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1  expression of genes related to skin barrier repair.
2 of postmitotic cell growth in gut epithelial repair.
3 vanced Glycation End-products (nRAGE) in DSB-repair.
4  reduced organ function and delays in tissue repair.
5  a new direction of immunomodulation for SCI repair.
6 ese pathways normally collaborate during DSB repair.
7 LigC ligates the resulting nicks to complete repair.
8  safeguard the health of women after fistula repair.
9 tive stress may serve to modulate active DNA repair.
10 ranscription-coupled nucleotide excision DNA repair.
11 ream BMP signaling pathway may help with CNS repair.
12 nsure appropriate skeletal muscle growth and repair.
13 inflammation and promoting connective tissue repair.
14 omplexes involved in DNA single-strand break repair.
15  terms of annexin gene expression and muscle repair.
16 roles of the extracellular matrix in cardiac repair.
17  for both normal bone formation and fracture repair.
18 ound to exhibit a significant delay in wound repair.
19 ion of a myeloid cell contribution to tissue repair.
20 dult organisms during tissue homeostasis and repair.
21 n injury exhibited enhanced functional brain repair.
22 ault prolapse compared with vaginal non-mesh repair.
23 ice towards blood-spinal cord barrier (BSCB) repair.
24 int was the composite of aneurysm rupture or repair.
25 ar genomes through double-stranded DNA break repair.
26 , which are critical for DNA replication and repair.
27 chinery now identified as key factors in DSB repair.
28 DNA damages processed by nucleotide excision repair.
29 uture use of hiPSC-CM tissues in human heart repair.
30 issue adhesives, wound dressings, and tissue repair.
31 V), organization of repetitive DNAs, and DNA repair.
32 nge leading to a complete, effective natural repair.
33  disease modeling, drug screening, and heart repair.
34 on factor activity during hepatic injury and repair.
35 naling pathway plays a dominant role in bone repair.
36 versions are believed to be central to nerve repair.
37 on require homologous recombination (HR) DNA repair.
38 stalling, chromosome fragility, and impaired repair.
39 scription initiation and nucleotide excision repair.
40 ation of the DNA damage checkpoint after DSB repair.
41  within the repetitive tract followed by DNA repair.
42 y be a paradigm for the regulation of tissue repair.
43  of a morphogen-responsive function in wound repair.
44  and MutLalpha function in in vitro mismatch repair.
45 ncing, while H2AX is important in DNA damage repair.
46  EPDCs during cardiovascular development and repair.
47 n and in epidermal wound healing and barrier repair.
48 plantation of sheath tissues improves tendon repair.
49 ular population, and contribute to cartilage repair.
50 me activation together with accelerated lung repair.
51  unusual patterns of cementum resorption and repair.
52 hey function in normal homeostasis and wound repair.
53 terious DNA damage and need to be accurately repaired.
54                   The fistula was surgically repaired.
55 R pathway, altered in 60% of lines; BRCA DNA repair, 44%; and SYNE1-SYNE2, 60%.
56 on [2], embryonic development [3, 4], tissue repair [5-8], and organismal aging [9].
57                   Cryptochromes lack the DNA-repair activity of the closely related DNA photolyases,
58                                  Maladaptive repair after AKI may lead to progressive fibrosis and de
59 ctions in transcription, replication and DNA repair and are hence implicated in development and cance
60 ing telomere ends from double-stranded break repair and ATM signaling, whereas POT1 represses ATR sig
61 mTORC2 are both required to enact DNA damage repair and cell survival, resulting in increased cancer
62 h nematodes as a model for investigating the repair and consequences of DNA crosslinks in metazoan de
63 s revealed pathways including apoptosis, DNA repair and early estrogen response that were differentia
64 ovel strategies are needed to enhance muscle repair and function and to slow this pathological remode
65 essential roles in nuclear architecture, DNA repair and genome stability, and silencing of transposon
66 he importance of sequence context for alt-EJ repair and have important implications for genome editin
67 ng a role for T cells in profibrotic cardiac repair and healing after ischemia, little is known about
68 ppo pathway involved in development, growth, repair and homeostasis.
