ライフサイエンスコーパス: for repairing

1 ells, indicating that NER is a major pathway for repairing 4-HNE-dG adducts in both human and E. coli

2 A glycosylase-1 (OGG1) is the primary enzyme for repairing 7,8-dihydro-8-oxoguanine (8-oxoG) via the

3 insic AP lyase activity, is the major enzyme for repairing 7,8-dihydro-8-oxoguanine (8-oxoG), a criti

4 The human Ogg1 glycosylase is responsible for repairing 8-oxo-7,8-dihydroguanine (8-oxoG) in both

5 e-DNA glycosylase (OGG1) is the major enzyme for repairing 8-oxoguanine (8-oxoG), a mutagenic guanine

6 Techniques for repairing a bicuspid valve might vary depending on t

7 NA end joining (NHEJ) pathway is responsible for repairing a major fraction of double strand DNA brea

8 e of Fpg substrates and was only responsible for repairing a subset of its own substrate lesions in v

9 f PAK2, may be utilized to develop therapies for repairing abnormal myelin in peripheral neuropathies

10 Senescent cells are beneficial for repairing acute tissue damage, but they are harmful

11 enchymal stem cells in clinical applications for repairing and/or regenerating periodontal tissue.

12 ve reduced viability, indicating a threshold for repairing anterior-posterior mispatterning.

13 t Apn1 and Apn2 represent alternate pathways for repairing AP sites.

14 derstanding of these mechanisms is necessary for repairing auditory circuits following acoustic traum

15 rived stem cells can offer a viable strategy for repairing basement membrane defects and conferring t

16 us therapeutic platforms have been developed for repairing bone defects.

17 gree of DNA recombination, which is required for repairing both DNA double-stranded (ds) breaks and b

18 al myoblasts (SMs) is one possible treatment for repairing cardiac tissue after myocardial injury.

19 athway (including Rho1 and a novel arrestin) for repairing cell-wall damage.

20 The NER pathway is responsible for repairing cisplatin bound to DNA.

21 ndrimer-based adhesives are of potential use for repairing corneal wounds.

22 re not needed for viability, but is required for repairing damage and for tolerating loss of Ctf4.

23 the base excision repair pathway responsible for repairing damaged bases in the DNA.

24 MENT Neural network reconnection is critical for repairing damaged brain.

25 ifferentiating to chondrocytes has potential for repairing damaged cartilage or to generate disease m

26 ssion in response to DNA damage is important for repairing damaged DNA for cell survival.

27 hepatocyte-like cells and thus hold promise for repairing damaged liver.

28 A number of new and innovative approaches for repairing damaged myocardium are currently undergoin

29 , thereby uncovering a new functional target for repairing damaged tissue and treating diseases such

30 ing natural ways of reprogramming host cells for repairing damaged tissues from infection, injury and

31 medicine seeks to exploit nature's solution for repairing damaged tissues, through the process of re

32 erative medicine offers promising strategies for repairing damaged tissues, with the aim of restoring

33 This approach offers a route for repairing diseased biocircuits and emulating their f

34 rmine the optimal stem cell type and regimen for repairing diseased myocardium.

35 Cellular treatments for repairing diseased tissues represent a promising cli

36 repair pathway, the major cellular mechanism for repairing DNA base damage.

37 Nature has devised many strategies for repairing DNA breaks.

38 onnected, with recombination being essential for repairing DNA damage and supporting replication of t

39 ted that TCR is the most important mechanism for repairing DNA damage in non-dividing cells such as n

40 The ability of p53R2 to supply dNTPs for repairing DNA damages requires the presence of a fun

41 Nonhomologous end joining (NHEJ) is required for repairing DNA double strand breaks (DSBs) generated

42 There are two major pathways for repairing DNA double strand breaks in mammalian cell

43 dimer with Ku80, called Ku, that is critical for repairing DNA double-stand breaks by nonhomologous e

44 recombination (HR) are the primary pathways for repairing DNA double-strand breaks (DSBs) during int

45 us end joining (NHEJ) is the primary pathway for repairing DNA double-strand breaks (DSBs) in many or

46 for restarting stalled replication forks and for repairing DNA double-strand breaks (DSBs) through a

47 or the homologous recombination (HR) pathway for repairing DNA double-strand breaks (DSBs), but surpr

48 ebrate cells have evolved two major pathways for repairing DNA double-strand breaks (DSBs), homologou

49 ous recombination (HR) is an important route for repairing DNA double-strand breaks (DSBs).

