ライフサイエンスコーパス: DDR

1 DDR activation and maintenance at telomeres depend on th

2 DDRs are upregulated in Alzheimer's and Parkinson's dise

3 DDRs regulate cell functions, and their extracellular do

4 focused dual guide RNA library targeting 852 DDR-associated genes.

5 c.7253dupT in TEX15, encoding a DDR factor important in meiosis, associated with heredit

6 DSB into neighboring chromatin, generating a DDR platform that protects against end disassociation an

7 s study, we demonstrate that HBoV1 induces a DDR that plays significant roles in the replication of t

8 ATM is a DDR kinase that has a central role in coordinating DNA r

9 bbp8, also known as CtIP), which regulates a DDR choice in double-stranded break (DSB) repair.

10 n maintenance of genomic stability through a DDR-independent pathway.

11 ITCH-H1.2 axis may confer TNBC cells with a DDR repression to counteract the replication stress and

12 Dysfunctional telomeres activate DDR signaling, genomic instability, and cellular senesce

13 s exhibit evidence for a partially activated DDR during mitosis, which leads to ongoing chromosome se

14 Here we show that all DDR complex components co-localize with Pol V, and we re

15 ATM loss altered DDR signaling, but did not directly impact homologous re

16 sites, a feature especially prominent among DDR genes.

17 TP53 (27%) and PTEN (12%) and DDR gene defects (BRCA2 7%; CDK12 5%; ATM 4%) were commo

18 Sirtuins share some DSB-binding capacity and DDR activation.

19 xicants and inhibitors of the cell cycle and DDR, with the prospect of personalized therapeutic strat

20 ed with Pol V recruitment-DR (DMS3-RDM1) and DDR' (DMS3-RDM1-DRD1 peptide), at 3.6 angstrom and 3.5 a

21 ; however, groupings of other DNA repair and DDR genes are correlated with APE2 with different patter

22 e mRNA expression of 13 other DNA repair and DDR genes from matched samples for 6 cancer types.

23 Replication stress and DDR deficiency are independent of each other, creating o

24 UPR and DDR alterations are associated with aging and with patho

25 the critical role of fibrillar collagen and DDRs in supporting the growth of tumours thriving within

26 lzheimer's and Parkinson's disease (PD), and DDRs knockdown reduces neurotoxic protein levels.

27 DSBs near a border produce highly asymmetric DDR platforms, with gammaH2Ax nearly absent from one bro

28 e mechanism by which nitric oxide attenuates DDR-dependent beta-cell apoptosis.

29 ospectively validate the association between DDR gene aberrations and response to olaparib in metasta

30 231 breast cancer cells were not affected by DDR kinase inhibition.

31 ociated with stimulation of tumour growth by DDRs and collagen I.

32 inases, leading to initiation of a canonical DDR (cDDR).

33 trated that they also activate non-canonical DDRs (ncDDRs) that regulate cell type-specific processes

34 ndings demonstrate that in G(1) phase cells, DDR signaling establishes a robust and extensive region

35 Instead of the classical ATM-Chk2 DDR, Mtb gains survival advantage through ATM-Akt signal

36 s mechanisms might be exploited by combining DDR inhibitors, ICIs and radiotherapy.

37 e (DDR) by phosphorylating 53BP1, a critical DDR mediator, to prevent its localization to damaged chr

38 ugh the initiation of a type I IFN-dependent DDR.

39 data provide novel insight in RNA-dependent DDR by coupling DSB-induced c-Abl activity on RNAPII to

40 inhibitors, each of them blocking different DDR pathway enzymes.

41 ts applicability in evaluating the different DDR outcomes utilized by human hematopoietic cell lines

42 1 (MRN) complex, at serine 649 (S649) during DDR.

43 DR and highlights the promise of engineering DDR factors to augment the efficiency of precision genom

44 2 signals and exposed to carcinogens escaped DDR-controlled apoptosis, contained more mutations and w

45 Unexpectedly, this slow-evolving DDR is not mediated by inhibitory Cdk1 phosphorylation b

46 to glycolytic ATP generation that allows for DDR signaling.

