ライフサイエンスコーパス: micronuclei

1 chromosomes in abnormal nuclear structures (micronuclei).

2 efore the appearance of anaphase bridges and micronuclei.

3 rophe, irregularly shaped nuclei or multiple micronuclei.

4 reaks via the formation of structures called micronuclei.

5 e fusion, resulting in formation of multiple micronuclei.

6 uent lagging of chromosomes and formation of micronuclei.

7 and accumulate cells with higher ploidy and micronuclei.

8 er chromatid exchanges (SCEs) and numbers of micronuclei.

9 olate status was an independent predictor of micronuclei.

10 H1 by shRNA suppressed induction of H2AX and micronuclei.

11 exclude part of their genome as damage-prone micronuclei.

12 ster chromatid exchanges, and show increased micronuclei.

13 aneous and radiation- or mitomycin C-induced micronuclei.

14 lymphoproliferative activity, and lymphocyte micronuclei.

15 re homozygous, rad51 nulls in their germline micronuclei.

16 re not associated with a higher frequency of micronuclei.

17 tions and are extruded into nuclear blebs or micronuclei.

18 ed the frequency of prevalence of cells with micronuclei.

19 res become elongated in both macronuclei and micronuclei.

20 ar convolution and the formation of multiple micronuclei.

21 inesis resulting in daughter cells with many micronuclei.

22 Brca2(Tr2014/Tr2014) MEFs frequently develop micronuclei.

23 ch we found associated with the formation of micronuclei.

24 and have increased numbers of macrocytes and micronuclei.

25 ells containing mitochondria surrounding the micronuclei.

26 of these DNA molecules in radiation-induced micronuclei.

27 sing altogether from transcriptionally inert micronuclei.

28 on of linker histone in mitotically dividing micronuclei.

29 n establishing transcriptional competence in micronuclei.

30 somes, leading to their mis-segregation into micronuclei.

31 n of thymic lymphoma with elevated levels of micronuclei.

32 of mis-segregated chromosomes trapped within micronuclei.

33 f mitotic errors leading to the formation of micronuclei.

34 ained bromodeoxyuridine (BrdU) and gammaH2AX micronuclei.

35 MP-AMP synthase) to the nuclear membrane and micronuclei.

36 nation, associated with anaphase bridges and micronuclei.

37 spindles, anaphase-lagging chromosomes, and micronuclei.

38 es damaged DNA out of the nucleus by forming micronuclei.

39 om enwrapping individual chromosomes to form micronuclei.

40 formation of ultra-fine anaphase bridges and micronuclei.

41 DNA from aberrant nuclear structures called micronuclei.

42 oss chromosomal aberrations, 53BP1 foci, and micronuclei.

43 neven chromosome segregations that resembles micronuclei.

44 frequency of acentric-bearing, lamin-coated micronuclei.

45 osomes in aberrant nuclear structures called micronuclei.

46 t of the nonsmokers (9.57 compared with 4.44 micronuclei/1000 cells; P < 0.0001).

47 mitotic chromosomes, their sequestration in micronuclei(5,6) and subsequent rupture of the micronucl

48 ersus 12% of controls) had >or=4 spontaneous micronuclei, 66% of cases (and no controls) had >or=4 sp

49 us 6% of the controls) had >or=5 NNK-induced micronuclei, 89% of cases (and no controls) had >or=6 in

50 ng activity associated with the formation of micronuclei, a clear sign of genome instability.

51 ultured cells also promotes the formation of micronuclei, a hallmark of chromosome instability.

52 to cell-killing activity and stimulation of micronuclei, a hallmark of genome instability.

53 genes also caused an increased frequency of micronuclei, a marker of genetically unstable cells.

54 o a striking increase in hepatocytes bearing micronuclei, a marker of genomic instability, which is s

55 Chromosomal instability (CIN) generates micronuclei-aberrant extranuclear structures that cataly

56 Although micronuclei accumulate DNA double-strand breaks and repl

57 Radiotherapy-induced tumour cell micronuclei activate cytosolic nucleic acid sensor pathw

58 with p21Waf1 expression, gamma-H2AX foci and micronuclei, adding SOD and catalase has no effect on th

59 on of either or both of these factors causes micronuclei after DNA damage, which disrupts intestinal

60 tial inhibition of Plk1 was the formation of micronuclei, an increase in tetraploid progeny, and sene

61 resulting in an increase in cells harboring micronuclei, an indication of defects in chromosome segr

62 n average increase in effect of 1.7-fold for micronuclei and 2.8-fold for apoptosis.

