ライフサイエンスコーパス: burst size

1 (+) T cell cultures to be determined (clonal burst size).

2 l gene expression, cytopathic effects and/or burst size.

3 the right half of cosN, does not affect the burst size.

4 ) and accompanied by a fourfold reduction in burst size.

5 rences decrease with increasing mean protein burst size.

6 rprisingly had only a modest impact on phage burst size.

7 hage-cell encounter rate, latent period, and burst size.

8 sm, is often observed if activators increase burst size.

9 ne acetylation, transcription frequency, and burst size.

10 beta-globin gene with modest stimulation of burst size.

11 frequencies increases burst fraction but not burst size.

12 ically reduce noise in mRNA copy numbers and burst size.

13 hnique for measuring protein copy number and burst size.

14 ations as the transcription rate and protein burst size.

15 per genome) and (ii) an 80% drop in average burst size.

16 T cell TCR binding, signal transduction, and burst size.

17 deoffs between phage latent period and phage burst size.

18 hat Gal4 dwell time sets the transcriptional burst size.

19 e linear relationship between lysis time and burst size.

20 whose virion production rate maximizes viral burst size.

21 tion rates lower than the one that maximizes burst size.

22 t extents and hence produce different photon-burst sizes.

23 marked change in the distribution of photon-burst sizes.

24 phages, which are cosN+, also had wild-type burst sizes.

25 w and high producer cells results in similar burst sizes.

26 stimuli caused a rapid and acute increase in burst sizes.

27 ractal properties, with power-law scaling of burst sizes across a remarkable 5 orders of magnitude an

28 a prominent effector of burst frequency and burst size acting via decreasing off-times and gene-spec

29 e found that the distribution (variation) of burst size against burst occurrence was greater in women

30 ation confocal spectroscopy and fluorescence burst size analysis are used to individually count and s

31 The concentration dependence, fluorescence burst size analysis, and fluorescence correlation analys

32 CCK reduced burst size and cluster size, whereas bombesin reduced bu

33 blocking plaque formation, sharply reducing burst size and enhancing the survival of host cells foll

34 The expected phage burst size and fitness curve were predicted from these m

35 or necrosis factor alpha (TNF) only modulate burst size and frequency along a constrained trend line

36 scGRO-seq can estimate burst size and frequency by directly quantifying transcr

37 amics of primary B-cells, but modulates both burst size and frequency in response to gamma-interferon

38 n of transcriptional bursting, including the burst size and frequency, has mainly relied on live-cell

39 wo key parameters of protein expression--the burst size and frequency--can be either determined direc

40 y meaningful properties, such as the average burst size and frequency.

41 tazanavir, which reduces the cellular virion burst size and hence inhibits replication only after ini

42 on muscle sympathetic nerve activity (MSNA) burst size and occurrence separately as subcomponents of

43 Ag-specific CD8 T cells negatively regulated burst size and TCR avidity in vivo.

44 ey variables that heavily influence effector burst size and the persistent memory pool size: the cell

45 We show that core promoter elements affect burst size and uncover synergistic effects between TATA

46 Both exhibit robust single-turnover burst sizes and ATP consumption rates higher than those

47 f the biophysical mechanisms, such as system burst sizes and degradation rates, that underlie observa

48 nitude and a scale-free relationship between burst sizes and durations.

49 tions, allowing us to estimate transcription burst sizes and extrinsic noise strength and calculate t

50 idual phage growth parameters-latent period, burst size, and adsorption rate.

51 per-plaque burst number versus per-infection burst size, and based on analysis of existing models of

52 infectivity, much greater stability, higher burst size, and decreased induction of cellular interfer

53 For each phage strain, the lysis time, burst size, and fitness (growth rate) were determined.

54 BCs, RBC age preference, RBC infection rate, burst size, and within-RBC interference.

55 The lysis times, burst sizes, and relative fitness were empirically deter

56 "slow" or if burst sizes are large, (ii) if burst sizes are already large, or (iii) if virion bindin

57 The histograms of the burst sizes are generated in <3 min with <1 pg of DNA.

58 When alpha<<1, the burst sizes are geometrically distributed, allowing larg

59 ly, (i) if virion adsorption is "slow" or if burst sizes are large, (ii) if burst sizes are already l

60 but only if adsorption is otherwise slow or burst sizes are large.