69 n into the role of IL-1 ligands in epidermal repair and innate immune response after damaging UVB exp
70 ction of factors normally involved in tissue repair and maintenance.
71 hich provides a mechanistic link between DNA repair and neurodegeneration.
72         It is a negative regulator of tissue repair and regeneration in multiple organs.
73 nnovative treatment strategies for long-term repair and regeneration of injured or diseased tissues a
74 hat may attenuate remodeling while promoting repair and regeneration.
75 cript reviews the role of the ECM in cardiac repair and remodeling and discusses matrix-based therapi
76 that cell-specific actions of Smad3 regulate repair and remodeling in the infarcted myocardium.
77 s to analyze very long-term outcome after MV repair and replacement for degenerative mitral regurgita
78 important biological processes including DNA repair and replication.
79 own for its functions in double-strand break repair and resolution of DNA replication stress.
80 ote unperturbed DNA replication and protect, repair and restart damaged forks.
81 avage that permits initiation of HR-mediated repair and restart of stressed forks.
82 gest H3-G34R slows resolution of HR-mediated repair and that unresolved replication intermediates imp
83  adhesion regulation during intestinal wound repair and the development of IBD.
84 e suggest that AhR may serve to adjust liver repair and to block tumorigenesis by modulating stem-lik
85 actors that affect UV-induced DNA damage and repair and ultimately UV carcinogenesis.
86 nment surrounding DSBs which facilitates DSB repair and which is framed by extensive ZMYND8 domains o
87 We set out to compare the incidence of bowel repair and/or resection in a large cohort of patients wi
88 tivation, imprinting and double-strand break repair, and mutations in SMCHD1 contribute to a type of
89 ibutor to transcription and DNA replication, repair, and recombination.
90 cell populations during cardiac development, repair, and regeneration.
91 tes, mitral reoperations within 12 months of repair, and survival were analyzed using multivariable C
92  interaction influences the process of wound repair are not well understood.
93  and graft trial) some women in the standard repair arm assigned to all treatment options were includ
94 ogrammed DNA double-strand breaks (DSBs) are repaired as crossovers, with the remainder becoming nonc
95 GFRalpha+ cells perform diverse roles in CNS repair, as multipotential progenitors that generate both
96  congenital heart disease requiring surgical repair at <7 days of life, lethal chromosomal anomaly, d
97 ) places patients undergoing elective hernia repair at increased risk for adverse postoperative event
98 e deaminase (AID) and requires base excision repair (BER) and mismatch repair (MMR).
99                   Furthermore, base excision repair (BER) is responsible for causing CAG repeat contr
100                                Base excision repair (BER) is the predominant pathway for coping with
101 DNA glycosylase1 (OGG1) during base excision repair (BER) pathway.
102 DNA repair intermediate during base excision repair (BER).
103 ing enzyme, which has been implicated in DNA repair, binds ssNucs preferentially over nucleosomes, an
104  markers and novel inflammatory, injury, and repair biomarkers.
105 e expectancy in patients ineligible for open repair, but can reduce aneurysm-related mortality.
106 tion is essential to rapid tissue growth and repair, but can result in replication-associated genome
107 n a decrease of mortality after elective AAA repair, but results of open repair have improved as well
108 ion as two distinct aspects of cellular self-repair by examining a few model organisms that have disp
109 uggesting that DNA double-strand break (DSB) repair by homologous recombination (HR) was compromised.
110 amage response (DDR) and is required for DSB repair by homologous recombination (HR).
111 s a gatekeeper function for replication fork repair by mediating the fork cleavage that permits initi
112      Analyzing genome-wide transcription and repair by next-generation sequencing, we identified loca
113  in response to DNA damage, which suppresses repair by nonhomologous end-joining and homologous recom
114 o-8-oxo-2'-deoxyguanosine (8-oxoG), which is repaired by 8-oxoguanine DNA glycosylase1 (OGG1) during
115 w model organisms that have displayed robust repair capacity, including Xenopus oocytes, Chlamydomona
116 n by distinctions in DNA damage induction or repair capacity.