63 f spontaneous chromosome instability such as micronuclei and 53BP1 nuclear bodies, known consequences

64 iciency is associated with the appearance of micronuclei and aberrant mitoses that are a by-product o

65 icentric chromosomes, nucleoplasmic bridges, micronuclei and aneuploidy.

66 was sufficient to increase the prevalence of micronuclei and binucleated cells in parallel with aberr

67 8 E6 promotes the growth of cells with micronuclei and causes chromothripsis, a mutagenic proce

68 ss, incomplete DNA replication, formation of micronuclei and chromatin bridges and eventually cell de

69 ng mechanisms underlying chromothripsis from micronuclei and chromatin bridges, as well as highlight

70 ults in a striking phenotype associated with micronuclei and chromosomal instability.

71 Here we identify micronuclei and chromosome bridges, aberrations in the n

72 generates structural defects of the nucleus, micronuclei and chromosome bridges, which initiate a mut

73 in the absence of 53BP1 results in increased micronuclei and cytoplasmic double-stranded DNA, leading

74 int MPS1 inhibitors that generate persistent micronuclei and diverse aneuploidy while skewing macroph

75 We tracked the fate of newly generated micronuclei and found that they undergo defective and as

76 ase to the medium decreases the formation of micronuclei and induction of p21Waf1 and gamma-H2AX foci

77 t nuclear morphology and a high frequency of micronuclei and large vacuoles.

78 h a high spontaneous frequency of cells with micronuclei and LST and specific alterations in DNA repa

79 Although both micronuclei and macronuclei contain H3 in typical nucleo

80 lls exposed to eleutherobin contain multiple micronuclei and microtubule bundles, and they arrest in

81 chromosomal instability and the formation of micronuclei and multinucleation through its interaction

82 laggings, mitotic bridges, and formation of micronuclei and multinucleation.

83 igns of aneuploidy including the presence of micronuclei and multiple nuclei.

84 mere attrition and an increased frequency of micronuclei and nuclear blebs.

85 duced by double-strand breaks, thus avoiding micronuclei and organ malformation.

86 V-C damage and increased mutation frequency, micronuclei and sister chromatin exchanges but are not s

87 hat lead to entrapment of chromosomes within micronuclei and their subsequent fragmentation in the ne

88 E6 decreased antiproliferative responses to micronuclei and time-lapse imaging revealed HPV8 E6 prom

89 total dose, when delivered acutely, induced micronuclei and transcriptional responses.

90 were associated with an increased number of micronuclei and with the presence of cytoplasmic ssDNA,

91 s normally restricted to unrearranged DNA of micronuclei and/or developing nuclei, but germline-limit

92 y the presence of increased multinucleation, micronuclei, and aberrant centrosomes.

93 plex was essential for the induction of DSB, micronuclei, and apoptosis in human cells by chromate.

94 tion-dependent formation of gamma-H2AX foci, micronuclei, and chromosomal aberrations (chromatid brea

95 anied by mitotic radiosensitivity, increased micronuclei, and chromosomal instability.

96 osomal translocations, deletions, mutations, micronuclei, and decreased plating efficiency.

97 -hydroxy-2'-deoxyguanosine, gamma-H2AX foci, micronuclei, and DNA deletions.

98 ases (P < .05) in centrosomal amplification, micronuclei, and micronuclei containing whole chromosome

99 xicity, including centrosomal amplification, micronuclei, and micronuclei containing whole chromosome

100 Analysis of cell growth, micronuclei, and phosphorylated Ser-139 residue of the h

101 ses mitotic spindle and cytokinesis defects, micronuclei, and polyploidy.

102 chromosome segregation errors, formation of micronuclei, and subsequent DNA damage.

103 sts (MEFs) had more aberrant chromosomes and micronuclei, and were genetically unstable.

104 unequal chromosome segregation, formation of micronuclei, and/or failure to complete cell division ar

105 The capture of DMs by micronuclei appears to be dependent on their lack of a c

106 Chromosome-containing micronuclei are a hallmark of aggressive cancers.

107 ow that CIN and pervasive cGAS activation in micronuclei are associated with ER stress signalling, im

108 ronucleus, and elimination of one of the new micronuclei are blocked if actinomycin D is added at lea

109 cGAS-containing cytoplasmic micronuclei are increased in BS cells.

