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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

26 Cellular treatments for repairing diseased tissues represent a promising cli

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

28 Nature has devised many strategies for repairing DNA breaks.

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

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

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

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

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

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

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

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

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

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

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

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

41 2, essential components of a repair pathway for repairing DNA double-strand breaks.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

62 5,6 mutants use a variation on this strategy for repairing heterochromatic DNA damage.

63 Many strategies for repairing injured myocardium are under active invest

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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