ライフサイエンスコーパス: genotoxic

1 fied from soil extracts was determined to be genotoxic.

2 s, when inappropriate cyclin E expression is genotoxic.

3 documents the replacement of the potentially genotoxic 3-nitro group by 3-chloro and 3-fluoro substit

4 irectly or after metabolic activation; 2) be genotoxic; 3) alter DNA repair or cause genomic instabil

5 or metabolism; 2) chemical or metabolite is genotoxic; 3) induces epigenetic alterations; 4) causes

6 Reactive oxygen species generate the genotoxic 8-oxoguanine (oxoG) and 8-oxoadenine (oxoA) as

7 antagonistic endocrine activities, mutagenic/genotoxic activities, cytotoxic activities, further acti

8 irradiated animals, covering three types of genotoxic activity.

9 Here, we show that genotoxic agent-activated Wnt/beta-catenin signaling is

10 hanism of rescue following the withdrawal of genotoxic agent.

11 Fto KO osteoblasts were more susceptible to genotoxic agents (UV and H(2)O(2)) and exhibited increas

12 DNA damage occurs on exposure to genotoxic agents and during physiological DNA transactio

13 le CHK1 inhibitors sensitize cancer cells to genotoxic agents and have shown single-agent preclinical

14 acids, for example when cells are damaged by genotoxic agents and in certain autoinflammatory disease

15 tion gaps are fundamental to the toxicity of genotoxic agents and underlie the BRCA-cancer phenotype

16 levated ILF2 expression exerts resistance to genotoxic agents by modulating YB-1 nuclear localization

17 implications for the development and use of genotoxic agents in cancer therapy.

18 undertook 31 CRISPR-Cas9 screens against 27 genotoxic agents in the retinal pigment epithelium-1 (RP

19 iation and sensitized leukemic blasts toward genotoxic agents in vitro and in vivo.

20 shows promising results in combination with genotoxic agents such as ionizing radiation or chemother

21 Genotoxic agents such as radiation and chemotherapeutics

22 Thus, genotoxic agents that are used chemotherapeutically to p

23 Administration of genotoxic agents to primary hepatocytes in vitro confirm

24 Genotoxic agents trigger a 'nuclear-to-cytoplasmic' NF-k

25 ntext of therapeutic strategies that combine genotoxic agents with immune checkpoint blockade.

26 rk in which DSBs are not directly induced by genotoxic agents, but rather are induced from cell death

27 Targeting MEK1/2 sensitizes AML blasts to genotoxic agents, indicating a role for NCAM1 as a bioma

28 n products have been implicated as causative genotoxic agents, no specific product has been identifie

29 In innate immune cells, the production of genotoxic agents, such as reactive nitrogen molecules, i

30 Macrophages produce genotoxic agents, such as reactive oxygen and nitrogen s

31 e counterparts in response to treatment with genotoxic agents, suggesting that FAN1 mutations cause c

32 response of ATAD5-depleted cells to several genotoxic agents.

33 ot fundamental to the mechanism of action of genotoxic agents.

34 adenovirus or herpesvirus) or treatment with genotoxic agents.

35 9M allele that sensitizes tel1Delta cells to genotoxic agents.

36 Human ingestion of cytotoxic and genotoxic aldehydes potentially induces deleterious heal

37 ts a mild and safe alternative to the use of genotoxic alkyl halides and sulfonate esters.

38 tensive study of proliferation dynamics of a genotoxic and a non-genotoxic compound.

39 Alkenylbenzenes are natural toxins with genotoxic and carcinogenic effects in rodents, which are

40 bons (PAHs) are considered to be potentially genotoxic and carcinogenic in humans.

41 Aflatoxins are the most potent genotoxic and carcinogenic mycotoxins.

42 first insight into how we might measure the genotoxic and cytotoxic effect of plasma jet treatments

43 mparatively little research on the potential genotoxic and cytotoxic effects of plasma jet treatment.

44 ences in proliferative responses between non-genotoxic and genotoxic carcinogens during the initial s

45 As non-genotoxic and genotoxic carcinogens have different cance

46 ivation of p53 and increased apoptosis under genotoxic and hematopoietic stress.