110 Micronuclei are whole chromosomes or chromosome segments

111 of nonviable cells with multiple, fragmented micronuclei, are common features observed.

112 While research has detailed how micronuclei arise from cells entering anaphase with lagg

113 Here, we report that cGAS localizes to micronuclei arising from genome instability in a mouse m

114 A high basal level of micronuclei as a predictive biomarker for AsiDNA treatme

115 Cytotoxicity (MTT test) and genotoxicity (micronuclei assay) were not detectable.

116 ent of DNA damage using the comet assay, the micronuclei assay, and the gamma-H2AX immunostaining ass

117 mokers using this novel flow-cytometry based micronuclei-assay.

118 This method, unlike available micronuclei assays, allows rapid evaluation of a large n

119 nexin-V/propidium iodide binding, comet, and micronuclei assays, showed that the reduction in viabili

120 urvival assays or 1 Gy for cytokinesis block micronuclei assays.

121 Damaged TIPs are segregated into micronuclei at a significantly higher frequency than dam

122 x safeguards against lagging chromosomes and micronuclei at mitotic exit by promoting chromosome alig

123 lopment of somatic macronuclei from germline micronuclei, at each sexual generation.

124 erved during meiotic prophase, a period when micronuclei become transcriptionally active.

125 in the peripheral blood for the presence of micronuclei before these cells are removed by the spleen

126 re heavily-damaged lymphocytes with multiple micronuclei/binucleated cell, whereas partial-body expos

127 nted chromosomes localize within sub-nuclear micronuclei bodies (MN bodies) and undergo ligation by N

128 p1p is missing from transcriptionally silent micronuclei but is enriched in heterochromatin-like chro

129 In support, extracts from micronuclei, but not macronuclei, contain a kinase activ

130 V600E) expression increased the frequency of micronuclei by both clastogenic and aneugenic events.

131 s also activate this pathway, recognition of micronuclei by cGAS may act as a cell-intrinsic immune s

132 dy, chromosome breakage and the formation of micronuclei by targeting cellular ligases through a sT d

133 Micronuclei can persist in cells over several generation

134 PCS), lagging chromosomes, anaphase bridges, micronuclei, centrosome amplification, multinucleated ce

135 some damage (dicentrics, acentric fragments, micronuclei, chromatid gaps/breaks) was scored.

136 ve mitotic events result in the formation of micronuclei colocalizing with cGAS, which is activated b

137 rapidly by pores or probes or else by small micronuclei consistently associates nuclear rupture with

138 Macronuclei, but not micronuclei, contain a 36-kDa polypeptide that is immuno

139 macronuclei, but not transcriptionally inert micronuclei, contain a robust histone methyltransferase

140 During S phase, BS cells expel micronuclei containing sites of DNA synthesis.

141 also generate acentric lagging chromatin and micronuclei containing these chromosomes.

142 centrosomal amplification, micronuclei, and micronuclei containing whole chromosomes were found in m

143 centrosomal amplification, micronuclei, and micronuclei containing whole chromosomes.

144 nes from tumor cells via their entrapment in micronuclei contributes to the improved therapeutic resp

145 creased the formation of centromere-negative micronuclei, demonstrating that induced DSB were ineffic

146 osimetry, we developed metrics that describe micronuclei distributions in binucleated cells and serve

147 DNA damage) and normochromatic erythrocytes (micronuclei) during chemical or immune-mediated colitis.

148 double membrane-bound structures, similar to micronuclei, during telophase of a DNA elimination mitos

149 to chromosomal errors by encapsulation into micronuclei, elimination via cellular fragmentation, and

150 CIN leads to the formation of rupture-prone micronuclei, exposing genomic double-stranded DNA (dsDNA

151 me misalignment, and subsequent formation of micronuclei following mitosis completion.

152 Both activities were lost from germ line micronuclei following the programmed arrest of micronucl

153 A second mechanism is activated after micronuclei form and then rupture, and involves CIP2A an

154 Whole-chromosome-containing micronuclei form when mitotic errors produce lagging chr

155 Further, POLQ knockdown enhances cytosolic micronuclei formation and activates signaling of cyclic

156 g CIP2A display increased radio-sensitivity, micronuclei formation and chromosomal instability.

