ライフサイエンスコーパス: OIS

1 OIS cells are also characterized by marked epigenetic ch

2 OIS is a serious blinding condition that occurs in the s

3 OIS is characterized by a stable proliferation arrest an

4 .277 [0.220 to 0.446]; lean vs OIR P = .002; OIS: 0.340 [0.048 to 0.491]; OIS vs OIR P = .08), and a

5 [31.6 to 83.3] pg/mL; lean vs OIR P = .002; OIS: 54.3 [39.3 to 77.2] pg/mL; OIS vs OIR P = .011).

6 mumol x kg-1 x min-1; lean vs OIR P = .004; OIS: 2.63 [1.22 to 4.52] mumol x kg-1 x min-1; OIS vs OI

7 S: 2.63 [1.22 to 4.52] mumol x kg-1 x min-1; OIS vs OIR P = .09), a blunted median (IQR) improvement

8 we used 2D-Optical Imaging Spectroscopy (2D-OIS) to measure changes in cerebral haemodynamics within

9 ed using 2D-optical imaging spectroscopy (2D-OIS).

10 s OIR P = .002; OIS: 0.340 [0.048 to 0.491]; OIS vs OIR P = .08), and a reduced median (IQR) PYY resp

11 Moreover, depletion of XPO7 alleviated OIS and increased tumor formation in a mouse model of li

12 Of these, 40 (34%) experienced an OIS event.

13 r initiation, we introduce the concept of an OIS spectrum, where oncogenic dosage-dependent cellular

14 Sample dilution with an OIS and the surfactant Triton X-100 (inorganic media) or

15 llowing Ras-induced C/EBPbeta activation and OIS to proceed.

16 sis on the involved side was worse in AF and OIS compared to BRAO, CRAO, and NA-AION (p<0.0001).

17 n-induced, p53-independent growth arrest and OIS and p53-dependent apoptosis protect developing thymo

18 beta-catenin still results in DNA damage and OIS, but the thymocytes survive and eventually progress

19 Iso-orientation maps obtained by fMRI and OIS were well matched, indicating that areas of the high

20 Compared with the lean and OIS groups, the OIR group showed a less marked median (I

21 ing can identify critical features of RS and OIS and discover determinants of acute senescence and SA

22 ign LLC, Clifton Park, NY), and AutoMontage (OIS, Sacramento, CA).

23 Using a variety of biomarkers, OIS has been previously reported in a wide range of huma

24 Both OIS and RS are accompanied by A-to-B and B-to-A compartm

25 tivation may represent a mechanism to bypass OIS.

26 transformation was associated with decreased OIS and SASP and a protumorigenic tumor microenvironment

27 oting genes and the avoidance of deleterious OIS- or TIS-related tumor secretomes, which can promote

28 ression could be contained via p53-dependent OIS and TSH is a major disruptor of this balance.

29 Upon DNMT1 depletion, OIS cells transition to a 3D genome conformation akin to

30 Genetically disabling OIS in Kras mice caused RelA to promote tumor proliferat

31 ture B (eBm5) cells was able to discriminate OIS patients from controls with a specificity of 88%.

32 r results define the oncogenic dosage-driven OIS spectrum, reconciling the senescence and tumour init

33 HG and INK4A, which becomes activated during OIS and interacts with the MIR31HG promoter.

34 -dependent kinase inhibitor p21(CIP1) during OIS.

35 mechanisms behind DNA repair defects during OIS remain poorly understood.

36 hat an increased nuclear pore density during OIS is responsible for SAHF formation.

37 he levels of these DNA repair factors during OIS.

38 RES-dependent translation is impaired during OIS ex vivo and on DNA damage in vivo.

39 s dramatic genome-wide relocalization during OIS, including its removal from SASP gene chromatin.

40 Here, we show that during OIS, a switch between cap- and internal ribosome entry s

41 egulation of vitamin D receptor (VDR) during OIS, and a role for the vitamin D/VDR axis regulating th

42 we demonstrate that cells frequently escape OIS induced by oncogenic H-Ras and B-Raf, after a prolon

43 ws human prostate epithelial cells to escape OIS caused by the activated Ras oncogene or by reduced e

44 serrated neoplasia requires cells to escape OIS via inactivation of tumor suppressor pathways.