47 cept not only enabled a simple prediction of genotoxic and non-genotoxic carcinogens, but also had th

48 environmental carcinogens promote cancer via genotoxic and nongenotoxic pathways, but nongenetic mech

49 Stem cells need to be protected from genotoxic and proteotoxic stress to maintain a healthy p

50 quired factors, impairs cellular response to genotoxic and replicative stress and could identify pati

51 deacylation; the latter are postulated to be genotoxic and to contribute to colorectal cancer formati

52 indicates that GEBR-32a is not cytotoxic and genotoxic, and does not seem to possess emetic-like side

53 In this study, we focused on a genotoxic aspect of exposure of esophageal cells to acid

54 Euterpe oleracea) provide prebiotic and anti-genotoxic benefits in the colon.

55 The variety of non-genotoxic cancer pathways complicates the search for rel

56 Inflammatory gene expression following genotoxic cancer therapy is well documented, yet the eve

57 ferative responses between non-genotoxic and genotoxic carcinogens during the initial stages of the r

58 As non-genotoxic and genotoxic carcinogens have different cancer risks, the o

59 led a simple prediction of genotoxic and non-genotoxic carcinogens, but also had the power to discrim

60 cinogenicity assays is the prediction of non-genotoxic carcinogens.

61 Mixtures of these genotoxic chemicals produced mutation responses that dif

62 manipulation or by growth in the presence of genotoxic chemicals, induces respiration.

63 cell lines induced synthetic lethality with genotoxic chemotherapeutics, including PARP inhibitors,

64 found that in response to UV irradiation or genotoxic chemotherapeutics, SOX9 is actively degraded i

65 re fundamental to the mechanism of action of genotoxic chemotherapies.

66 ATM, are associated with resistance against genotoxic chemotherapy (del17p) and poor outcome (del11q

67 r mechanism promoting acquired resistance to genotoxic chemotherapy.

68 nce suggests precolibactins are converted to genotoxic colibactins by colibactin peptidase (ClbP)-med

69 liferation dynamics of a genotoxic and a non-genotoxic compound.

70 enome integrity by AhR-mediated 'sensing' of genotoxic compounds from the diet.

71 This non-genotoxic conditioning method may provide an attractive

72 Here we describe a non-genotoxic conditioning protocol for fully MHC-mismatched

73 urrent allotransplantation protocols involve genotoxic conditioning which has harmful side-effects an

74 NF8 homeostasis under both physiological and genotoxic conditions and that targeting ATX3 may be a pr

75 ysiological changes required for coping with genotoxic conditions.

76 rmediate-sized repeats both under normal and genotoxic conditions.

77 NHL is based on the combination of different genotoxic cytostatics and anti-CD20 monoclonal antibody

78 Both, ATR- and CHK1 inhibitors induce genotoxic damage and apoptosis in human and murine SCLC

79 ematopoietic cells from TOP2 poison-mediated genotoxic damage and, therefore, reduce the rate of ther

80 Because resistance to genotoxic damage is achieved mainly through execution of

81 ng budding yeast, we demonstrate that global genotoxic damage or even a single unrepaired double-stra

82 ls in S-phase and led to the accumulation of genotoxic damage, particularly in S-phase.

83 proteins that function to protect cells from genotoxic damage.

84 ng them to undergo cell death in response to genotoxic damage.

85 on of the lead compounds showed that in vivo genotoxic degradants might be generated.

86 Genotoxic DNA double-strand breaks (DSBs) can be repaire

87 iotic crossover recombination by potentially genotoxic DNA double-strand breaks (DSBs).

88 ar proteins producing proteotoxic stress and genotoxic DNA-histone crosslinks.

89 ome maintenance factors and another in which genotoxic DNA:RNA hybrids, called R-loops, impair DNA re

90 Premenopausal women undergoing commonly used genotoxic (DNA-damaging) chemotherapy experience an acce

91 Treatment of preexisting CSCs with a genotoxic drug combination (5-fluorouracil, doxorubicin,

92 p53-induced apoptosis in melanoma following genotoxic drug exposure.

93 p53-dependent nuclear gene expression during genotoxic drug treatment.

94 w expression of NBAT1 provided resistance to genotoxic drugs by promoting p53 accumulation in cytopla

95 he use of G9a inhibitors in combination with genotoxic drugs to treat p53-positive tumors.