157 ome instabilities including chromosome loss, micronuclei formation and chromosome breakage that are f

158 ed frequencies of chromosomal aberration and micronuclei formation and exhibit an enhanced proliferat

159 omosomal instability manifested by increased micronuclei formation and numerical chromosomal aberrati

160 g quiescent HSPCs bypasses long deletion and micronuclei formation and preserves efficient on-target

161 M, or of BRCA1 and FANCM, leads to increased micronuclei formation and synthetic lethality in ALT cel

162 matin, and consistent with a mitotic origin, micronuclei formation and the proinflammatory response f

163 pathway senses unnatural cell fusion through micronuclei formation as a danger signal, and consequent

164 as assessed by sister-chromatid exchange and micronuclei formation assays.

165 CENPA expression and micronuclei formation correlate highly with activation o

166 plification, sister chromatid exchanges, and micronuclei formation in cells exposed to genotoxic agen

167 ies by Harding et al. demonstrate a role for micronuclei formation in DNA damage-induced immune activ

168 t stress leads to a decline in fertility and micronuclei formation in pollen mother cells.

169 derate degree of chromosomal instability and micronuclei formation in short-term cultures established

170 ver, downregulation of POLQ by ZEB1 fostered micronuclei formation in TNBC tumor cell lines.

171 The frequency of micronuclei formation in unirradiated bystander cells in

172 s therapeutic combination promotes increased micronuclei formation in vitro and subsequently drives i

173 Mitotic chromosome misalignment and micronuclei formation increased in the knockout cells an

174 ctivating immune signaling through increased micronuclei formation utilizing a cell cycle checkpoint

175 Micronuclei formation was induced by both DP and BDE-209

176 s, the biological Bragg peak and the highest micronuclei formation was observed at the depth of 14.5

177 cantly (P < .05 to .001) higher frequency of micronuclei formation was observed in mice that received

178 ncreased gene mutations, gene amplification, micronuclei formation, and chromosomal instability.

179 We also observed type I IFN gene expression, micronuclei formation, and death of chemically induced c

180 mbers, formed multipolar spindles, displayed micronuclei formation, and elevated nuclear DNA content.

181 and RNA-Seq, GOF p53-induced origin firing, micronuclei formation, and fork protection were traced t

182 sed levels of DNA damage, lagging chromatin, micronuclei formation, breaks and quadriradials.

183 e Gravin rescued chromosome misalignment and micronuclei formation, but a mutant Gravin that cannot b

184 recombination repair in human cells, reduced micronuclei formation, promoted DNA end protection, and

185 eta-galactosidase, increased p21 expression, micronuclei formation, reduced Lamin B1, and increased e

186 Chromocenter disruption led to micronuclei formation, resulting in cell death.

187 , stabilizes replication forks, and promotes micronuclei formation, thus facilitating the proliferati

188 inhibitor treatment, which potently induces micronuclei formation, upregulates cytoplasmic dsRNA sen

189 umber of centrosome, multipolar spindles and micronuclei formation.

190 rtially rescued DHA-induced cytotoxicity and micronuclei formation.

191 As micronuclei formed from lagging chromosomes also activat

192 That micronuclei frequency can be measured in biopsies and do

193 We measured micronuclei frequency in reticulocytes from peripheral b

194 monstrate that chromosomes mis-segregated to micronuclei frequently undergo chromothripsis-like rearr

195 bility (measured as the number of cells with micronuclei) from compromised replication fork repair(6)

196 ntly re-engages this pathway in KL cells via micronuclei generation.

197 We assessed base lesions, micronuclei, homologous recombination (HR; using fluores

198 , fluorescence in situ hybridization (FISH), micronuclei imaging, and the telomere shortest length as

199 eased occurrence (more than 2-fold) of extra micronuclei, implying faulty control of micronuclear div

200 elated with mitotic and meiotic divisions of micronuclei in a fashion that closely coincides with chr

201 rg et al. have described a method to measure micronuclei in an enriched reticulocyte population using

202 plies single-laser flow-cytometry to measure micronuclei in an enriched transferrin-positive reticulo

203 ted anaphase chromatin-bridge formation, and micronuclei in daughter cells of proband skin fibroblast

204 hreads form centromeric-chromatin-containing micronuclei in daughter cells.