47 The elevated ATP levels resulting from DDR-stimulated respiration drove enlargement of dNTP poo

48 luated the prevalence and effect of germline DDR (gDDR) mutations on metastatic castration-resistance

49 161 patients had DDR gene aberrations, 98 of whom were randomly assigned

50 tivity in advanced prostate tumors harboring DDR gene alterations, particularly in tumors with BRCA1/

51 During the past 2 decades, understanding how DDR drives cancer development and contributes to the agi

52 Our findings identify DDR mutations, histone imbalances and aberrant subtelome

53 amage sites is a useful strategy to identify DDR proteins.

54 chromosome mis-segregation due to imperfect DDR signaling in response to dysfunctional telomeres cre

55 damage response (DDR), the role of TDP-43 in DDR has not been investigated.

56 However, the role of alterations in DDR genes beyond BRCA1/2 in mediating PARP inhibitor sen

57 Defects in DDR pathways lead to an accumulation of mutations that c

58 tion appears to be a key initiating event in DDR-dependent OCT4 locus reactivation although full reac

59 e are approximately 450 proteins involved in DDR, and a number of these other targets are being inves

60 greatly unknown how the IDPs are involved in DDR.

61 BM-specific mutations in DDR genes and elevated microsatellite instability (MSI)

62 ation of these factors causes a reduction in DDR foci both in vivo and in an in vitro system that rec

63 (DDRNAs), have been shown to play a role in DDR signalling and DNA repair.

64 f 53BP1 foci, which plays important roles in DDR.

65 binds SET, we investigated a role for SET in DDR inhibition by protein VII.

66 other, creating opportunities for therapy in DDR-proficient PC and after platinum therapy.

67 ically significant P/LP germline variants in DDR genes frequently are present in patients with advanc

68 bition assists E4orf4 in reducing Ad-induced DDR signaling and improves the efficiency of virus repli

69 NA breaks, is a hallmark of the HCMV-induced DDR.

70 An essential aspect of the MVM-induced DDR is establishment of a potent premitotic block.

71 epigenetic link among ATRX loss, RS-induced DDR initiation and telomere maintenance via homologous r

72 In contrast to BKPyV infection, DDR inhibition did not disrupt cell cycle control in uni

73 es in radiosensitization through influencing DDR and support the rationale of blocking TRIP12 to impr

74 e nitric oxide, mitochondrial toxins inhibit DDR signaling in beta cells by a mechanism that is assoc

75 the adenovirus (Ad) E4orf4 protein inhibits DDR signaling, but the mechanisms were not identified.

76 transcription of short units, including key DDR genes and multiple classes of non-coding RNAs.

77 sphorylates its downstream targets to launch DDR signaling.

78 tely to DNA damage, but instead mount a G2/M DDR that evolves slowly and involves a phosphorylation-i

79 tabolic flexibility is necessary to maintain DDR signaling under conditions in which mitochondrial ox

80 stem that rapidly quantifies the three major DDR pathways utilized at the individual DSB created by C

81 A significantly greater mean DDR% was found in the MF group than the placebo group at

82 ression requires the removal of ATR-mediated DDR signaling from autosomes.

83 istinct E3 ubiquitin ligase, ITCH, modulates DDR machinery in triple-negative breast cancer (TNBC).

84 ding and DNA sculpting functions in multiple DDR processes to maintain genome stability.

85 se phenotypes and for XPG's role in multiple DDRs, here we determined the crystal structure of human

86 AKT inhibition rescued the activity of NHEJ-DDR proteins in autophagy- and PTEN-deficient cells.

87 SP14 inhibition rescued the activity of NHEJ-DDR proteins in autophagy-deficient cells.

88 ppressorium repolarization involves a novel, DDR-independent S-phase checkpoint, triggered by appress

89 e observed with collagen I in the absence of DDR induction.

90 648 complements the current armamentarium of DDR-targeted agents and has potential in combination wit

91 Biomarkers of DDR deficiency, including a novel signature of homologou

92 w that dilncRNAs drive molecular crowding of DDR proteins, such as 53BP1, into foci that exhibit liqu

93 In H2ax-Y142A meiosis, the establishment of DDR signals on the chromosome-wide domain of the sex chr

94 po pathway core components, as a function of DDR and collagen expression, that were associated with s

95 ility (MSI) levels support the importance of DDR in the brain metastasis of CRC.

96 Inhibition of DDR restored satellite cell differentiation ability.

97 cells to nitric oxide-mediated inhibition of DDR signaling.

98 hemotherapy, consistent with a local loss of DDR, and identify a potential therapeutic strategy to ta

99 The presence of DDR germline variants could guide cancer screening for p

100 iched in later stages, but the prevalence of DDR defects in diagnostic samples is similar to mCRPC.

