ライフサイエンスコーパス: TLD

1 TLD in Escherichia coli is accompanied by blocked replic

2 TLD is the mode of action of common anticancer drugs and

3 d developmental roles in other systems-BMP-1/TLD (tolloid) (astacins), MMPs (matrix metalloproteases)

4 se the possibility that members of the BMP-1/TLD family may be involved in activating latent myostati

5 he propeptide resistant to cleavage by BMP-1/TLD proteinases can cause significant increases in muscl

6 bone morphogenetic protein-1/tolloid (BMP-1/TLD) family of metalloproteinases can cleave the myostat

7 The unexpectedly large number of BMP-1/TLD-like protease genes (23) results primarily from expa

8 on domains of all four known mammalian BMP-1/TLD-like proteases [BMP-1, mammalian Tolloid (mTLD), mam

9 human ataxia-telangiectasia like disorder (A-TLD) were derived.

10 f ROS to background levels largely abolished TLD.

11 cteria from double-stranded DNA breakage and TLD.

12 e opposing effects of SOG inhibiting DPP and TLD processing SOG to release DPP from the inhibitory co

13 There are similarities between TLD of bacteria and death of eukaryotic cells.

14 I, and report crystal structures of the Bye1 TLD bound to Pol II and three different Pol II-nucleic a

15 ist TLD and suggest strategies for combating TLD resistance during chemotherapies.

16 Thymineless death (TLD) is the rapid loss of viability in bacterial, yeast,

17 This phenomenon, called thymineless death (TLD), underlies the action of several antibacterial, ant

18 llular condition known as thymineless death (TLD), which is the basis of action for several common an

19 hesis is not required for thymineless death (TLD).

20 he sensitivity of GK11 to thymineless death (TLD).

21 se to thymine starvation [thymineless death (TLD)].

22 Neither T-lymphocyte depletion (TLD) of the bone marrow nor irradiation appeared to infl

23 ed religation of topoisomerase I-linked DNA (TLD) in the presence of camptothecin.

24 n molecule that contains a tRNA-like domain (TLD) and an internal open reading frame (ORF).

25 that Bye1 binds with its TFIIS-like domain (TLD) to RNA polymerase (Pol) II, and report crystal stru

26 contains a transfer RNA (tRNA)-like domain (TLD), which enters the ribosome as a tRNA and places an

27 ed by placing a thermoluminescent dosimeter (TLD) strip (six TLD chips) on the abdomen of eight patie

28 performed with thermoluminescent dosimeters (TLD) placed inside a CIRS anthropomorphic phantom.

29 with 50 to 60 thermoluminescent dosimeters (TLDs).

30 antom by using thermoluminescent dosimetric (TLD) and CT pencil chamber measurements.

31 e source of double-strand ends (DSEs) during TLD, as previously proposed; models are suggested.

32 up to 2 mM) inhibited PARP-1/NAD-facilitated TLD religation in a dose-dependent manner.

33 Many explanations for TLD have been advanced, with recent efforts focused on r

34 cleotide excision repair as explanations for TLD.

35 nded DNA were necessary but insufficient for TLD, whereas reduction of ROS to background levels large

36 recombination nor SOS induction causes hyper-TLD in recB cells, and RecQ is not the sole source of do

37 persensitivity to thymine deprivation (hyper-TLD) in mutants that lack the UvrD helicase, which oppos

38 We report that hyper-TLD in uvrD cells is partly RecA dependent and cannot be

39 The hyper-TLD of recB cells requires neither RecA nor RecQ, implyi

40 The hyper-TLD of ruvABC cells requires RecA but not RecQ or RecJ.

41 estigated the possible involvement of ROS in TLD.

42 vivo, Bye1 is recruited to chromatin via its TLD and occupies the 5'-region of active genes.

43 and fork' structure on the ribosome when its TLD moves to the ribosomal P site and translation resume

44 Like TFIIS, Bye1 binds with its TLD to the Pol II jaw and funnel.

45 Occupying the empty A site with its TLD, the tmRNA enters the ribosome with the help of elon

46 model is presented for a molecular basis of TLD.

47 ved cells and may be the underlying cause of TLD.

48 and the SOS DNA-damage response as causes of TLD.

49 d from the replication origin: the extent of TLD correlates with the progression of damage.

50 e current proposals account for only part of TLD and because reactive oxygen species (ROS) are implic

51 rticipation of ROS in the terminal phases of TLD provides a specific example of how ROS contribute to

52 e characterized the onset and progression of TLD in Escherichia coli and found that DNA damage is the

53 vides a major impetus for further studies on TLD.

54 onal as-yet-unknown function of UvrD promote TLD resistance.

55 esults define pathways by which cells resist TLD and suggest strategies for combating TLD resistance

56 thermoluminescent dosimeter (TLD) strip (six TLD chips) on the abdomen of eight patients examined wit

57 ent transfection assays, we demonstrate that TLD cleaves SOG and that cleavage is stimulated by DPP.

58 secondary axis induction assay, we show that TLD negates the inhibitory effects of SOG/CHD on DPP/BMP

59 Radiation risk was estimated based on the TLD readings and expressed as the dose absorbed by parti

60 The map clarifies that the TLD is located near helix 34 and protein S19 of the 30S

61 as tRNA for normal translation, so that the TLD is oriented toward the ORF.

62 ibosome and the tmRNA at the point where the TLD is accommodated into the ribosomal P site.

63 The mean PSDs measured with the TLDs were 1.0+/-0.5 Gy in the RAO and 1.5+/-0.4 Gy in th

64 We conclude that ROS contribute to TLD by converting single-stranded DNA lesions into doubl

65 ic protein 1 (BMP-1) and Drosophila Tolloid (TLD) are prototypes of a family of metalloproteases with

66 e and thymidine, mutant GK11 did not undergo TLD but was defective for in vitro growth, and the defec

67 tic processing of fibrillar collagens, while TLD affects dorsal-ventral patterning by releasing TGFbe

68 ses for conventional urography measured with TLD strips and calculated as entrance skin dose were 151

69 nt skin doses for CT urography measured with TLD strips and calculated from phantom data (CT dose ind