ライフサイエンスコーパス: repair pathway

1 ts integrate ASCC3/AlkBH3 into a complex DNA repair pathway.

2 key proteins in the single-strand DNA break repair pathway.

3 ithout a functional homologous recombination repair pathway.

4 netic mutation harness the homology-directed repair pathway.

5 volved in a common interstrand DNA crosslink-repair pathway.

6 rror-free manner by the uracil base excision repair pathway.

7 de excision repair, forming a novel excision repair pathway.

8 over multiple steps of the DNA base excision repair pathway.

9 ), a universal DNA double strand break (DSB) repair pathway.

10 angements by suppressing the insertional DNA repair pathway.

11 ncy in the homologous recombination (HR) DNA repair pathway.

12 on-catalyzed oxidation and the base excision repair pathway.

13 is a potential therapeutic target in the DNA repair pathway.

14 machinery and the mitoNEET cluster transfer repair pathway.

15 as EHMT1) are critical components of the DNA repair pathway.

16 ral oncogenes were shown to disrupt this DSB repair pathway.

17 the error-free homologous recombination (HR) repair pathway.

18 coli lines, each deficient in a distinct DNA repair pathway.

19 nction upstream of BRCA2 in the stalled fork repair pathway.

20 hways, including E2Fs, Wnt, Myc, and the DNA repair pathway.

21 the canonical non-homologous end joining DNA repair pathway.

22 stabilization by the Fanconi anemia (FA) DNA repair pathway.

23 of the non-homologous end-joining (NHEJ) DSB repair pathway.

24 NHEJ)-mediated DNA double-strand break (DSB) repair pathway.

25 -prone non-homologous end-joining (NHEJ) DNA repair pathway.

26 r new insights into this deceptively complex repair pathway.

27 an genes for coevolution with 6 distinct DNA repair pathways.

28 utilizes endogenous DNA double strand break repair pathways.

29 s, damaged DNA is sensed and targeted by DNA repair pathways.

30 minase are processed by multiple error-prone repair pathways.

31 eaks and responsible for multiple DNA damage repair pathways.

32 es, and the host may respond with DNA damage repair pathways.

33 omotes cancer cell growth independent of DNA repair pathways.

34 ells exhibiting deficiencies in parallel DNA repair pathways.

35 proteins in immune signaling and DNA damage-repair pathways.

36 ss requiring the coordination of several DNA repair pathways.

37 of chemotherapeutic drugs by modulating DNA repair pathways.

38 epistatic, suggesting they involve different repair pathways.

39 1 in the regulation of genes involved in DNA repair pathways.

40 e cancers, and their positions in DNA damage repair pathways.

41 unctional mismatch and transcription-coupled repair pathways.

42 nterstrand crosslinks initiates two distinct repair pathways.

43 tative candidate genes involved in UV damage repair pathways.

44 were evaluated in 127 genes from 6 major DNA repair pathways.

45 ologous end joining or the homology directed repair pathways.

46 talling and checkpoint signaling to activate repair pathways.

47 ni anemia (FA), and homologous recombination repair pathways.

48 DNA replication, rather than by various DNA repair pathways.

49 s and form protein complexes that act in DNA repair pathways.

50 ficantly altered immune reactivation and DNA repair pathways.

51 ted genes are enriched in cell cycle and DNA repair pathways.

52 y and cisplatin by regulating DNA damage and repair pathways.

53 changes to DNA by activation of various DNA repair pathways.

54 lucidating the balance between competing DSB repair pathways.

55 of how PARP-2 is specialized toward specific repair pathways.

56 in size, but their extent is similar in both repair pathways.

57 nomic instability and promote defects in DNA repair pathways.

58 ir pathway choice between NHEJ and other DSB repair pathways.

59 vulnerability to drugs targeting DNA-damage repair pathways.

60 etions differ in their dependencies on these repair pathways.

61 by the same genotoxin are mended by separate repair pathways.

62 tus that maintains genomic integrity through repair pathways.

63 a key intermediate during the base excision repair pathway, abasic sites are frequent DNA lesions th

64 ition (EMT) but increased MYC target and DNA-repair pathway activities.

65 s homologous recombination (HR)-mediated DNA repair pathway activity of samples.