61 bacterial densities are especially high, or burst sizes are large.

62 on" and "off" transitions, together with the burst sizes, are modulated in single cells to increase g

63 This suggested burst size as a neural code for stimuli optimality (and

64 ing a two-state model with a distribution of burst sizes as the most potent of the seven for describi

65 lysis-timing mutants, should increase phage burst sizes, as more time is available for phage-progeny

66 investigation into the biology of HSV-1, its burst size at the single-cell level has not been rigorou

67 with a mathematical model, the in vivo viral burst size averaged 4.0 x 10(4) and 5.5 x 10(4) virions

68 Burst size [B = alpha(mu - nu)], the number of phages re

69 cts of food deprivation and concentration on burst size (BS), burst number (BN), and other parameters

70 ritable variations in gene function--such as burst size, burst frequency, cell cycle-specific express

71 to BP is greater in older women than men in burst size but not burst occurrence.

72 n be modulated by altering burst fraction or burst size, but how regulatory elements control bursting

73 s demonstrated that hok/sok decreased the T4 burst size by 40%, increased the time to form mature pha

74 clustered arrangements reduce the effective burst size by more than 50% and cause substantial superi

75 Second, if increases in burst size can contribute to plaque size (i.e. larger pl

76 cle that are not captured in an SCA, such as burst size, cell-to-cell transmission, or infected-cell

77 We first show altering transcriptional burst size contributes to premeiotic transcription and a

78 o glucose (increased total intake, increased burst size, decreased number of pauses), relative to fru

79 ptional activators alter burst frequency and burst size, depending on the expression level of the loc

80 Reduction in burst size depends on efficient expression of the EGS co

81 As expected, burst size did not vary with stimulus orientation in the

82 d variation in splicing contributed to these burst size differences.

83 High-quality burst size distribution histograms were obtained for DNA

84 Burst-size distributions are, in addition, shaped by mRN

85 plex multiprotein regulation can have peaked burst-size distributions in contrast to the geometric di

86 the recBCD(+) host cell cytoplasm and a low burst size due, at least in part, to a decreased ability

87 scription factor complex, primarily modifies burst size (duration x intensity).

88 l pool is a direct consequence of the clonal burst size during the primary response may no longer be

89 acts of infected cell identity on multiround burst size, even among preferentially infected cell type

90 ith one-step growth curves revealing reduced burst sizes for the generalist phages.

91 allowing large bursts even while the average burst size [Formula: see text] is small.

92 tic life cycle, including a relatively large burst-size, has evolved to promote survival in the face

93 Photon-burst size histograms were constructed, from which the s

94 Due to influenza's higher burst size, however, the overall cost of a T4 phage infe

95 ng lifetimes, high infection rates and large burst sizes; (ii) large, stable, and high-density popula

96 ription burst frequency or by increasing the burst size in [Formula: see text], the noise shows only

97 lysogeny propensities rather than the phage burst size in any individual phase.

98 confirmed by a significantly enhanced virus burst size in cells in which silencing was knocked down

99 quency is primarily encoded in enhancers and burst size in core promoters, and that allelic single-ce

100 These include an increased burst size in multiply infected cells, the saturation of

101 Concomitantly, the average clonal burst sizes in EC-stimulated CTL cultures were significa

102 , had broader host range and produced larger burst sizes in WT compared with P1.

103 T4 rnh null mutations reduce burst sizes, increase sensitivity to DNA damage, and inc

104 on of polymerase shuttling typically reduces burst size, increases burst frequency, and thus limits t

105 The burst size indicates that the dimeric enzyme has a singl

106 sponse to EBV and find that a larger primary burst size is associated with proportionally greater dec

107 arly a constant, whereas the increase in the burst size is conceivably sensitive, when responding to

108 will expand its host range if its effective burst size is positive.

109 plaques at normal efficiency even though the burst size is reduced to about half that obtained on the

110 T cell burst size is regulated by the duration of TCR engagemen

111 s in vivo as judged by plaque morphology and burst size measurements.