117 tracks, and failure to sustain expression of repair cell markers, including Shh, GDNF, and BDNF.
118 ation also results in abnormal morphology of repair cells and regeneration tracks, and failure to sus
119  control long-term survival and phenotype of repair cells have not been studied, and the molecular si
120 rt long-term survival and differentiation of repair cells will help identify, and eventually correct,
121 n of CFTR in CF and the action of drugs that repair CFTR gating defects.
122 rgets of miR-424 that function in DNA damage repair, CHK1 and Wee1, are suppressed in HPV-positive ce
123 differences in food availability affect self-repair choice and regeneration success in cydippid larva
124 sheds light on how eukaryotes utilize RNA to repair chromosome breaks.
125 ggests that histone chaperones sequester the repair complex for oxidized bases in non-replicating chr
126                Here we show that the XPC DNA repair complex is a potent accelerator of global and loc
127 adiation and inefficient double-strand break repair correlated with severe late radiation toxicity.
128                                        These repairs could represent cancer mutations leading to GEP
129     The demand for organ transplantation and repair, coupled with a shortage of available donors, pos
130 ns of elongation complexes and transcription-repair coupling events in genes throughout the genome.
131 ve anti-inflammatory drugs frequently do not repair damaged bone.
132     We evaluated genetic instability and DNA repair defects by direct and indirect assays in 12 breas
133 repair pathways that essentially monitor DSB repair defects.
134 proportion of mutant neoantigens in mismatch repair-deficient cancers make them sensitive to immune c
135 s the mutation profiles observed in mismatch repair-deficient colorectal cancers.
136 rrow (BM) chimera mice revealed that mucosal repair depended on TNF production by BM-derived cells an
137 y at the matched end is </=150 bp, efficient repair depends on the recombination enhancer, which teth
138    Bioinformatic analyses suggest that these repair differences arise from transiently forming loops
139 hasis on the enzymes that synthesize DNA and repair discontinuities on the lagging strand of the repl
140 hPSCs) has generated opportunities for heart repair, disease modeling, and drug development.
141                     Homologous recombination repairs DNA double-strand breaks and must function even
142 -deficient muscle we find that poor myofiber repair due to the lack of AnxA2 does not result in chron
143 cts on epithelial cell regeneration and lung repair during fibrosis.
144 involved in nonhomologous end joining (NHEJ) repair, enhance amplification of viral DNA.
145 purinic/apyrimidinic endonuclease 1 is a DNA repair enzyme involved in genome stability and expressio
146   The Rh-PPO mechanism is reminiscent of DNA repair enzymes that displace mismatched bases, and is di
147 mismatch repair (MMR) pathway recognizes and repairs errors in base pairing and acts to maintain geno
148 nical processes of double-strand break (DSB)-repair, especially the auxiliary factor(s) that can stim
149                                  Three-prime repair exonuclease 1 (TREX1) is an anti-viral enzyme tha
150 norhabditis elegans mutants, we identify DNA repair factors that protect against the genotoxicity of
151 ipants were women who underwent transvaginal repair for POP or SUI with mesh between January 1, 2008,
152 nhibitor-based regimen because of a mismatch repair gene anomaly are presented.
153                By targeting the DNA mismatch repair gene MLH1 CGI, we could generate a PSC model of a
154 ation in organoids deficient in the mismatch repair gene MLH1 is driven by replication errors and acc
155 repeats/CRISPR-associated) homology-directed repair gene-editing.
156 he induction of anti-inflammatory and tissue repair genes in the lungs after helminth infection or in
157        Notably, reduced responsiveness of HR repair genes to irradiation and inefficient double-stran
158 tudies indicate that failure of white matter repair goes beyond the intrinsic incapacity of oligodend
159 atment options were included in the standard repair group of both trials.
160 eneration, but due to its tissue opaqueness, repair has been primarily assessed using destructive his
161 ter elective AAA repair, but results of open repair have improved as well.