66 red DSB-clusters, compromises first-line DSB-repair pathways, allowing alt-EJ to function as rescuing

67 ter understanding on the role of various DNA repair pathway alterations, especially the evidence supp

68 of ZNF281 impairs the efficiency of the NHEJ repair pathway and decreases cell viability upon DNA dam

69 ent of the non-homologous end joining (NHEJ) repair pathway and DNA damage in alveolar type II (ATII)

70 tes the activation of the Fanconi anemia DNA repair pathway and facilitates replication traverse of D

71 x affects the non-homologous end joining DNA repair pathway and hypersensitises human cancer cells to

72 ion repair (BER) pathway is an important DNA repair pathway and is essential for immune responses.

73 conjugating enzyme of the Fanconi anemia DNA repair pathway and it is overexpressed in several cancer

74 e strand breaks repair via homology-directed repair pathway and prostate tumorigenesis.

75 ts identify a novel player in the DNA damage repair pathway and provides a link in ductal carcinoma i

76 ein required for the nucleotide excision DNA repair pathway and represents a therapeutic target in on

77 ole in the non-homologous end joining (NHEJ) repair pathway and the DNA damage response (DDR).

78 atch affects the substrate channeling of the repair pathway and the mechanism underlying the coordina

79 REV1 is known to be a key player in DNA repair pathway and to interact with HSP90.

80 To study DSB repair pathways and associated factors, inducible site-s

81 alignancies must simultaneously activate DNA repair pathways and avoid the cell cycle arrest that nor

82 ition of G9a catalytic activity disrupts DNA repair pathways and increases sensitivity to ionizing ra

83 amage and apoptosis, induction of DNA damage repair pathways and ROS detoxification systems, cellular

84 association between DNA damage-response and repair pathways and the age at onset of disease.

85 In some cases, DNA repair pathways and the N(6)-methyladenine DNA modificat

86 We also noted involvement of distinct DNA repair pathways and translesion synthesis polymerases (P

87 1 (MAG1), which is part of the base-excision repair pathway, and the DNA photolyase gene PHotoreactiv

88 een age at onset and genetic variants in DNA repair pathways, and we therefore tested whether the mod

89 site will utilize the microhomology-mediated repair pathway; and (iii) MENTHU, a tool for identifying

90 Two major players during this repair pathway are Rad51 and Rad54.

91 DNA repair pathways are aberrant in cancer, enabling tumor c

92 lowing radiation induced DNA damage, several repair pathways are activated to help preserve genome in

93 Efficient DNA repair pathways are crucial in these organelles to fix d

94 nes encoding direct repair and base-excision repair pathways are required by B. abortus to face this

95 We show that PARP-mediated repair pathways are upregulated in prostate cancer follo

96 Although many DNA repair pathways are well understood, new pathways contin

97 ing pathways and reveals the DNA replication/repair pathway as central in promoting these effects.

98 wide association studies have identified DNA repair pathways as modifiers of somatic instability and

99 portant both for the basic study of cellular repair pathways as well as for potential new translation

100 Using an in vivo DSB repair pathway assay, we find that Ino80 is selectively

101 run" activation of PARP-1 initiates the DNA repair pathway at a specific point.

102 enome and detected signatures of error-prone repair pathways at the breakpoints.

103 on (HR) and nonhomologous end-joining (NHEJ) repair pathways but exclusively for heterochromatic DSBs

104 It typically does not compete with canonical repair pathways but, in NHEJ-deficient cells, is engaged

105 (MRN) and Ku70-Ku80 (Ku) direct distinct DSB repair pathways, but the interplay between these complex

106 Vpr also interferes with the base-excision repair pathway by antagonizing the uracil DNA glycosylas

107 ercept the more error-prone alternative NHEJ repair pathway by recruiting Ku and associated NHEJ fact

108 Mag1 initiates the base excision repair pathway by removing alkylated bases from DNA, and

109 eregulation of the cell cycle and DNA damage repair pathways by modulating transcription factors p53

110 gements (LST), and the status of several DNA repair pathways by transcriptome and genome analysis.