205 cent protein (GFP)-tagged Cna1p localizes in micronuclei in dots whose number and behavior during mit

206 show that this assay can effectively detect micronuclei in human blood samples.

207 Reticulocytes with micronuclei in human peripheral blood are not generally

208 Newly synthesized Cna1p-GFP enters micronuclei in mitosis and accumulates in the nucleoplas

209 ploidies, we found no lagging chromosomes or micronuclei in mitotic polyploid cells.

210 the MAPK pathway in mediating v-ras-induced micronuclei in NIH 3T3 cells was examined by inhibiting

211 Micronuclei in peripheral blood reticulocytes can be use

212 tic nuclei, anaphase bridges during mitosis, micronuclei in pollen tetrads, and 30% seed abortion.

213 oth the apoptotic wave and the appearance of micronuclei in red blood cells are likely cellular conse

214 ucleus at mitotic exit, and the formation of micronuclei in vitro and in vivo.

215 Binucleation and micronuclei increase as telomeres shorten, which all fav

216 se in both CREST negative and CREST positive micronuclei, indicating that both clastogenic and aneuge

217 n, activation, and downstream signaling from micronuclei induced by ionizing radiation, replication s

218 addition, Tax-1 PBM was responsible for the micronuclei induction activity of Tax-1 relative to that

219 We show that, due to their small size, micronuclei inherently lack the capacity of primary nucl

220 may be important for the differentiation of micronuclei into macronuclei during development.

221 The generation of micronuclei is a reflection of DNA damage, defective mit

222 er alterations (aneuploidy) and formation of micronuclei-key intermediates of a rapid mutational proc

223 We show that the isolated micronuclei lack functional lamin B1 and become prone to

224 t that LT, dependent on Bub1 binding, causes micronuclei, lagging chromatin, and anaphase bridges, wh

225 and play an unexpected role in the germ line micronuclei late in conjugation that is unrelated to tra

226 hosphate-adenosine monophosphate synthase in micronuclei, leading to further activation of the downst

227 n drives increased production of immunogenic micronuclei, leading to systemic tumor response with pot

228 us DNA damage by alkaline comet assay, basal micronuclei levels, the number of large-scale chromosoma

229 ions were restricted to mitotically dividing micronuclei; macronuclei, which are amitotic, showed no

230 hput method for quantifying the formation of micronuclei, markers of genome instability, in mouse ery

231 Pulverization of chromosomes in micronuclei may also be one explanation for 'chromothrip

232 e two kinds of nuclei: Macronuclei (MAC) and Micronuclei (MIC).

233 ce of somatic macronuclei (MAC) and germline micronuclei (MIC).

234 rosis) and occurrence of chromosomal damage (micronuclei MN, nculeoplasmic bridge NPBs and nuclear bu

235 (classical) chromosomal aberrations (CAs) or micronuclei (MN) as markers of DNA damage.

236 Micronuclei (MN) frequency in lymphocytes is a marker of

237 ge as reflected in a significant increase of micronuclei (MN) in cells.

238 ions from a particle microbeam, the yield of micronuclei (MN) in the nontargeted cells was increased,

239 tely 380 keV/microm), a 1.4-fold increase of micronuclei (MN) was detected demonstrating a bystander

240 As standard the assay detects micronuclei (MN), cytotoxicity and cell-cycle profiles f

241 We examined nuclear DNA damage, micronuclei (MN), intracellular ROS production, and the

242 ruit their own nuclear envelope (NE) to form micronuclei (MN).

243 A in aberrant extranuclear structures called micronuclei (MN).

244 in high genomic instability characterized by micronuclei, multiple nuclei, and a wide distribution of

245 predict cancer risk based on the numbers of micronuclei, nucleoplasmic bridges, and nuclear buds def

246 analyzed on a continuous scale, spontaneous micronuclei, nucleoplasmic bridges, and nuclear buds wer

247 of NNK-induced chromosomal damage endpoints (micronuclei, nucleoplasmic bridges, and nuclear buds) pe

248 h percentiles of spontaneous and NNK-induced micronuclei, nucleoplasmic bridges, and nuclear buds, re

249 Such micronuclei occur after mis-segregation of DNA during ce

250 ansfer from somatic macronuclei to germ-line micronuclei occurs rarely if at all.

251 the spontaneous induction of DNA damage and micronuclei of SIRT2 deficiency in cancer cells.