162 or(s) that can stimulate accurate and timely repair, have remained elusive.
163 t that T reg cells can participate in tissue repair in a manner separable from their immunosuppressiv
164 munomodulatory approach to stimulating nerve repair in a nerve-guidance scaffold was used to explore
165 latonin and its metabolites enhanced the DNA repair in melanocytes exposed to UVB and stimulated expr
166  role for EAF2 in androgen regulation of DNA repair in prostate cancer cells.
167 chlea undergoing development, maturation and repair in response to damage.
168              CHAF1A inhibits NEIL1 initiated repair in vitro Subsequent restoration of the chaperone-
169 activates cell cycle arrest and disrupts DNA repair, in part by increasing p21 expression.
170 ment with AsiDNA, a novel first-in-class DNA repair inhibitor.
171  DNA synthesis and removal of a reactive DNA repair intermediate during base excision repair (BER).
172                                              Repairing IR1 improves EBNA-LP levels and the quality of
173    We reveal that defective ATM-mediated DNA repair is a consequence of P62 accumulation, which impai
174 of coronary endothelial cells during cardiac repair is essential for identifying improved approaches
175 s pathogenic microbial interactions in wound repair is important.
176                                 However, how repair is initiated at telomeres is largely unknown.
177 ioners need to understand when open surgical repair is required and when alternative management strat
178 roteins and reorganizes chromatin during DNA repair is unclear.
179 ve repair, particularly edge-to-edge leaflet repair, is a well-established alternative for patients w
180 ce and chromatin state modulate cleavage and repair kinetics.
181 se apurinic sites are subject to error-prone repair, leading to substitution and short frameshift mut
182 nding channel, shielding them from other DNA repair machineries.
183  properly removed by the nucleotide excision repair machinery.
184 e-seq and compared them to the complementary repair maps of the human genome obtained by excision rep
185 ion sequencing (NGS) to generate genome-wide repair maps.
186                 Expression of the DNA damage/repair marker, gamma-H2AX and DNA damage response marker
187                Targeting PARP-associated DNA repair may represent a novel therapeutic strategy for gl
188  type 2 ILCs (ILC2s) have been implicated in repair mechanisms that restore tissue integrity after in
189  chemokine receptor CXCR4 promote epithelial repair mechanisms.
190                       Compared with non-mesh repair, mesh repair of anterior compartment prolapse was
191 forts, including: tumor testing for mismatch repair (MMR) deficiency in Lynch syndrome establishing a
192                                     Mismatch repair (MMR) is a conserved mechanism exploited by cells
193                                     Mismatch repair (MMR) is a near ubiquitous pathway, essential for
194                                     Mismatch repair (MMR) is one of the main systems maintaining fide
195                             The DNA mismatch repair (MMR) pathway recognizes and repairs errors in ba
196 by uracil-DNA glycosylase (UNG) and mismatch repair (MMR) pathways to generate mutations at G-C and A
197 ires base excision repair (BER) and mismatch repair (MMR).
198 ity, proofreading activity, and DNA mismatch repair (MMR).
199 he efficacy of steroid dosing on sarcolemmal repair, muscle function, histopathology, and the regener
200             We analyzed the outcome after MV repair (n=1709) and replacement (n=213) overall, by prop
201  cardiac catheterization (n=5) after primary repair (n=4) or after surgical RV revalvulation for sign
202 posal that for sustained cooperation, guilty repair needs to override angry retaliation.
203 r replication-dependent and -independent ICL repair networks, and establish nematodes as a model for
204                                   Intact AAA repairs numbered 4956.
205          Compared with non-mesh repair, mesh repair of anterior compartment prolapse was associated w
206                                cAMP-enhanced repair of cisplatin-induced DNA damage was dependent on
207 ecules that may be further optimized for the repair of CNS damage.
208  BRCA and NHEJ pathways are required for the repair of CX-5461 and CX-3543-induced DNA damage and fai
209             Alternative end-joining (alt-EJ) repair of DNA double-strand breaks is associated with de
210                               Defects in the repair of DNA interstrand crosslinks (ICLs) are associat
211                                          The repair of DNA strand breaks improves, as do serum protei
212 lear metalloprotease that is involved in the repair of DNA-protein crosslinks (DPCs).