111 s illustrate that specific rereplication DSB repair pathways can have major effects on cellular physi

112 protein of nonhomologous end-joining (NHEJ) repair pathway, can directly interact with DNA polymeras

113 e mediated by either of two end-joining (EJ) repair pathways [canonical nonhomologous end joining (C-

114 BRCA-deficient cells utilize error-prone DNA-repair pathways, causing increased genomic instability,

115 action of RNF8 from chromatin to balance DNA repair pathway choice and promote cell survival after io

116 P53-binding protein 1 (53BP1) mediates DNA repair pathway choice and promotes checkpoint activation

117 l4 ligase activity, and has implications for repair pathway choice and resection regulation upon DSB

118 In this Review, we first discuss repair pathway choice between NHEJ and other DSB repair

119 vealing a mechanism of compartmentalized DSB repair pathway choice by sequestration of a fatty acylat

120 hylated at lysine 20 (H4K20me0), linking DSB repair pathway choice directly to sister chromatid avail

121 Kcs T2609 phosphorylation in promoting cNHEJ repair pathway choice during CSR.

122 on timing, and DNA double-strand break (DSB) repair pathway choice from yeast to human.

123 rolysis primes the MR function and regulates repair pathway choice in cells.

124 53BP1 is a key regulator of DSB repair pathway choice in eukaryotic cells and functions

125 in S phase and providing a mechanism of DSB repair pathway choice in mammalian cells.

126 This detailed characterization of repair pathway choice in response to CRISPR-Cas9 enables

127 DSB repair pathway choice is largely dictated at the step of

128 hosphorylation status of NBS1 determines the repair pathway choice of dysfunctional telomeres.

129 horylation status of the NBS1(S432) dictates repair pathway choice of dysfunctional telomeres.

130 MT5-mediated arginine methylation during DSB repair pathway choice through its ability to regulate ac

131 that, rather than being deterministic in DSB repair pathway choice, 53BP1 functions as a DSB escort t

132 udy uncovers a critical role for Ape1 in DNA repair pathway choice, and provides a mechanistic unders

133 P13 emerges as an important regulator of DNA repair pathway choice-promoting HDR, while suppressing N

134 activities are crucial for proper DNA damage repair pathway choice.

135 modelling during resection is underlying DSB repair pathway choice.

136 suggesting that Wwox contributes to DNA DSB repair pathway choice.

137 ory mechanism for ATM that also controls DNA repair pathway choice.

138 t a ubiquitylation cascade that controls DNA repair pathway choice.

139 critical determinant of double-strand break repair pathway choice.

140 by ACLY participates in the mechanism of DNA repair pathway choice.

141 nt with p97-driven Ku release also affecting repair pathway choice.

142 tablishes CEP-1 as a critical determinant of repair pathway choice.

143 aster regulator of double-strand break (DSB) repair pathway choice.

144 rge-scale genome organization influences DNA repair pathway choice.

145 gesting that genomic location influences DNA repair pathway choice.

146 RIF1 and MAD2L2/Shieldin, to coordinate DNA repair pathway choices.

147 efficiency of this process is limited by DSB repair pathways competing with HDR, such as non-homologo

148 ssing cells with defects in other DNA damage repair pathway components may also exhibit "BRCAness," w

149 scripts of Hspa1a and other genes in the DNA repair pathway containing consensus m6A motifs required

150 Surprisingly, both DNA repair pathways contributed substantially to break forma

151 hogenesis, we have identified that the wound repair pathway, controlled by the epidermal growth facto

152 General DNA repair pathways convert these lesions to double-stranded

153 genetic diversity profoundly alters meiotic repair pathway decisions via at least two distinct mecha

154 These findings provide evidence that DNA repair pathway defects and immunomodulatory genes togeth

155 Therapeutic strategies targeting DNA repair pathway defects have been widely explored, but of

156 single nucleotide variants [SNVs]), the DNA repair pathway (deletion 17p, TP53, and ATM SNVs), and M

157 quitin ligase with a key role in several DNA repair pathways, directly affects L1 retrotransposition

158 efficiency and fidelity of the base excision repair pathway during the repair of opposing base damage

159 remodelling enzymes facilitate different DNA repair pathways, during different stages of the cell cyc

160 nding of the nature of these lesions and the repair pathways engaged is critical to realizing the ful

161 ing from each Cas9 variant and the resulting repair pathway engagement.