45 contra- or ipsilateral forepaws also evoked OIS activation in the posteriorly located 'hindlimb' reg

46 reas ectopic expression of hTERT facilitated OIS escape.

47 to RAS-induced tumorigenesis by facilitating OIS escape, highlighting its physiological role as a tum

48 ths after onset was 6% (95% CI: 2%, 17%) for OIS, 3% (95% CI: 0.4%, 19%) for AF, and 1% (95% CI: 0.3%

49 ivation of mTORC1 and mTORC2 is required for OIS evasion in human melanomas harboring oncogenic BRAF

50 the DNA damage response is not required for OIS in HMEC.

51 anscription factor C/EBPbeta is required for OIS in primary fibroblasts but is downregulated by H-Ras

52 ondrial Ca(2+) load and promotes escape from OIS-induced senescence.

53 CNA1 in the cytoplasm and caused escape from OIS.

54 In a hepatocyte OIS model in vivo, ectopic expression of NRAS(G12V) does

55 hnology and methodology that have made human OIS easier to implement and more accessible, including i

56 EBV peptides, may be useful for identifying OIS in immunosuppressed patients.

57 tivity for detecting over-immunosuppression (OIS) events in kidney recipients in the short term.

58 for the detection of over-immunosuppression (OIS) events.

59 bition on SASP gene expression do not impair OIS and, furthermore, abolish the ability of the SASP to

60 et of ocular condition was 52% in AF, 22% in OIS, 22% in BRAO, 21% in CRAO, and 6% in NA-AION patient

61 our data demonstrate that cells arrested in OIS retain the potential to escape senescence by mechani

62 ntify a functional role for PP2A-B56alpha in OIS of melanocytic cells.

63 ore, they implicate the RPL5-MDM2 complex in OIS and demonstrate a link between spliceosomal and ribo

64 en proposed as major causes of DNA damage in OIS cells.

65 he involved side was significantly higher in OIS, AF, and CRAO compared to NA-AION (p=0.002, p=0.003,

66 or 3 (TFF3) was found to be overexpressed in OIS hepatocytes and in hepatocellular carcinoma.

67 of C-MYC in melanoma cells and their role in OIS are unknown.

68 e-associated heterochromatin foci (SAHFs) in OIS but not in RS.

69 dentify the lncRNA MIR31HG as upregulated in OIS and find that knockdown of MIR31HG promotes a strong

70 (HMEC) undergo a p16/RB- and p53-independent OIS in response to oncogenic RAS that requires TGF-beta

71 ppressed C-MYC in melanoma cells and induced OIS, whereas depletion of PP2A-B56alpha in normal human

72 In this cross-sectional study, lean, OIS, and OIR youth demonstrated different associations b

73 ng the mechanisms that initiate and maintain OIS in epithelial cells may provide a foundation for fut

74 located SII region that yielded the maximal OIS response to stimulation of the contralateral central

75 M or CHK2 was unable to prevent RAS-mediated OIS, arguing that the DNA damage response is not require

76 IR P = .002; OIS: 54.3 [39.3 to 77.2] pg/mL; OIS vs OIR P = .011).

77 onset of ocular condition occurred in 17% of OIS, 11% of AF, 7% of CRAO, 6% of NA-AION, and 3% of BRA

78 ion of DNA repair factors, in the context of OIS.

79 Although the contribution of OIS to disease progression is undetermined, recent evide

80 ore was robust to alternative definitions of OIS ranging from mild to severe.

81 potassium channel KCNA1 as a determinant of OIS escape that can license tumor growth.

82 Here, we show that engagement of OIS in primary human melanocytes, specifically by melano

83 ient to trigger immunosurveillance escape of OIS hepatocytes, resulting in premalignant to malignant

84 naling molecules, safety nets in the form of OIS, growth arrest and apoptosis prevent accidental tran

85 Induction of OIS has been attributed to either RAS-mediated productio

86 However, the interactions of OIS cells with the immune system are still poorly define

87 oRNA (miRNA) screen to identify mediators of OIS and show that siRNA-mediated knockdown of p21(Waf1/C

88 summarize evidence in established models of OIS including B-Raf-induced nevi, transgenic lung cancer

89 e globally assessed histone modifications of OIS cells and discovered an increase in the active histo

90 ole of deoxyribonucleotides in regulation of OIS.