50 and G(2)/M cell cycle arrest and is critical for repairing DNA double-strand breaks and for RAD51-dep

51 ar, serine/threonine protein kinase required for repairing DNA double-strand breaks and for V(D)J rec

52 gous end-joining (NHEJ) is the major pathway for repairing DNA double-strand breaks in mammalian cell

53 imer with Ku80, called Ku that is well known for repairing DNA double-strand breaks through non-homol

54 omologous recombination is the major pathway for repairing DNA double-strand breaks.

55 2, essential components of a repair pathway for repairing DNA double-strand breaks.

56 One highly conserved pathway for repairing DNA DSBs is DNA non-homologous end-joining

57 ein and ssDNA may prove generally applicable for repairing DNA in many organisms.

58 Mono-ubiquitination of Fancd2 is essential for repairing DNA interstrand cross-links (ICLs), but th

59 The Fanconi anemia (FA) pathway is essential for repairing DNA interstrand crosslinks (ICL).

60 Recombination is important for repairing DNA lesions, yet it can also lead to genom

61 In higher organisms, a major pathway for repairing double stranded breaks in DNA is non-homol

62 ning (c-NHEJ) pathway is largely responsible for repairing double-strand breaks (DSBs) in mammalian c

63 The two major pathways for repairing double-strand breaks (DSBs), homologous re

64 a major pathway in multicellular eukaryotes for repairing double-strand DNA breaks (DSBs).

65 AddAB helicase and nuclease complex is used for repairing double-strand DNA breaks in the many bacte

66 DNA end joining (NHEJ) is the major pathway for repairing double-strand DNA breaks.

67 ther than C-NHEJ, serves as a primary method for repairing DSBs in malaria parasites.

68 highlight RT-DSBR as an alternative pathway for repairing DSBs in transcribed genes, with potential

69 versity in antigen receptors, relies on NHEJ for repairing DSBs introduced by the Rag1-Rag2 protein c

70 , considered a particularly accurate pathway for repairing DSBs, are linked to breast cancer suscepti

71 nd-joining (NHEJ) pathway is a key mechanism for repairing dsDNA breaks that occur often in eukaryoti

72 NHEJ is the primary pathway for repairing dsDNA breaks throughout the G0, G1 and ear

73 ologous recombination are the major pathways for repairing dsDNA breaks.

74 oval of the 5'-blocking residue, is required for repairing endogenous SSBs in the mt genome.

75 ethyltransferase (PCMT1) activity, essential for repairing ethanol-induced protein damage.

76 Orangutans select different tactics for repairing failed communication, depending upon how w

77 us end joining (NHEJ) is the primary pathway for repairing G1 phase-induced DNA double-strand breaks

78 Tetrahymena ribozymes hold promise for repairing genetic disorders but are largely limited

79 5,6 mutants use a variation on this strategy for repairing heterochromatic DNA damage.

80 ed to be permanent and thus lack a mechanism for repairing in situ molecular detachment or degradatio

81 Many strategies for repairing injured myocardium are under active invest

82 A key approach for repairing injured spinal cord is to seal the damaged

83 ld be developed into a therapeutic procedure for repairing injured spinal cord.

84 This approach offers a promising strategy for repairing ischemic injury and preventing heart failu

85 Thus human Tdp1 is thought to be responsible for repairing lesions that occur when topoisomerase I be

86 te that homologous recombination is required for repairing lesions using double-stranded, but not sin

87 cision repair (BER), the predominant pathway for repairing methylated bases.

88 ind that MMR-PCNA interactions are important for repairing mismatches formed during meiotic recombina

89 The rate micros(T) for repairing molecular damage by means of DNA-repair en

90 eterminants of axonal sprouting is important for repairing motor circuits after injury to achieve fun

91 d, structure-specific endonuclease important for repairing multiple types of DNA lesions.

92 osylase 1 (OGG1) provides the major activity for repairing mutagenic 7,8-dihydro-8-oxoguanine (8-oxoG

93 enue to explore the potential of these cells for repairing myelin disorders in adulthood.

94 nerve regeneration by using it as a scaffold for repairing nerve defects.