112 y infected CD4(+) T lymphocytes or the viral burst size must be proportionally higher than previous m

113 Under typical clinical circumstances, burst sizes needed to be 3 to 5 mm in order to be reliab

114 latent phase of approximately 60 min, and a burst size of 20 to 30 particles per cell at 28 degrees

115 (26 h) suggested an 11 h latent period and a burst size of 871 by plaque assay, whereas phageFISH ide

116 5 min, the phage WCT72P1 and WAG25P1 had the burst size of about 45 virions and 61 virions per infect

117 The clonal burst size of CD4 T cells is predicted to be less than t

118 absence of efficient antibodies, the optimal burst size of lytic viruses would be only a few virus pa

119 ither kind of EGS construct is used in vivo, burst size of phage lambda is reduced by > or = 40%.

120 is NCK203 to lyse 15 min early, reducing the burst size of phi31 100-fold.

121 ty of the response controlled in part by the burst size of T cells expanded from effector/memory prec

122 hibitor of host RNA polymerase, restores the burst size of T7 phage on udk-overexpressing hosts to no

123 cyclophosphamide treatment and how increased burst size of the mutated virus will affect the growth o

124 decrease from 4 mm to eventually 1 mm if the burst size of the virus is triple that which is currentl

125 The initial burst size of these mutations was similar to that of the

126 lated globin genes are cotranscribed in cis, burst sizes of both genes are comparable.

127 of CD8(+) T cells, BLC-stimulated very large burst sizes of CTL were observed from both naive and mem

128 e body, we estimate an average in vivo viral burst size on the order of 104 virions per cell.

129 of consecutive MSNA bursts; while individual burst size only had a mild influence.

130 th (i) latent period reductions, (ii) larger burst sizes, or (iii) faster virion binding to bacteria.

131 to the early antigen load and initial clonal burst size, persist in the host as a stable pool of memo

132 rulence as measured by in vitro growth rate, burst size, plaque morphology, and interferon-gamma sens

133 In the limit gamma->0, the average burst size reaches a maximum set by the closing rate hc.

134 st frequency approximately halves, while the burst size remains mostly unchanged.

135 ven though they have qualitatively different burst-size statistics and regulatory parameters.

136 aused a more than a 4-fold reduction of E217 burst size, suggesting a catalytic amount of the protein

137 een shown to be dependent upon initial virus burst size surpassing a critical growth threshold of 510

138 We introduce a new concept of effective burst size that accounts for the fact that successful ho

139 nheritable changes in plating efficiency and burst size that depended on which host strain it most re

140 infectious virus with delayed kinetics and a burst size that was significantly decreased for the ICP0

141 wo intuitive parameters, burst frequency and burst size, the cell-cycle dependence of which has not b

142 Whereas the Sp1BS element regulates burst size, the Inr element regulates burst frequency.

143 include the optimization of effector T cell burst sizes, the use of adjuvants, cytokines and co-stim

144 A fundamental property of viruses is their burst size-the amount of progeny produced during one rou

145 y, whereas stronger expression loci modulate burst size to increase activity.

146 achieving an order-of-magnitude increase in burst size using a mechanism called lysis inhibition (LI

147 analyzed to identify factors contributing to burst size variation.

148 s the human genome, both burst frequency and burst size vary by chromosomal location, and transcripti

149 eriod and the relative contribution of phage burst size versus latent period toward plaque size.

150 P(i) burst size was 0.31, indicating that the equilibrium of

151 oximately 100 supercoils per second (average burst size was 6.2 supercoils).

152 The P(i)-burst size was low (0.46 mol/mol), indicating that the e

153 A linear relation between DNA length and burst size was seen from 564 bp to 27.5 kbp.

154 ion of BISC found bursting frequency but not bursting size was strongly associated with gene expressi

155 of A3G (hypermutation and reduction of viral burst size) were necessary to replicate the experimental

156 ikely driven by random variation in parasite burst size, which is linked to the rate of host cells lo

157 primarily regulates frequency, MYC regulates burst size, while cohesin and Bromodomain-containing pro

158 trolled stress response is regulated via the burst size, while that of the sigma(54)-controlled stres

159 h of replication cycle, virus half-life, and burst size, will also be important to the process optimi

160 ilibrium is postulated, to reconcile reduced burst sizes with full activity of the mutant enzymes.

161 phages showed short replication times, large burst sizes with rapid adsorptions.

162 ne LNCaP and a significant increase of virus burst size, with no reduction in specificity of CV706-ba

163 These data suggest that the response of burst size within each burst is augmented for the barore

164 Quantitation of the "burst size" within naive cells further demonstrated that