96 patients being hypersensitive to particular genotoxic drugs, indicating that the underlying defect i

97 cusing on a matrix of DNA repair mutants and genotoxic drugs, we quantify 76 gene-drug interactions b

98 tions and sensitized NBAT1-depleted cells to genotoxic drugs.

99 , impacting genome stability and response to genotoxic drugs.

100 d milk did not cause any changes in cyto- or genotoxic effects and antigenotoxic capability of protec

101 e and the molecular mechanism underlying its genotoxic effects have remained unknown for more than a

102 lopropane has been shown to be essential for genotoxic effects in vitro, this ClbS-catalyzed ring-ope

103 tal exposure, only few animal studies on the genotoxic effects of chronic LDR radiation have been per

104 ed a meat based diet to compare the possible genotoxic effects of red vs. white meat, and the interfe

105 Genotoxic effects were seen after continuous radiation (

106 aralysis of meiotic chromosome mobility in a genotoxic environment is not a universal response among

107 ence of slight but significant cytotoxic and genotoxic events associated with the US-nanoprobe combin

108 isted, and TERT-positive ALT cells surviving genotoxic events propagated through subsequent generatio

109 These genotoxic events were accompanied by changes in plasma c

110 Combined genotoxic exposure and DNA repair deficiency alters muta

111 Studies where benzene was the primary genotoxic exposure and that had adequate assessment of b

112 Physiologically, we show that, upon genotoxic exposure, p300-mediated AFF1 acetylation is dy

113 Environmental genotoxic factors pose a challenge to the genomic integr

114 sequestration of free iron necessary for the genotoxic Fenton reaction.

115 omplex secondary metabolite produced by some genotoxic gut Escherichia coli strains.

116 tically increases the formation potential of genotoxic halonitromethanes (HNMs), including during O(3

117 al biosensor recApr-Luc2 was built to detect genotoxic hazard in recycled ash.

118 red functional RecA expression to respond to genotoxic heavy metals (Cr>Cd approximately Pb), and pol

119 de proof-of-principle for CD117-ADC as a non-genotoxic, highly-targeted conditioning agent in allotra

120 which convert dietary sources of sulfur into genotoxic hydrogen sulfide (H(2)S), have been associated

121 he quantitation of metabolites and potential genotoxic impurities (PGIs).

122 d important consequences for bioanalysis and genotoxic impurity quantification.

123 s compromised angiogenesis during early age, genotoxic injury, and viral infection, and impaired hema

124 We provided evidences showing that genotoxic injury, such as low dose irradiation, may prom

125 anced ectopic progenitor proliferation after genotoxic injury, thereby preventing both IR- and cyclop

126 insult, and the role of USP22 in response to genotoxic insult was further confirmed using mouse adult

127 Depletion of USP22 sensitized cells to genotoxic insult, and the role of USP22 in response to g

128 response that is crucial for cell fate upon genotoxic insult.

129 RNAPII degradation, essential for surviving genotoxic insult.

130 l mediator of the USP22-mediated response to genotoxic insult.

131 es DNA repair to facilitate survival against genotoxic insults and found that FASN suppresses NF-kapp

132 hat FASN regulates cellular response against genotoxic insults by up-regulating PARP-1 and DNA repair

133 ositive ALT cells showed higher tolerance to genotoxic insults compared with their TERT-negative coun

134 chanism of fork stabilization in response to genotoxic insults.

135 The genome is constantly attacked by genotoxic insults.

136 tion advantage of these cells was not due to genotoxic integrations of the therapeutic provirus.

137 e to morbidity and mortality associated with genotoxic irradiation or chemotherapy conditioning.

138 aCometChip', enabling the detection of bulky genotoxic lesions that are missed by current genotoxicit

139 y of ATM and p53 through the accumulation of genotoxic levels of DNA damage.

140 sed meat has been linked to the formation of genotoxic N-nitroso compounds (NOCs) and lipid peroxidat

141 tomyces as a means of self-resistance to the genotoxic natural product azinomycin B.

142 roach to the bacterial colibactin pathway, a genotoxic NRPS-PKS hybrid pathway found in certain Esche

143 variety of environmental stresses, including genotoxic, oxidative, and nutritional stresses.

144 Similarly, genotoxic, oxidative, or dicarbonyl stress also caused n

145 trating that CerS6 is a component of the non-genotoxic p53-dependent cellular stress response.