95 FEN-1 has specific endonuclease activity for repairing nicked double-stranded DNA substrates that

96 Thus, TDP1 seems to be critical for repairing nuclear and mitochondrial DNA damage cause

97 lymer modified mortar is effective technique for repairing of cracks in shear deficient RC beams.

98 ults of experimental investigation conducted for repairing of cracks in shear deficient reinforced co

99 with interleukin-17 (IL-17) to induce genes for repairing of damaged epithelium.

100 s a primary homologous recombination pathway for repairing one-ended double-strand DNA breaks, includ

101 odeling, and may provide an effective method for repairing OPOA.

102 lar chaperones provide additional mechanisms for repairing or degrading non-native proteins and for i

103 ecause of the lack of alternative treatments for repairing or replacing damaged bile ducts.

104 se by providing an unlimited source of cells for repairing or replacing damaged tissue.

105 , there will remain an ongoing clinical need for repairing or replacing these prostheses in the futur

106 ot of the other DNA glycosylases responsible for repairing oxidatively damaged bases in mammalian gen

107 ases (DGs) with overlapping substrate ranges for repairing oxidatively damaged bases via the base exc

108 n repair (BER) pathway is mainly responsible for repairing oxidized and abasic sites into DNA.

109 e many cell types being examined are optimal for repairing particular lesions.

110 e transfer of BMPs and offers a new approach for repairing periodontal defects.

111 es preserves the pool of reduced thioredoxin for repairing proteins vital to survival.

112 The NEIL3 pathway is the major pathway for repairing psoralen-ICL, and the FA/BRCA pathway is o

113 dy evaluated the use OF bioactive glass (BG) for repairing/regenerating periodontal intrabony defects

114 effectiveness of PMM, an indigenous product, for repairing reinforced concrete beams, resulting more

115 ded as a mediator of this pathway, essential for repairing replication-associated DSBs during mitosis

116 Although biochemical mechanisms for repairing several forms of genomic insults are well

117 ken replication forks, where BIR is required for repairing single-ended DSBs (seDSBs), SMARCAD1 displ

118 ase stack, explaining the preference of AlkB for repairing ssDNA lesions over dsDNA ones.

119 biomarkers and immunotherapeutic treatments for repairing T-cell responses in lymphoma.

120 Current strategies for repairing the adult CNS following injury include cel

121 Club cells are local progenitors critical for repairing the airway epithelium after exposure to va

122 a are capable of using endogenous mechanisms for repairing the cellular damage.

123 d to further enhance successful neurogenesis for repairing the damaged brain.

124 may be an attractive and innovative solution for repairing the damaged heart.

125 o define an evolutionarily conserved pathway for repairing the epidermal surface barrier.

126 We studied an extracellular matrix scaffold for repairing the infarcted left ventricle.

127 l integrin expression, suggesting strategies for repairing the injured spinal cord.

128 and 8 carrying a wild-type genomic sequence for repairing the mutated Fah (fumarylacetoacetate hydro

129 e neural tissue has raised new possibilities for repairing the nervous system.

130 otic cells, and there are two major pathways for repairing them: homologous recombination (HR) and no

131 Two major mechanisms are responsible for repairing these breaks in mammalian cells, non-homol

132 Several mechanisms for repairing these mutagenic UV-induced DNA lesions hav

133 tilized technique to produce additional skin for repairing tissue defects in many conditions, such as

134 essential for ICL repair but is dispensable for repairing TOP1 inhibitor-induced DNA lesions.

135 hway, polymerase beta, and FEN1 are critical for repairing trapped PARP-DNA complexes.

136 n repair, the DNA repair pathway responsible for repairing up to 20000 endogenous lesions per cell pe

137 cision repair (BER), the pathway responsible for repairing uracil in DNA.

138 ucleotide excision repair is a major pathway for repairing UV light-induced DNA damage in most organi

139 otide excision repair and photolyase enzymes for repairing UV-induced DNA damage and regaining preirr

140 Y family translesion polymerase, is required for repairing UV-induced DNA damage, and loss of PolH is

141 erma pigmentosum C (XPC), a protein critical for repairing UVB-induced DNA damage.

142 y (under 40 min per construct) and potential for repairing volumetric defects.

143 mains the "gold-standard" therapeutic option for repairing wounds that cannot be closed by primary or