ライフサイエンスコーパス: competent cell

1 fate of donor DNA as it is processed by the competent cell.

2 e (DHAP) concentration to levels seen in TPI-competent cells.

3 here it has ready access to activated immune competent cells.

4 tion and enhance this process in leukotriene-competent cells.

5 tions which are found infrequently in repair competent cells.

6 associated with the membranes of genetically competent cells.

7 r enzymes in whole-cell extracts from repair-competent cells.

8 process requires engraftment of donor immuno-competent cells.

9 signaling but is cleared from IFN signaling-competent cells.

10 as a stop signal for the migration of immune-competent cells.

11 ring their differentiation into functionally competent cells.

12 r circadian rhythmicity in transcriptionally competent cells.

13 l pathways impair peptidoglycan synthesis in competent cells.

14 onal migration of transplanted remyelination-competent cells.

15 tive Vero cells but severe impairment in IFN-competent cells.

16 ltaneously increasing the frequency of IL-10-competent cells.

17 a and that the fragment must also include wg-competent cells.

18 increase chemotherapy-induced damage in BRCA-competent cells.

19 ClpC and ClpP localize to the cell poles of competent cells.

20 population of undifferentiated, regeneration-competent cells.

21 as a recombination intermediate in wild-type competent cells.

22 uction of this noise decreases the number of competent cells.

23 d from the plasma membrane of mineralization-competent cells.

24 s are as sensitive to NDV as other caspase-8-competent cells.

25 eased radiosensitivity compared with TGFbeta competent cells.

26 within a mammalian host, yet generate mating-competent cells.

27 t caused induction of prostin-1 in PLC gamma competent cells.

28 kinetics of transfer during fusion in fusion-competent cells.

29 ficient tumor cells while sparing checkpoint-competent cells.

30 clustering occurred only in chemotactically competent cells.

31 ule phosphorylation site) in chemotactically competent cells.

32 ls that can differentiate into mature immune-competent cells.

33 eases in the levels of ICL and MAs in repair-competent cells 24 h after 8-MOP/UVA treatment, there wa

34 To distinguish the minority of competent cells, a translational fusion between ComK, th

35 nd only in mitochondria, both in respiratory-competent cells and in rho0 cells in which the bc1 compl

36 protein to productively replicate in the IFN-competent cells and in the cells of mosquito origin was

37 r replication was severely attenuated in IFN-competent cells and in young calves.

38 ression is restricted to the putative fusion-competent cells and is not detected in unfused founder c

39 A and SsbB are directed to the cell poles in competent cells, and that the uptake of transforming DNA

40 We report that in editing-competent cells BCR ligand-induced RAG mRNA expression i

41 Furthermore, in contrast to autophagy-competent cells, both proliferation and transformation i

42 ctivity were highly attenuated in interferon-competent cells but not in cells unable to establish ant

43 yl methanesulfonate (MMS) response in repair-competent cells, but it greatly amplified the MMS sensit

44 The protocol involves the transduction of competent cells by a chimeric retroviral vector containi

45 (sc) expression defines a group of neurally-competent cells called the proneural cluster (PNC).

46 nstrated that latently infected, replication-competent cells can be generated in vitro after eliminat

47 Initially we confirmed that respiratory-competent cells can be produced following incubation of

48 tion, and by increasing the pool of division-competent cells capable of anchorage-independent growth.

49 in approximately 25% of the mismatch repair-competent cell clones analyzed (cell lines HeLa and PMS2

50 Thus, IDO-competent cells constitute a distinctive B-lymphoid cell

51 led EFF-1 is specifically targeted to fusion-competent cell contacts via reciprocal localization to t

52 Platelets are immunologically competent cells containing cytokines such as TGF-beta1 t

53 density difference between competent and non-competent cells depends on the competence-specific growt

54 ells with phenotypic attributes matching IDO-competent cells developed normally and expressed IDO in

55 ctuation in this signaling helps to sort out competent cells during successive cell-fate determinatio

56 Moreover, DNMAML1-enriched EMT-competent cells exhibited robust upregulation of ZEBs, d

57 Competent cells express specialized proteins that assemb

58 Here we show that IDO-competent cells express the B-lineage commitment factor

59 ine adducts are substrates for repair by NER competent cell extracts but not XP12BE cell extracts def

60 Overall, increased glycolysis in autophagy-competent cells facilitates Ras-mediated adhesion-indepe

61 a unique gene regulatory network in germline-competent cells for PGC specification.

62 ee species have three cell types: two mating-competent cell forms (a and alpha) and the product of th

63 t cells and by the release of mineralization-competent cell fragments (matrix vesicles and apoptotic

64 Replication-competent cell-free extracts from other human cells were

65 the majority of vesicles in fully secretion-competent cells had no Munc18-1 associated within distan

66 hich can take up sterols aerobically in heme-competent cells have been selected.