146 Here we expose human intestinal organoids to genotoxic pks(+) E. coli by repeated luminal injection o

147 study elucidates a mechanism behind the low genotoxic potential of foamy virus, identifies a unique

148 rs are required.IMPORTANCE Understanding the genotoxic potential of viral vectors is important in des

149 ts described suggest that DP poses a greater genotoxic potential than BDE-209.

150 s retained significant anti-oxidant and anti-genotoxic potential through digestion and fermentation.

151 ch regulation must be balanced against their genotoxic potential.

152 yl- and nitro-PAH emissions and assess their genotoxic potential.

153 96% with E10 and by 82-96% with E85, and the genotoxic potentials dropped by 72 and 83%, respectively

154 anned due to its carcinogenic, mutagenic and genotoxic properties, which represent a serious risk to

155 es synthetic precolibactin 886 to form a non-genotoxic pyridone, which suggests precolibactin 886 lie

156 ecolibactins, leads to the production of non-genotoxic pyridone-based isolates derived from the diver

157 Soon after exposure to genotoxic reagents, mammalian cells inhibit transcriptio

158 regulation suppresses aberrant, potentially genotoxic recombination activities, and the mobilization

159 Here, we define a novel genotoxic response whereby spatially separated signals i

160 hospho-proteins is well known to support the genotoxic response, whether multi-BRCT domains can acqui

161 All major genotoxic responses to FA, including replication inhibit

162 cApr-Luc2 could be useful for evaluating the genotoxic risk of pollutants present in ash that might b

163 Thus, our work uncovers a mechanism by which genotoxic Salmonella exhausts the RPA response by induci

164 ctive intermediates are converted to a known genotoxic scaffold, providing metabolic support of our m

165 pplicability of the system by identifying as genotoxic specific components of HPTLC-separated influen

166 bly arrested proliferation, often induced by genotoxic stress [1].

167 to sublethal low-dose ionizing radiation, a genotoxic stress affecting the soma and the germ line, a

168 5-fluorouracil, which induces metabolic and genotoxic stress and activates p53, further implicated C

169 s in adult tissues are constantly exposed to genotoxic stress and also accumulate DNA damage with age

170 PSGs enhance resistance to genotoxic stress and confer fitness during aging.

171 deficiency leads to increased sensitivity to genotoxic stress and delayed DNA double-strand break (DS

172 A damage in placental cells, suggesting that genotoxic stress and ensuing placental senescence and cy

173 Yeast cells activate RNR in response to genotoxic stress and iron deficiency by facilitating red

174 pressor p53 becomes activated in response to genotoxic stress and is essential for arresting the cell

175 tosolic double-stranded (ds)DNA arising from genotoxic stress and pathogen invasion.

176 tress responses are also activated following genotoxic stress and play a crucial role in the outcome

177 noubiquitylation of Nup60 is stimulated upon genotoxic stress and regulates the DNA-damage response a

178 s to heightened apoptotic priming, intrinsic genotoxic stress and susceptibility to DNA damage checkp

179 ageal squamous cells against DNA damage from genotoxic stress and that GSTT2 expression can be induce

180 isms important for cancer cell adaptation to genotoxic stress and thereby to achieve cancer cell-spec

181 re characterized by increased sensitivity to genotoxic stress associated with sustained induction of

182 Exposure to genotoxic stress by environmental agents or treatments,

183 nterestingly, we found that arsenite-induced genotoxic stress causes a PLK1-dependent signaling respo

184 tic genes in mice were resistant to specific genotoxic stress compared to sister cells recovered from

185 wed that CaWss1 promotes cell survival under genotoxic stress conditions that generate DPCs and that

186 of programmed cell death under salinity and genotoxic stress conditions.

187 suggest that regulation of p53 responses to genotoxic stress contributes to the tumour suppressor fu

188 Genotoxic stress drives damaged DNA out of the nucleus b

189 s or in a repair-competent background due to genotoxic stress from celluar processes such as transcri

190 Specifically, there is evidence that genotoxic stress from chemotherapy or radiation therapy,

191 A repair by NHEJ in conferring resistance to genotoxic stress in advanced prostate cancer and suggest

192 ing pathway is associated with resistance to genotoxic stress in aggressive prostate cancer cells.