252 The macro- and micronuclei of Tetrahymena reside in the same cytoplasm

253 In growing cells, H2A.Y is incorporated into micronuclei only during S phase, which occurs immediatel

254 originates from aberrations of nuclei called micronuclei or chromosome bridges(5-8).

255 d, along with interphase cells that harbored micronuclei or multiple nuclei, consistent with unbalanc

256 lear shapes characterized by blebs, lobules, micronuclei, or invaginations are hallmarks of many canc

257 chromosomes frequently missegregate and form micronuclei, promoting additional chromothripsis.

258 Micronuclei quantification was also possible in patient

259 reduced proliferation, frequent formation of micronuclei, recruitment of cGAS, and activation of the

260 We therefore conclude that micronuclei represent an important source of immunostimu

261 These micronuclei retain DNA damage markers and frequently rej

262 ient cells showed chromosome rearrangements, micronuclei, sensitivity to replication stress and DNA d

263 f functional lamin B1 partly correlates with micronuclei size, suggesting that the proper assembly of

264 Cancer cells frequently contain micronuclei-small, nucleus-like structures formed by chr

265 Here we discuss basic studies on micronuclei stability and transactions that affect their

266 r cells following pharmacologic induction of micronuclei, stimulating mitochondrial antiviral signali

267 ased mitotic defects, chromatin bridges, and micronuclei, suggesting HDAC1/2 are necessary for accura

268 rized by genome instability, accumulation of micronuclei, susceptibility to cancer, and immunodeficie

269 dye, and genotoxicity was evaluated with the micronuclei test.

270 in and Cdc20, and exhibit a greater level of micronuclei than do wild-type cells.

271 veloped a general and rapid method to purify micronuclei that are known to entrap extrachromosomal el

272 8 E6 makes the micronuclei that can result from anaphase bridges more c

273 phosphorylation can be detected in germline micronuclei that divide mitotically but not in somatic m

274 ibution from chromosome-containing fragments/micronuclei that frequently emerge and may persist or be

275 hese mitotic errors generate an abundance of micronuclei that predispose chromosomes to subsequent ca

276 lypeptide is detected with PKA antibodies in micronuclei, that is not detected in macronuclei.

277 chromatin fragments with characteristics of micronuclei; these were found to activate cGAS/STING, do

278 of missegregated chromosomes trapped within micronuclei through a process known as chromothripsis(1-

279 imaging revealed HPV8 E6 promoted cells with micronuclei to complete mitosis.

280 sensor cGAS gains access to the cargo within micronuclei to drive type I IFN responses.

281 inger et al. further improved the scoring of micronuclei to enable the use of bench-top instruments i

282 These micronuclei undergo dynamic changes including loss of ac

283 During meiosis, micronuclei underwent abnormal chromosome condensation a

284 Although cGAS localized to ruptured micronuclei via binding to self-DNA, we failed to observ

285 eated cells, an increase in cells containing micronuclei was noted in comparison with controls.

286 cluding apoptotic cells and cells expressing micronuclei, was determined as a function of time in cul

287 A significant fraction of the micronuclei were CREST-negative, reflective of lost acen

288 rrant mitotic segregation, since most of the micronuclei were CREST-positive, reflective of lost chro

289 ed, suggesting a failure of cytokinesis, and micronuclei were formed, indicative of genomic instabili

290 gation, and the protein localizes to meiotic micronuclei when bidirectional germ line transcription o

291 rete dots in those nuclei destined to become micronuclei, whereas it remains diffuse and is gradually

292 easured as chromosomal damage in the form of micronuclei which is radiation quality dependent.

293 We also detected the presence of numerous micronuclei, which are known to induce cGAS, in the cyto

294 tion is also associated with the presence of micronuclei, which are shown to contain unstable chromos

295 tranded DNA breaks leads to the formation of micronuclei, which precede activation of inflammatory si

296 s encapsulate missegregated chromosomes into micronuclei while undergoing cellular fragmentation and

297 ridges and then shattered, thereby producing micronuclei whose encapsulated ecDNAs are substrates for

298 that chromosome segregation errors generate micronuclei whose rupture activates cGAS.

299 le causing unrestrained activity at ruptured micronuclei, with catastrophic consequences for genome s

300 As for fragments, micronuclei yields for combined treatments were consiste