mutant cells to have elevated levels of SOS expression, a percentage similar to that of cells wi

137 epair and contributes to the pathogenesis of SOS, whereas timely infusion of bone marrow has therapeu

138 of bone marrow during the necrotic phase of SOS nearly eradicates histologic features of SOS.

139 n a wild-type host over the natural range of SOS-inducing conditions.

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

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

142 ") is predicated upon feedback regulation of SOS.

143 coincides with a productive reorientation of SOS at the membrane and increased accessibility of both

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

145 Here we present a new crystal structure of SOS that contains the N-terminal histone domain in addit

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

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

148 unless Ras is bound to an allosteric site on SOS, and the Dbl homology (DH) and Pleckstrin homology (

149 d accessibility of both Ras binding sites on SOS.

150 believed to modulate its activity in ongoing SOS events.

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

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

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

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

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

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

157 n despite having an appropriately positioned SOS box to which LexA binds in vitro.

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

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

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

161 cBCD loads RecA4142 onto this end to produce SOS(Con) expression.

162 model suggests that recA(C) alleles promote SOS(C) expression by mimicking RecA filament structures

163 ggest that L. pneumophila lacks a prototypic SOS response and competence development in response to g

164 hat compound-binding interferes with the Ras/SOS interactions.

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

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

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

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

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

170 recA SOS constitutive [recA(Con)] mutants induce the SOS resp

171 Herein, it is shown that recA4142 SOS(Con) expression is additionally dependent on ruvAB (

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

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

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

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

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

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

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

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

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

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

182 ed by translocation of the Son of Sevenless (SOS) protein to the plasma membrane.

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

184 f both the Shc adaptor and son of sevenless (SOS)1/2 GEFs, and Rit activation was inhibited by RNA in

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

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

187 silencing of SOS1/2, implicating a TrkA/Shc/SOS signaling complex in Rit regulation.

188 Included in the SOS regulon is sidA (SOS-induced inhibitor of cell division A), a membrane pr

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

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

191 Furthermore, although spontaneous SOS induction has been observed to occur in only a small

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

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

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

195 quinolones, antibiotics that elicit a strong SOS response.

196 19 controls from the Swedish Obese Subjects (SOS) cohort.

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

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

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

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

201 ors are not allele specific and can suppress SOS(C) expression of recA730 and recA4142 in cis and in

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

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

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

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

206 ) initiates sinusoidal obstruction syndrome (SOS), which is most commonly a consequence of myeloablat

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

208 fit an equilibrium linkage model employing T.SOS binding in the pathway to higher order complex forma

209 mm, and this binding was tightened in the T.SOS.HCII complex, characterized by K(complex) of approxi

210 rther increase in mutagenesis, implying that SOS induction of DinB, although necessary, is insufficie

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

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

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

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

215 The SOS response leads to overexpression of the TisB toxin a

216 The SOS response to DNA damage in bacteria is a well-known c

217 The SOS response to DNA damage was not induced under these c

218 vities of recombination protein RecA and the SOS DNA-damage response as causes of TLD.

219 ires DinB error-prone DNA polymerase and the SOS DNA-damage- and RpoS general-stress responses.

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

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

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

223 a protein-based TA system upregulated by the SOS response.

224 division inhibition was not mediated by the SOS-induced regulator YneA nor by RecA-independent repre

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

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

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

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

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

230 e 2 TA system that is upregulated during the SOS DNA damage response.

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

232 recA4142 (F217Y) constitutively express the SOS response.

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

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

235 During F plasmid conjugation, however, the SOS response is suppressed by PsiB, an F-plasmid-encoded

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

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

238 Included in the SOS regulon is sidA (SOS-induced inhibitor of cell divis

239 DinI's function in the SOS response remains controversial, since its interactio

240 te a predicted role for IsrA and GlmZ in the SOS response, and we expand on current knowledge of the

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

242 constitutive [recA(Con)] mutants induce the SOS response in the absence of DNA damage.

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

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

245 teracts with the LexA repressor inducing the SOS response.

246 Escherichia coli initiates the SOS response when single-stranded DNA (ssDNA) produced b

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

248 ytic pathway, measured in a host lacking the SOS response, was almost undetectably low, probably less

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

250 Disruption of the SOS box did not prevent induction, indicating that an al

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

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

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

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

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

256 ing of the regulation and termination of the SOS response is much more limited.

257 The induction of the SOS response is well understood and involves the cleavag

258 gene products is upregulated as part of the SOS response to DNA damage.

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

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

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

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

263 repair, recombination, and induction of the SOS response.

264 r of division that is induced as part of the SOS response.

265 subunits and is up-regulated as part of the SOS response.

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

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

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

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

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

271 We show that suppressing the SOS network in Escherichia coli with engineered bacterio

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

273 shows amino acid sequence similarity to the SOS response regulator LexA from Escherichia coli.

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

275 ther stresses, Escherichia coli utilizes the SOS response, which regulates the expression of at least

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

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

278 te the division blockage associated with the SOS response.

279 narrow intersubdomain groove, and the third SOS is bound near the two-fold axis of the protein.

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

281 A total of three SOS molecules are bound to the E2 dimer.

282 on of many DNA repair proteins by binding to SOS 'boxes' in their operators.

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

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

285 Two SOSs are bound inside a narrow intersubdomain groove, an

286 thymidine glycol and is bypassed only under SOS-induced conditions.

287 on to the DH-PH unit and the catalytic unit (SOS(HDFC), residues 1-1049).

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

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

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

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 res of Escherichia coli LexA in complex with SOS boxes.

297 ses show that most residues interacting with SOS also contribute to heparin binding, although in vary

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

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

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