162 vide a broad overview of replication-coupled repair pathways, explaining how they fix polymerase mist

163 Targeting the PARP DNA repair pathway extensively sensitized IDH1-mutated gliom

164 leotide excision repair (NER) is a major DNA repair pathway for a variety of DNA lesions.

165 define the specificity of the base excision repair pathway for discreet, detrimental modifications,

166 us end-joining (NHEJ) pathway is the primary repair pathway for DNA double strand breaks (DSBs) in hu

167 on-homologous end joining (NHEJ) is the main repair pathway for DNA double-strand breaks (DSBs) in ce

168 g non-homologous end joining (NHEJ), a major repair pathway for DNA double-strand breaks (DSBs).

169 ous recombination, which is an essential DNA repair pathway for fixing damaged chromosomes.

170 pair processes, the requirement of known DNA repair pathways for integration is controversial.

171 giectasia- and Rad3-related (ATR) DNA damage repair pathways for viral genome amplification.

172 excision repair (BER) is one of several DNA repair pathways found in all three domains of life.

173 at least one mutation in nucleotide excision repair pathway genes in African Americans, whereas >40%

174 40% of tumors had mutations in base excision repair pathway genes in Caucasians.

175 ermline loss-of-function mutations in FA DNA repair pathway genes.

176 erations of genes involved in the DNA damage repair pathway have been associated with sarcoma risk an

177 alk between glutamine metabolism and the DNA repair pathway identified in this study highlights a pot

178 rials: Pathway inhibition, alteration of DNA Repair pathways, Immunotherapy, cancer Metabolism and ta

179 Here, we report an antibiotic specific DNA repair pathway in Bacillus subtilis that is composed of

180 stablishes base excision as an alternate ICL repair pathway in bacteria.

181 , which was mediated by impairing DNA damage repair pathway in CC.

182 a rationale for targeting the Plasmodium DSB repair pathway in combination with ART.

183 ing (the predominant DNA double-strand break repair pathway in higher eukaryotes) and is stimulated b

184 ) pathway is a major DNA double-strand break repair pathway in mammalian cells and is required for ly

185 most prominent DNA double strand break (DSB) repair pathway in mammalian cells.

186 hat elicits an immune system-mediated tissue repair pathway in tendons and ligaments.

187 ous end joining (NHEJ) is the most used DSBs repair pathway in the cells, how NHEJ factors are sequen

188 oring the importance of MMEJ as a collateral repair pathway in the context of homologous recombinatio

189 nteraction supports NHEJ as the dominant DSB repair pathway in Wwox-sufficient cells.

190 derstanding of the roles of the affected DNA repair pathways in development.

191 induces senescence and downregulation of DNA repair pathways in glioma cells.

192 de that an in-depth understanding of DNA DSB repair pathways in human cells will lead to novel therap

193 will highlight DNA double-strand break (DSB) repair pathways in human cells, how DNA repair failures

194 comprehensively profile double-strand break repair pathways in isogenic paired cell lines, we demons

195 er (BLRR) for non-invasive monitoring of DSB repair pathways in living cells and animals.

196 which plays an essential role in several DNA repair pathways in mammalian cells.

197 Targeting these repair pathways in P. falciparum may be used to block ad

198 (Cdh1) plays a critical role in choosing the repair pathways in S/G2 cells.

199 tigations about the involvement of other DNA repair pathways in the removal of these lesions and for

200 d convergence between Wnt signalling and DNA repair pathways in tumorigenesis and tissue regeneration

201 d roles in maintaining genome stability, DNA repair pathways including base excision repair (BER) are

202 PF-ERCC1 participates in multiple DNA damage repair pathways including nucleotide excision repair (NE

203 glycosylase NEIL3 has been implicated in DNA repair pathways including the base excision repair and t

204 associated with metabolic, apoptotic or DNA repair pathways (including APBA3, PARP1 and RAB11).