193 Upon genotoxic stress in G2, high levels of H2A.X lead to per

194 patient HSPCs but rescued physiological and genotoxic stress in HSPCs from FA mice, showing that MYC

195 ous vegetables, to be a widespread source of genotoxic stress in intestinal epithelial cells.

196 s to silence repetitive elements and prevent genotoxic stress in the germ line.

197 We evaluated the possible origins of genotoxic stress in the mouse gut by examining factors a

198 wild-type strain, suggesting the presence of genotoxic stress in the mouse gut.

199 breaks in developing lymphocytes exposed to genotoxic stress increases the risk for aberrant recombi

200 populations are expected to be less prone to genotoxic stress induced by these treatments and therefo

201 The protective role of IRE1alpha under genotoxic stress is conserved in fly and mouse.

202 and that disruption of this immune sensor of genotoxic stress leads to behavioural abnormalities.

203 unusual event that is often associated with genotoxic stress or viral infection.

204 Genotoxic stress reduces this ubiquitination in cytosol

205 Apoptotic death of cells damaged by genotoxic stress requires regulatory input from surround

206 o indicated the involvement of TRIM21 in the genotoxic stress response and suppressing tumorigenesis.

207 However, whether ATR affects the genotoxic stress response in non-replicating, non-cyclin

208 sphoproteome datasets revealed activation of genotoxic stress response pathways, including deregulati

209 innate immunity, lymphocyte development and genotoxic stress response.

210 energy, in addition to cell development and genotoxic stress response.

211 t role in regulating the level of p53 in the genotoxic stress response.

212 ion of histones by PARP-1 has been linked to genotoxic stress responses, its role in physiological pr

213 , immunophenotyping studies, and analysis of genotoxic stress responses.

214 , CTCF-deficient cells are hypersensitive to genotoxic stress such as ionizing radiation (IR).

215 constantly threatened by multiple sources of genotoxic stress that cause DNA damage.

216 vement of ZNF281 in the cellular response to genotoxic stress through the control exercised on the ex

217 protein response transducer IRE1alpha under genotoxic stress to modulate repair programs and sustain

218 efective TERT variants that bestowed similar genotoxic stress tolerance, indicating that telomere syn

219 l-extrinsic (chemical- or metabolism-induced genotoxic stress) challenges.

220 zes, the evolution of extreme sensitivity to genotoxic stress, and a hyperactive TP53 signaling pathw

221 organization, leading to cell cycle arrest, genotoxic stress, and innate immunity.

222 ession of gammaH2A.X and of genes related to genotoxic stress, as well as STAT3 phosphorylation, was

223 and break (DSB) is the most critical type of genotoxic stress, but the involvement of DSB repair in P

224 cGAS induces potent interferon responses to genotoxic stress, but weaker responses to viral infectio

225 In response to genotoxic stress, cells employ diverse adaptive mechanis

226 During genotoxic stress, cellular transformation requires that

227 Following genotoxic stress, cGAS can also respond to endogenous DN

228 In response to genotoxic stress, CHK1-mediated phosphorylation of RAD51

229 Upon genotoxic stress, dynamic relocalization events control

230 In response to genotoxic stress, multiple kinase signaling cascades are

231 Upon genotoxic stress, PCNA ubiquitination allows for replica

232 n of apoptosis following exogenously induced genotoxic stress, prophase-arrested oocytes are highly c

233 traviolet radiation, or to asbestos, survive genotoxic stress, resulting in a higher rate of cellular

234 nt cells (SCs) accumulate with age and after genotoxic stress, such as total-body irradiation (TBI).

235 Here, we show that following genotoxic stress, the RNA-binding motif protein 7 (RBM7)

236 and organelle quality control, prevention of genotoxic stress, tumor suppression, pathogen eliminatio

237 Under genotoxic stress, when RNF8 is rapidly recruited to site

238 Short term IL-22 production protects against genotoxic stress, whereas uncontrolled IL-22 activity pr

239 ic differentiation results in an overload of genotoxic stress, which causes aborted differentiation a

240 ng germination, indicative of high levels of genotoxic stress, which is induced following maturation

241 ULIN Tyr56 phosphorylation, which depends on genotoxic stress-activated ABL1/c-Abl.

242 x1-FBXO31) ubiquitin ligase complex mediates genotoxic stress-induced cyclin D1 degradation.