101 tes DART synthesis and delays recruitment of DDR factors and DSB signalling.

102 hus critical to understand the regulation of DDR in cells especially in the light of a strong linkage

103 overed an unexpected tumor-promoting role of DDR in cancer cell reprogramming, providing novel therap

104 thesis, which stimulates phase separation of DDR factors in the shape of foci.

105 s consistent with spatial re-distribution of DDRs in cells.

106 ese findings identified divergent effects of DDRs on primary tumour growth and experimental lung meta

107 diated transcriptional repression depends on DDR signaling but does not require the generation of ina

108 hology to impaired DSB repair and persistent DDR signaling in motor neuron disease, and suggest that

109 80 and promotes RAP80 recruitment and proper DDR.

110 The Discoidin Domain Receptors (DDRs) constitute a unique set of receptor tyrosine kinas

111 The role of Discoidin Domain Receptors (DDRs) is poorly understood in neurodegeneration.

112 and in an in vitro system that reconstitutes DDR events on nucleosomes.

113 r mean percentage of defect depth reduction (DDR) was found in the RSV group (30.80% +/- 8.35%, 41.86

114 ss this need with our Data-Driven Reference (DDR) approach, which employs stably expressed housekeepi

115 stly sensitized to inhibitors of the related DDR kinase ATR.

116 2 pathways are central in DNA damage repair (DDR) and their over-activation may confer aggressive mol

117 Germline mutations in DNA damage repair (DDR) genes are identified in a significant proportion of

118 germline P/LP variants in DNA-damage repair (DDR) genes, of which 28 (42%) had biallelic inactivation

119 DNA damage repair (DDR) inhibition and immune checkpoint blockade (ICB) hav

120 les that influence choice of DNA-DSB repair (DDR) pathways by HSPC is required for therapeutic levels

121 es that function in the DNA damage response (DDR) also improve phenotypes in Mecp2/Y mice.

122 other components of the DNA damage response (DDR) also result in Pol theta addiction.

123 romosome end (telomere) DNA damage response (DDR) and cellular apoptosis in a T-cell line (highly per

124 analyzing the telomeric DNA damage response (DDR) and cellular apoptosis in highly permissive SupT1 c

125 TOP2ccs, suppressed the DNA damage response (DDR) and completely protected cells from ETO-induced gen

126 frames involved in the DNA damage response (DDR) and determine their impact on CRISPR-mediated HDR.

127 we identified multiple DNA damage response (DDR) and DNA repair pathways that stimulate the dramatic

128 hrough execution of the DNA damage response (DDR) and DNA repair pathways, knowledge of the changes i

129 a critical role in the DNA damage response (DDR) and embryonic stem cell development.

130 H1 ability to block the DNA damage response (DDR) and ensuing growth arrest through suppression of AT

131 ides with activation of DNA damage response (DDR) and impaired ability to differentiate into myotubes

132 critical player in the DNA damage response (DDR) and instrumental in the non-homologous end-joining

133 vates the ATR-dependent DNA damage response (DDR) and is required for DSB repair by homologous recomb

134 f genes involved in the DNA damage response (DDR) and mRNA processing.

135 tically involved in the DNA damage response (DDR) and pinpointing their roles in tumor suppression.

136 owing to defects in the DNA damage response (DDR) and/or increased replication stress.

137 genes involving in the DNA-damage response (DDR) are often tumor prone owing to genome instability c

138 in system regulates the DNA damage response (DDR) by modifying histone H2A at Lys15 (H2AK15ub) and tr

139 tic cells attenuate the DNA damage response (DDR) by phosphorylating 53BP1, a critical DDR mediator,

140 duced inhibition of the DNA damage response (DDR) by reducing ATM and ATR signaling.

141 Plk1 contributes to the DNA damage response (DDR) by targeting multiple factors downstream of the cor

142 The DNA damage response (DDR) coordinates DNA metabolism with nuclear and non-nuc

143 e downregulation of the DNA damage response (DDR) enables aggressive tumors to achieve uncontrolled p

144 The DNA damage response (DDR) encompasses the cellular response to DNA double-str

145 duced activation of the DNA damage response (DDR) enhances viral titers and prevents host DNA damage.