205 MRE11/RAD50/NBS1 (MRN) complex mediates DNA repair pathways, including double-strand breaks induced

206 Deficiencies in DNA repair pathways, including mismatch repair (MMR), have b

207 etition from other double-strand break (DSB) repair pathways, including non-homologous end-joining (N

208 ly, both lineages lost genes involved in DNA repair pathways, including the DNA glycosylase gene 3-Me

209 This repair pathway involves eight factors, including XRCC4-l

210 Other DNA repair pathways involving ATM and DNA-PKcs are unaffecte

211 tion of the overactivated Ku80-dependent DNA repair pathway is a promising therapeutic approach in C9

212 SIRT6 activates the DDR before the repair pathway is chosen, and prevents genomic instabili

213 in vivo and a robust ribonucleotide excision repair pathway is critical to keeping incorporation leve

214 y, either a DPC tolerance mechanism or a DPC repair pathway is essential for C. albicans to maintain

215 Two-way crosstalk between BER and c-NHEJ repair pathway is mediated by Pol-beta and Ku70.

216 glycosylase-1 (OGG1)-initiated base excision repair pathway is primarily responsible for 7, 8-dihydro

217 pace and time to differentially regulate DNA repair pathways is insufficiently understood.

218 otential crosstalk between metabolic and DNA repair pathways is poorly understood.

219 gh PARP1 and XRCC1 are implicated in the SSB repair pathway, it remains unclear how SSB repair and SS

220 ion of the DNA damage response (DDR) and DNA repair pathways, knowledge of the changes in DNA repair

221 th a backup, error-prone double-strand break repair pathway known as microhomology-mediated end-joini

222 Errors in this DNA repair pathway lead to genomic instability and cancer pr

223 inappropriate activity of these alternative repair pathways, leading to chromosome mis-segregation.

224 Multiple DNA repair pathways maintain genome stability and ensure tha

225 Together, we demonstrate that a critical DNA repair pathway maintains the structure and function of h

226 particularly cancers in which defects in DNA repair pathways make tumour cells highly sensitive to th

227 Multiple DNA repair pathways may be involved in the removal of the sa

228 ated) nonhomologous end-joining, whereas DNA repair pathways mediated by poly(ADP)ribose polymerase 1

229 response network and two Fanconi anaemia DNA repair pathway members showed elevated expression in the

230 tion does not require other post-replication repair pathway members, or the PCNA modification sites i

231 Despite the major importance of this repair pathway, MutS-MutL are absent in almost all Actin

232 is believed to primarily function in the DSB repair pathway, non-homologous end joining.

233 Thomson Syndrome, promotes the two major DSB repair pathways, non-homologous end joining (NHEJ) and h

234 These results define the repair pathways of DNA interstrand crosslinks caused by

235 genetic interaction of Ubp7 with DNA damage repair pathways of homologous recombination and nucleoti

236 ciated with the homologous recombination DNA repair pathway or PARP inhibitor sensitivity, first in a

237 ations arise either from inactivation of DNA repair pathways or in a repair-competent background due

238 es associate with recombination-mediated DNA repair pathways, particularly the RecFOR pathway.

239 des presynaptic stimulation of the bacterial repair pathway perhaps by contributing to the RecA homol

240 We demonstrate that cell membrane repair pathways play the main role in this stimulated ne

241 ated, error-prone, double strand break (DSB) repair pathway, referred to as Theta Mediated End Joinin

242 ion factors at DSBs, providing insights into repair pathway regulation.

243 The major DNA repair pathway removing DNA lesions caused by exposure t

244 these cells require replication-coupled DNA-repair pathways, replication-stress signaling and replic

245 ation of the FRC population, and blocked the repair pathways required for its regeneration.

246 the base excision repair (BER) and mismatch repair pathways, respectively, in CSR.

247 to elucidate how loss of the 53BP1-dependent repair pathway results in PARPi resistance in BRCA1 pati

248 complex is directly involved in an excision repair pathway(s) that repairs DNA damage with ribonucle

249 that ruxolitinib-induced deficiencies in DSB repair pathways sensitized MPN cells to synthetic lethal

250 reatments that target RNA processing and DNA repair pathways simultaneously as effective cancer thera

251 While these cells employ ubiquitous repair pathways, specialized mechanisms that ensure high

252 We propose that errors in DNA repair pathways, such as non-homologous end joining and

253 ates are channeled into cardioprotective and repair pathways, such as the pentose-phosphate pathway a

254 ng therapeutic agents via utilization of DNA repair pathways, suggesting that DNA repair capacity (DR