67 reporter system and that only proliferation-competent cells have the ability to rapidly adapt ERK an

68 We present evidence that Drosophila immune-competent cells have the potential to express more than

69 assay to measure the function of the immune-competent cells in PD effluent from PD patients.

70 in thymic cellularity and enrichment for ILK-competent cells in the spleen and lymph nodes.

71 e, with an increase in the number of S-phase competent cells in the upper suprabasal layers, while th

72 equently induce activation of various immune-competent cells, including dendritic cells, thereby prov

73 triplex in a plasmid transfected into repair competent cells, indicating that approximately 25% of th

74 ribe Il10 illustrated that the pool of IL-10-competent cells is dominated by CD4 T cells and macropha

75 In leukotriene-competent cells, LTC4 augmented phagocytosis to the grea

76 Upon dilution into fresh medium, competent cells maintain this appearance for about 2 h.

77 eased upon activation of a variety of immuno-competent cells may be important mediators that give ris

78 vector (pET-28a(+)) and converted it to the competent cell of BL21(DE3) to gain recombinant MAF-1 fu

79 In the competent cells of a comGA mutant culture, chromosomal r

80 that are activated during the development of competent cells of B. subtilis, a developmental program

81 Competent cells of Bacillus subtilis efficiently bind an

82 ssing and transport of transforming DNA into competent cells of Bacillus subtilis is described.

83 IL-10-competent cells of the B lineage are rare in vivo and, a

84 As the immune-competent cells of the brain, microglia play an increasi

85 Transformable (competent) cells of Bacillus subtilis are blocked in cel

86 has been traversed occurred in gap junction-competent cells only.

87 ed heterodicentric chromosome fusions in ATM-competent cells, only those mutant repeat sequences with

88 ed fewer lung metastases than syngeneic MKK4-competent cells (P = 0.0034).

89 IL-4-competent cells persisted in cured animals, and memory r

90 y leading to cell branching and formation of competent cell poles.

91 ly activated at a low level in all Sevenless-competent cells prior to Sevenless signaling, and this r

92 In contrast, the majority of non-competent cells rapidly resume growth, exhibiting chaini

93 Competent cells resemble stationary phase cells; the maj

94 Chemotaxis-competent cells respond to a variety of ligands by activ

95 is a poorly understood process during which competent cells respond to inducing conditions, allowing

96 of infections with these two viruses in IFN-competent cells showed that W956IC activated NF-kappaB,

97 s recruited to sites of fusion by the fusion-competent cell-specific receptor Sns and acts as a posit

98 sin production and cell lysis of its own non-competent cells, suggesting a possible active mechanism

99 ted an approximate 20-fold enrichment of ILK-competent cells, suggesting these cells have a competiti

100 s of the ComG proteins in DNA binding to the competent cell surface are discussed in the light of the

101 of severe inflammation by engaging signaling-competent cell surface receptors.

102 l for the binding of transforming DNA to the competent cell surface.

103 horylated in vitro by expression in the TKX1-competent cells that carry an inducible tyrosine kinase

104 self-renewal, proliferation, or survival of competent cells that it inappropriately contacts.

105 In repair-competent cells the 1-NP adduct induced 1.7% CpG deletio

106 Although in silencing competent cells there was no correlation between the fra

107 , dendritic cells (DCs) are the first immune-competent cells to encounter antigens within skin or muc

108 ibutes were not essential for B-lymphoid IDO-competent cells to regulate T cells.

109 ion that enables the resultant gametogenesis-competent cells to respond to feminizing or masculinizin

110 Immune-competent cell trafficking to synovial tissue is integra

111 ficient in IL-1alpha expression or IL-1alpha-competent cells treated with IL-1alpha-specific small in

112 Restoring KCNA1 expression in transformation-competent cells triggered variation in membrane potentia

113 coupled to fusion receptors; in other fusion-competent cell types it may be triggered by different up

114 o increased survival or activity of division-competent cell types under anchorage-independent growth

115 protein Maf is synthesized predominantly in competent cells under the direct control of the transcri

116 Enrichment of EMT-competent cells was more evident in the presence of p53

117 To validate the identification of competent cells, we demonstrated the coincident expressi

118 , single strands from native donor DNA enter competent cells, where they associate with an unidentifi

119 ant host hepatocytes must be replaced by AGT-competent cells, which is beyond the capacity of current

120 ceptor-mediated signaling pathways in immuno-competent cells will provide a new insight for understan

121 nisms for the inhibition of cell division in competent cells with Maf acting downstream of ComGA.