213 rates with Mre11 and Rad50 to coordinate the repair of double-stranded DNA breaks.
214  control of the cell cycle allows for timely repair of genetic material prior to replication.
215 defined as intraoperative enterotomy, suture repair of intestine, or bowel resection.
216 ologue, Ddes_1165, that is implicated in the repair of nitrosative damage.
217 t play a central role in the maintenance and repair of our bones are formed from bone marrow myeloid
218 PNKP; an XRCC1 protein partner important for repair of oxidative SSBs.
219 y-five patients aged median 12.0 years after repair of tetralogy of Fallot and similar lesions were s
220 hways that bypass such obstacles, postponing repair of the offending damage to complete the cell cycl
221 Here, we review research on regeneration and repair of the optic system.
222 ween vaginal and, separately, abdominal mesh repair of vaginal vault prolapse compared with vaginal n
223 locked with bricks and mortar, cement floors repaired or constructed, and rain gutters and a tank for
224 e cell cycle and accounts for nearly all DSB repair outside of the S and G2 phases.
225 ntrol class II and III) ventral hernia (CVH) repair over 24 months.
226                   Transcatheter mitral valve repair, particularly edge-to-edge leaflet repair, is a w
227              53BP1 is a key regulator of DSB repair pathway choice in eukaryotic cells and functions
228 horylation status of the NBS1(S432) dictates repair pathway choice of dysfunctional telomeres.
229 hosphorylation status of NBS1 determines the repair pathway choice of dysfunctional telomeres.
230 modelling during resection is underlying DSB repair pathway choice.
231 ing from each Cas9 variant and the resulting repair pathway engagement.
232 most prominent DNA double strand break (DSB) repair pathway in mammalian cells.
233 des presynaptic stimulation of the bacterial repair pathway perhaps by contributing to the RecA homol
234 tion (HR) is a DNA double-strand break (DSB) repair pathway that protects the genome from chromosomal
235 is the predominant double-strand break (DSB) repair pathway throughout the cell cycle and accounts fo
236 hogenesis, we have identified that the wound repair pathway, controlled by the epidermal growth facto
237 s an adverse effect on the DNA base excision repair pathway, the major DNA repair system that deals w
238  association between DNA damage-response and repair pathways and the age at onset of disease.
239                                Efficient DNA repair pathways are crucial in these organelles to fix d
240 gements (LST), and the status of several DNA repair pathways by transcriptome and genome analysis.
241 clei and LST and specific alterations in DNA repair pathways that essentially monitor DSB repair defe
242          Yra1 and Def1 were required for DSB repair per se, while Sit4 was required for rapid inactiv
243               To analyze IL-6 effects in the repair phase, compounds were injected from day 7 onwards
244  maintaining the molecular and morphological repair phenotype that promotes axonal regeneration.
245 centrations that are associated with the DNA repair process.
246 s in symptomatic ALS mice may represent BSCB repair processes, supporting hBM34+ cell transplantation
247 ther with apoptotic cells induced the tissue repair program in macrophages.
248 I is driven in part by corruption of a nerve repair program.
249                                          DNA repair protein counteracting oxidative promoter lesions
250  However, how H4 acetylation (H4Ac) recruits repair proteins and reorganizes chromatin during DNA rep
251 tivity of DNA polymerase-delta, although the repair proteins Msh2, Mlh1 and Exo1 influence the extent
252 verse contributions of several recombination/repair proteins to telomere maintenance in Ustilago mayd
253 eon case volume on degenerative mitral valve repair rates and outcomes.
254                                       Mitral repair rates, mitral reoperations within 12 months of re
255 cribed strand/nontranscribed strand (TS/NTS) repair ratio demonstrated that deletion of mfd globally
256 s study, we identified the Tudor-interacting repair regulator (TIRR) that specifically associates wit
257 Here we show that the budding yeast mismatch repair related MutLbeta complex, Mlh1-Mlh2, specifically
258 ed XR-seq method, tXR-seq does not depend on repair/removal of the damage in the excised oligonucleot
259 iated with increased DNA damage, reduced DNA repair responses, and elevated cellular senescence.