255 identified mutations that disrupt DNA damage repair pathways, suggesting that Rhizobium may cause DNA

256 ion factor (HLTF) DNA helicase and other DNA repair pathway targets, and by another mutation that pre

257 d replication (BIR) is a double strand break repair pathway that can promote genetic instabilities si

258 bination (HR) is a universally conserved DNA repair pathway that can result in the exchange of geneti

259 plication (BIR) is a DNA double-strand break repair pathway that leads to genomic instabilities simil

260 ta underscore a unique replication-dependent repair pathway that leads to the mitochondrial common de

261 gous recombination (HR) is a template-driven repair pathway that mends DNA double-stranded breaks (DS

262 tion (HR) is a DNA double-strand break (DSB) repair pathway that protects the genome from chromosomal

263 ision repair (BER) is the major cellular DNA repair pathway that recognises and excises damaged DNA b

264 ed downregulation of genes within DNA damage repair pathways that are controlled by MOF, as correlate

265 defects in DNA repair, although the specific repair pathways that are disrupted have not been elucida

266 ous end joining (NHEJ) are the two major DSB repair pathways that are highly conserved from yeast to

267 All organisms possess DNA repair pathways that are used to maintain the integrity

268 l to efficiently enhance recombinational DNA repair pathways that depend on long-range resection for

269 clei and LST and specific alterations in DNA repair pathways that essentially monitor DSB repair defe

270 n-coupled DNA repair (TCR) are among the DNA repair pathways that evolved to maintain genome integrit

271 Given the broad range of homeostatic and repair pathways that HS regulates, these changes in prot

272 Suppression of host DNA-repair pathways that remove TOP2betacc trigger HSV-1 rea

273 d multiple DNA damage response (DDR) and DNA repair pathways that stimulate the dramatic increase of

274 Here we discuss the DNA repair pathways that underlie genome editing and strateg

275 Specifically, we show that the base excision repair pathway, the main pathway utilized for the repair

276 ase involved in initiating the base excision repair pathway, the major cellular mechanism for repairi

277 s an adverse effect on the DNA base excision repair pathway, the major DNA repair system that deals w

278 is the predominant double-strand break (DSB) repair pathway throughout the cell cycle and accounts fo

279 SBs), which are highly toxic, have specified repair pathways to address them.

280 or doxorubicin, acting upstream of different repair pathways to block histone polyADP-ribosylation (P

281 Cells possess an armamentarium of DNA repair pathways to counter DNA damage and prevent mutati

282 -mediated hDNA2 ubiquitination activates DNA repair pathways to maintain nuclear genome integrity.

283 lls inactivate DNA double-strand break (DSB) repair pathways to preserve genome stability.

284 Cells employ a variety of DNA repair pathways to protect themselves from these pro-mut

285 Eukaryotic cells deploy overlapping repair pathways to resolve DNA damage.

286 The main repair pathways used to resolve DSBs are Non-Homologous

287 of new series of compounds that modulate DNA repair pathways via a unique mechanism of action.

288 cision repair and the interstrand cross-link repair pathways via its DNA glycosylase and/or AP lyase

289 enic drivers and the DNA damage response and repair pathway warrant further prospective evaluation.

290 The PARP1-associated DNA repair pathway was extensively compromised in mutant cel

291 n of USP22, enrichment of cell-cycle and DNA repair pathways was observed in the USP22-sensitive tran

292 relationships between genes in the major DNA repair pathways, we uncovered functional relationships b

293 that both cAMP and Fanconi anemia DNA damage repair pathways were affected by SCNAs in growth hormone

294 The six major mammalian DNA repair pathways were discovered as independent processes

295 many cancers exhibit an impairment of a DNA repair pathway, which can lead to dependence on specific

296 s a component of the Fanconi anemia (FA) DNA repair pathway, which is frequently found defective in h

297 has been excised by the nucleotide excision repair pathway, while others participate in trans-lesion

298 injury), biological processes include tissue repair pathways with upregulated genes related to neurit

299 on (HR) and nonhomologous end-joining (NHEJ) repair pathways, with defective localization of Brca1 an

300 utilizing genes from the nucleotide excision repair pathway without provoking PAEC apoptosis.