146 cer drugs targeting the DNA damage response (DDR) exploit genetic or functional defects in this pathw

147 1 assembles a cohort of DNA damage response (DDR) factors to distinctly execute its repertoire of DSB

148 e cancer is enriched in DNA damage response (DDR) gene aberrations.

149 Alterations in DNA damage response (DDR) genes are common in advanced prostate tumors and ar

150 sion of BRCA1 and other DNA damage response (DDR) genes.

151 upports the role of the DNA damage response (DDR) in the negative regulation of tumorigenesis.

152 o better understand the DNA damage response (DDR) in these cells, we exposed pregnant mice to ionizin

153 y linked Gene 33 to the DNA damage response (DDR) induced by hexavalent chromium (Cr(VI)), but the mo

154 how recent research on DNA damage response (DDR) inhibitors in combination with radiotherapy may be

155 DNA damage response (DDR) involves dramatic transcriptional alterations, the

156 The DNA damage response (DDR) is a DNA damage surveillance and repair mechanism t

157 The DNA damage response (DDR) is an evolutionarily conserved process essential fo

158 us genome, the cellular DNA damage response (DDR) is considered a barrier to successful infection.

159 IFICANCE STATEMENT: The DNA damage response (DDR) is essential for prevention of a broad spectrum of

160 A proper DNA damage response (DDR) is essential to maintain genome integrity and preve

161 s lesions that activate DNA damage response (DDR) kinases, leading to initiation of a canonical DDR (

162 s due to a p53-mediated DNA damage response (DDR) limiting the efficiency of generating viable edited

163 telomeres may activate DNA damage response (DDR) machinery resulting in telomere attrition.

164 immediate-response G2/M DNA damage response (DDR) may be deficient.

165 ognized by the cellular DNA damage response (DDR) network as DNA damage whose repair may lead to inhi

166 oint kinase 2 (CHK2), a DNA damage response (DDR) pathway activated during metabolic and hypoxic stre

167 MSCI is directed by a DNA damage response (DDR) pathway centered on the phosphorylation of histone

168 The DNA damage response (DDR) pathway coordinates the identification, signaling,

169 sized that blocking the DNA damage response (DDR) pathway should further sensitize cancer cells by in

170 n important role in the DNA damage response (DDR) pathway.

171 nhibited the endogenous DNA damage response (DDR) pathways by combinations of activating TopBP1 prote

172 ion repair and ATR-Chk1 DNA damage response (DDR) pathways, it remains unknown how the APE2 gene is a

173 /ZNF280C as a potential DNA damage response (DDR) protein.

174 r inclusions containing DNA damage response (DDR) proteins are causally linked to abnormal synaptic f

175 al function through the DNA damage response (DDR) remains poorly understood.

176 nitric oxide suppresses DNA damage response (DDR) signaling in the pancreatic beta-cell line INS 832/

177 Defective DNA damage response (DDR) signaling is a common mechanism that initiates and

178 lso has a major role in DNA damage response (DDR) signaling, and our results show that macroH2A1 alte

179 tes ATM-Chk2 pathway of DNA damage response (DDR) signaling, resulting in altered cell cycle.

180 regulator of IR-induced DNA damage response (DDR) signaling.

181 er analysis reveals two DNA damage response (DDR) signatures could emerge early and are enhanced in B

182 aling is crucial in the DNA damage response (DDR) to mediate the repair of damaged DNA.

183 on is activation of the DNA damage response (DDR) to prevent severe host and viral DNA damage that im

184 chief mobilizer of the DNA damage response (DDR) upon DNA double-strand breaks.

185 suggest that the human DNA damage response (DDR) utilizes small RNA species, which are produced as l

186 es a sustained cellular DNA damage response (DDR) which the virus exploits to prepare the nuclear env

187 1 infection initiates a DNA damage response (DDR), activating all three phosphatidylinositol 3-kinase

188 the interplay among the DNA damage response (DDR), cyclic GMP-AMP synthase-stimulator of interferon g

189 own for its role in the DNA damage response (DDR), especially after double-strand breaks.

190 upstream kinase of the DNA damage response (DDR), is rapidly activated following DNA damage, and pho

191 the association between DNA damage response (DDR), replication stress, and novel therapeutic response

192 g proteins, like FUS in DNA damage response (DDR), the role of TDP-43 in DDR has not been investigate

193 to inhibit the cellular DNA damage response (DDR), which acts as an antiviral defense system.