260 oth NHEJ and HR and severely compromised DSB repair resulting in chromosomal instability.
261 myelinating SCs in the later phases of nerve repair, resulting in slowed axon regeneration, cutaneous
262       Improper DNA double-strand break (DSB) repair results in complex genomic rearrangements (CGRs)
263 godeoxynucleotide-mediated homology-directed repair revealed that insulin signaling is up-regulated i
264 outcomes in adults after tetralogy of Fallot repair (rTOF).
265 T Although injured peripheral nerves contain repair Schwann cells that provide signals and spatial cl
266 e of the cells that form them, denervated or repair Schwann cells, remains obscure.
267 aps of the human genome obtained by excision repair sequencing to gain insight into factors that affe
268  concomitant with defective ATM-mediated DNA repair signaling and accumulation of protein-linked DNA
269 lore in conjunction with neuronal rescue and repair strategies.
270 plex in cell, presumably after completion of repair, suggests that histone chaperones sequester the r
271  base excision repair pathway, the major DNA repair system that deals with oxidative DNA damage.
272 ed transcription coupled nucleotide excision repair (TC-NER) (category 1: XP-A, B, D, F, and G) and p
273             Eukaryotic transcription-coupled repair (TCR) is an important and well-conserved sub-path
274  integrating nuclease-encoding cassettes and repair templates into the plant genome.
275                    Fifty-seven patients with repaired tetralogy of Fallot (age >/=16 y; mean age, 35.
276 sfunction or secondary outcome parameters in repaired tetralogy of Fallot.
277 chromatin-remodeling enzyme required for DNA repair that possesses a poly(ADP-ribose) (PAR)-binding m
278 conserved sub-pathway of nucleotide excision repair that preferentially removes DNA lesions from the
279 ll-derived neural progenitor cells (NPCs) to repair the FTD-associated N279K MAPT mutation.
280                                           By repairing the deletion, we resurrected 11 alleles of KIR
281 es AAA formation, whereas VSMC proliferation repairs the vessel wall.
282 iology of PARP-1 in DNA damage detection and repair, the mechanistic and functional understanding of
283 le of each cell type in the process of wound repair, the nature of the dynamic interplay between thes
284 open questions remain, elucidating how cells repair themselves is important for our mechanistic under
285                       Genetic defects in DNA repair underlie other neurodegenerative disorders (eg, a
286 ompleted initial training programs in hernia repair, underwent interval proficiency assessments, and
287 , branched, and fenestrated) and open aortic repair using flow cytometry.
288  in-service water distribution pipeline leak repair via clogging.
289  of TCTP in promoting DNA double-stand break repair via facilitating DNA homologous recombination pro
290 Q and NONO, promotes DNA double-strand break repair via the canonical nonhomologous end joining (c-NH
291 flail leaflet referred to mitral surgery, MV repair was associated with lower operative mortality, be
292 e the elongation complexes were blocked, and repair was associated with the dissociation of these com
293                                   To mediate repair, we exploit the catalytic domain of Adenosine Dea
294 ases in non-replicating chromatin, and allow repair when oxidized bases are induced in the genome.
295 templated processes, including base excision repair where Pol beta catalyzes two key enzymatic steps:
296 ontrolling OB-ISCs in homeostasis and injury repair, which is likely to be crucial in prevention of d
297 e down-regulation of BMI1, which impedes DNA repair while elevated levels can sensitize breast cancer
298 ructural problems such as leaking roofs were repaired, windows screened, open eaves blocked with bric
299 emporal monitoring after endovascular aortic repair, with excellent correlation and interobserver agr
300 of how DNA double-stranded breaks (DSBs) are repaired, with many components of the ubiquitin (Ub) con
301 sease, diabetes, obesity, and primary suture repair without mesh are associated with increased umbili

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