243 Here we show that Sam68 is critical for genotoxic stress-induced NF-kappaB activation in the gam

244 the critical role of Sam68 in orchestrating genotoxic stress-initiated NF-kappaB activation signalin

245 data reveal a novel function of Sam68 in the genotoxic stress-initiated nuclear signaling, which is c

246 leolytic degradation only in the presence of genotoxic stress.

247 r non-corrected cells, even without imposing genotoxic stress.

248 cetylation of a key elongation factor during genotoxic stress.

249 2AX phosphorylation for plant survival under genotoxic stress.

250 while sosA inactivation sensitizes cells to genotoxic stress.

251 taining cellular homeostasis and response to genotoxic stress.

252 , with the gene induced by multiple types of genotoxic stress.

253 tial new regulator of RNAPII turnover during genotoxic stress.

254 ia have evolved a network of genes to combat genotoxic stress.

255 form for caspase-2 activation in response to genotoxic stress.

256 ic features, and increased susceptibility to genotoxic stress.

257 ll cycle arrest and apoptosis in response to genotoxic stress.

258 le minute 2 (MDM2) is induced in response to genotoxic stress.

259 ulators of DNA replication in the absence of genotoxic stress.

260 p53-binding kinetics are modulated following genotoxic stress.

261 ished functions in sensing and responding to genotoxic stress.

262 is but also with increased susceptibility to genotoxic stress.

263 sponse to metformin, hypoxia-like (CoCl2) or genotoxic stress.

264 on with the DROSHA-processing complex during genotoxic stress.

265 limiting H2A.X synthesis and cell death upon genotoxic stress.

266 sensitive to DNA double-strand break-induced genotoxic stress.

267 3 stabilization and activity following acute genotoxic stress.

268 from radiotherapy- and chemotherapy-induced genotoxic stress.

269 acilitating its stabilization in response to genotoxic stress.

270 e deficiencies, and increased sensitivity to genotoxic stress.

271 dergo dramatic genome changes in response to genotoxic stress.

272 in the root meristem, even in the absence of genotoxic stress.

273 d degradation, is necessary for responses to genotoxic stress.

274 l organisms might be a significant source of genotoxic stress.

275 responses are crucial for plant growth under genotoxic stress.

276 d histone modification in plant growth under genotoxic stress.

277 st decrease in apoptosis in response to most genotoxic stresses compared with wild-type p53 but exhib

278 ing infections, C. albicans has to cope with genotoxic stresses generated by the host immune system.

279 Genotoxic stresses lead to centrosome amplification, a f

280 yptococcus cells polyploidize in response to genotoxic stresses that cause DNA double-strand breaks.

281 key intracellular molecule participating in genotoxic stresses-induced NF-kappaB activation.

282 vealing a variant that improves growth under genotoxic stresses.

283 pathways to protect their genomes from both genotoxic stressors and foreign DNA from invading pathog

284 We then analyzed how genotoxic stressors may promote the release of IGFBP-4 a

285 Ps), some of which are cytotoxic, mutagenic, genotoxic, teratogenic, and potential carcinogens both i

286 ne that have been shown to be more cyto- and genotoxic than regulated DBPs.

287 comparable to chloramination, 3.9 times more genotoxic than the nondisinfected controls.

288 zonated wastewater was at least 3 times less genotoxic than the samples treated with chlorine-based d

289 ted species are typically more cytotoxic and genotoxic than their chlorinated analogs.

290 rnary complex formation after treatment with genotoxic therapeutics has not been fully explored.

291 al for effective targeting of ERG protein by genotoxic therapeutics in fusion-positive PCa.

292 tion, outcome prediction, dose optimization, genotoxic therapy evaluation, and target engagement imag

293 gulation across cancer types correlates with genotoxic therapy resistance.

294 P inhibition, especially in combination with genotoxic therapy.

295 ate, but subsequently resolve, L1-instigated genotoxic threats independent of piRNAs and differentiat

296 How genotoxic TOP2 DNA-protein cross-links are resolved is u

297 IN-mediated Wnt/beta-catenin activation upon genotoxic treatments promotes drug resistance and metast

298 be a decisive factor for tumor responses to genotoxic treatments.

299 Treatment of cells with the non-genotoxic UPR agonist thapsigargin led to a rapid inhibi

300 nd foamy virus vectors to be remarkably less genotoxic, well below what was expected from their integ