194 requires a coordinated DNA Damage Response (DDR), which includes phosphorylation of histone H2Ax, fo

195 .2 is re-deposited in a DNA damage response (DDR)-dependent manner to promote homologous recombinatio

196 repair pathway and the DNA damage response (DDR).

197 esection as part of the DNA damage response (DDR).

198 r response pathway, the DNA damage response (DDR).

199 tability and activate a DNA damage response (DDR).

200 , which coordinates the DNA damage response (DDR).

201 n shown to regulate the DNA damage response (DDR).

202 eosome level during the DNA damage response (DDR).

203 a key component of the DNA damage response (DDR).

204 actor in initiating the DNA damage response (DDR).

205 ence as outcomes of the DNA damage response (DDR).

206 braxas) and facilitates DNA damage response (DDR).

207 esion that triggers the DNA damage response (DDR).

208 d domains (IDPs) in the DNA damage response (DDR).

209 response (UPR) and the DNA damage response (DDR).

210 se II are necessary for DNA-damage-response (DDR) focus formation.

211 al partner in multiple DNA damage responses (DDR) and a pathway coordinator and structure-specific en

212 DNA damage responses (DDR) to double-strand breaks (DSBs) alter cellular trans

213 ely dephosphorylate 53BP1, thereby restoring DDR, is unclear.

214 Y nuclear compartment-the XY body-sequesters DDR factors to permit meiotic progression from the mid-p

215 for MSCI: the initiation of MSCI sequesters DDR factors from autosomes to the sex chromosomes at the

216 te (BAY 2287411) in combination with several DDR inhibitors, each of them blocking different DDR path

217 ted to augment DICER activity, show stronger DDR signalling and faster DNA repair upon exposure to io

218 t intracellular signaling of the B. subtilis DDR is achieved via production of L-malic acid, which af

219 efine novel therapeutic strategies targeting DDR and replication stress.

220 marker-driven therapeutic strategy targeting DDR and replication stress in PC.

221 e the therapeutic opportunity that targeting DDR provides.

222 We demonstrated that HIV-induced telomeric DDR plays a critical role in inducing telomere loss, pre

223 We demonstrated that HIV-induced, telomeric DDR plays a pivotal role in triggering telomere erosion,

224 ght on the molecular mechanisms of telomeric DDR and CD4 T-cell homeostasis during HIV infection.IMPO

225 ght on the molecular mechanisms of telomeric DDR and its role in CD4 T-cell homeostasis during HIV in

226 Here, we found that DDR signaling poises a series of epigenetic events, resu

227 causes of glucose dependence, implying that DDR kinases coordinate metabolism and epigenetic changes

228 Here, we show that DDR activation and DNA repair can be pharmacologically b

229 PCR methods, and dNTP analyses, we show that DDR activation in the budding yeast Saccharomyces cerevi

230 d an in situ labeling approach, we show that DDR-induced epigenetic reactivation of OCT4 regulates th

231 h RNA-seq data of blood platelets shows that DDR achieves the superior performance in classification

232 This suggests that DDR inhibitors may be used to specifically target BKPyV-

233 The DDR culminates in either transient cell-cycle arrest and

234 The DDR kinase Rad53(CHK1/CHK2) controls histone degradation

235 The DDR limits keratinocyte multiplication upon hyperprolife

236 SIRT6 activates the DDR before the repair pathway is chosen, and prevents ge

237 to better understand why BKPyV activates the DDR through the ATR and ATM pathways and how this preven

238 y demonstrating that the virus activates the DDR to maintain the cells in S phase in order to promote

239 ts suggest a role for MDC1 in activating the DDR in areas of the genome lacking or depleted of H2AX.

240 ected connection between respiration and the DDR and indicate that the benefit of increased dNTP synt

241 crosstalk between UPR stress sensors and the DDR, as well as their involvement in cancer biology.

242 feedback loop between DNA resection and the DDR.

243 fic gestational time points and assessed the DDR in PGCs.

244 in the light of a strong linkage between the DDR impairment and the occurrence of common human diseas

245 osis and cell proliferation triggered by the DDR.

246 y low levels of IL-22 and, consequently, the DDR in epithelial cells of mice on a glucosinolate-free

247 of ubiquitin at Thr12 (pUbT12) controls the DDR by inhibiting the function of 53BP1, a key factor fo

248 R have unique and essential roles during the DDR, collectively ensuring comprehensive genome maintena

249 s implicate BRAF and IKKalpha kinases in the DDR and reveal a combination strategy for cancer treatme

250 fier 1 and the function of UFMylation in the DDR is largely unknown.

251 helix, which plays an important role in the DDR pathway.

252 TR), work together as apical proteins in the DDR to maintain genome stability and cell survival in th

253 her H2AX amino acid residue important in the DDR, tyrosine 142 (Y142), is converted to alanine (H2ax-

254 ntial proportion of which participate in the DDR.

255 unteracting BRCA1-dependent functions in the DDR.

256 (NEK) family (NEK1, NEK10, and NEK11) in the DDR.

257 t overcome cellular responses, including the DDR.

258 ny viruses evolved mechanisms to inhibit the DDR network.

259 at the damage sites and from inhibiting the DDR.

260 adenovirus (Ad) E4orf4 protein inhibits the DDR.

261 laces greater reliance on ATR to mediate the DDR.

262 Key drivers of the DDR are multiple members of the phosphatidylinositol 3-k

263 However, a detailed understanding of the DDR at a physiological level is lacking.

264 ociation of Pol V requires components of the DDR complex DRD1, DMS3 and RDM1, but the assembly proces

265 arifies the previously enigmatic role of the DDR during BKPyV infection by demonstrating that the vir

266 is required for effective initiation of the DDR following DNA damage.

267 ocytes directly regulating components of the DDR in epithelial stem cells.

268 ta T cells, is an important regulator of the DDR machinery in intestinal epithelial stem cells.

269 n the recruitment of numerous members of the DDR machinery to DSBs.

270 rationale for targeting other members of the DDR pathway and the associated tumor cell genetics that

271 , knocking down H2AX, a common target of the DDR pathways, inhibits the epidermoid phenotype.

272 rase (PARP) is the best-known element of the DDR, and several PARP inhibitors have been licensed.

273 TM and ATR modulate multiple portions of the DDR, but DNA-PKcs is believed to primarily function in t

274 activity to inhibit various branches of the DDR, whereas it later inhibits DNA-PK itself.

275 ctivity is pivotal for the initiation of the DDR.

276 ATM orchestrates the DDR by modulating the expression of various miRNAs throu

277 stone mark, H2AK15pUbT12, that regulates the DDR by hampering the activity of 53BP1 at damaged chromo

278 repaired may trigger apoptosis; as such, the DDR pathway is of crucial importance as a cancer target.

279 landscape of antitumour agents targeting the DDR has rapidly expanded to include inhibitors of other

280 status of anticancer therapies targeting the DDR.

281 The results altogether show that the DDR is required to maintain the balance proliferation di

282 etween compact chromatin foci throughout the DDR.

283 omes entering directly into mitosis when the DDR was inhibited in BKPyV-infected cells.

284 espiration, raising the question whether the DDR also stimulates respiration.

285 ) are known to interact extensively with the DDR during the course of their replicative cycles.

286 gate a direct interaction of E4orf4 with the DDR.

287 tors upstream of ATM/ATR and regulates their DDR-related functions.

288 The synergistic activation of these DDR kinases promoted and maintained BKPyV-mediated S pha

289 ostate tumor DDR function and sensitivity to DDR-directed agents, we created a series of ATM-deficien

290 efine the role of ATM loss in prostate tumor DDR function and sensitivity to DDR-directed agents, we

291 These results support a model in which DDR genes are uniquely susceptible to CDK12 inhibition p

292 of PC (P < .001) but was not associated with DDR deficiency.

293 ic castration-resistant prostate cancer with DDR gene aberrations, supporting the implementation of g

294 efficacy of the MSLN-TTC in combination with DDR inhibitors in human ovarian cancer xenograft models.

295 e/adaptive immunity and its combination with DDR inhibitors, ionizing radiation (IR), and chemotherap

296 domain, a region sharing high homology with DDR proteins Topoisomerase 3alpha (TOP3alpha) and NEIL3

297 cruited at DSB sites to stably interact with DDR and NHEJ factors, specifically acting as a scaffold

298 treatment of hematological malignancies with DDR defects, where ATM/p53-dependent apoptosis is compro

299 Patients with DDR gene aberrations were randomly assigned (1:1) by a c

300 ed rationale for combining the MSLN-TTC with DDR inhibitors as new treatment strategies in MSLN-posit