91 tiles of low, intermediate, and high risk of OIS based on age and CD14 + 16 + tumor necrosis factor-a

92 a substantial shift in the estimated risk of OIS events.

93 In the adjusted model, the risk of OIS was more than 12 times higher in patients classified

94 , we have characterized a panel of potential OIS biomarkers in human and murine pancreatic intraepith

95 eas-specific inactivation of CXCR2 prevented OIS and was correlated with increased tumor proliferatio

96 own of the SWI/SNF component ARID1B prevents OIS and cooperates with RAS to induce liver tumors.

97 ("skin flutter") stimulus evoked a prominent OIS response ("activation") in an extensive anteroposter

98 we determined that RelA activation promotes OIS via elevation of the SASP factor CXCL1 (also known a

99 Indeed, many of the other proposed OIS biomarkers are detected in actively proliferating Pa

100 n arrest, suggesting that unlike quiescence, OIS requires depletion of dNTP pools and activated DNA r

101 However, the mechanisms that regulate OIS in PDAC are poorly understood.

102 ense and splice site) in genes that regulate OIS: the p16-Rb and ATM-ATR DNA damage response pathways

103 uggest a pivotal role for RelA in regulating OIS in preneoplastic lesions and implicate the RelA/CXCL

104 have determined that nuclear RelA reinforces OIS to inhibit carcinogenesis in the Kras mouse model of

105 Trp53 inactivation reversed OIS and enabled tumor transplants to grow in nude mice w

106 replicative and oncogene-induced senescence (OIS) and diminishes the DNA-damage response.

107 referred to as oncogene-induced senescence (OIS) and replicative senescence (RS), respectively, and

108 s a mediator of oncogene-induced senescence (OIS) and the senescence-associated secretory phenotype (

109 Oncogene-induced senescence (OIS) and therapy-induced senescence (TIS), while tumor-s

110 Oncogene-induced senescence (OIS) can occur in response to oncogenic insults and is c

111 Oncogene-induced senescence (OIS) constitutes a failsafe program that restricts tumor

112 al human cells, oncogene-induced senescence (OIS) depends on induction of DNA damage response.

113 Oncogene-induced senescence (OIS) is a critical tumor-suppressing mechanism that rest

114 Oncogene-induced senescence (OIS) is a potent tumor suppressor mechanism.

115 Oncogene-induced senescence (OIS) is a stable cell cycle arrest that occurs in normal

116 Oncogene-induced senescence (OIS) is a tumor-suppressive mechanism typified by stable

117 Oncogenic RAS-induced senescence (OIS) is an autonomous tumour suppressor mechanism associ

118 Oncogene-induced senescence (OIS) is an inherent and important tumor suppressor mecha

119 Oncogene-induced senescence (OIS) is considered a powerful tumor suppressor mechanism

120 Although oncogene-induced senescence (OIS) is considered a tumor suppressor mechanism, the acc

121 is mediated by oncogene-induced senescence (OIS) is considered to function as a safeguard during dev

122 Oncogene-induced senescence (OIS) is one form of senescence that occurs in response t

123 mor initiation, oncogene-induced senescence (OIS) is proposed to limit the progression of preneoplasm

124 Oncogene-induced senescence (OIS) is thought to be a barrier to malignant transformat

125 tions result in oncogene-induced senescence (OIS) of intestinal crypt cells.

126 is required for oncogene-induced senescence (OIS) of primary fibroblasts, but also displays pro-oncog

127 Oncogene-induced senescence (OIS) protects normal cells from transformation by Ras, w

128 , leading to an oncogene-induced senescence (OIS) response.

129 h arrest called oncogene-induced senescence (OIS) that serves as a fail-safe mechanism against malign

130 nfiltration and oncogene-induced senescence (OIS) was demonstrated by strong beta-gal staining and ab

131 Oncogene-induced senescence (OIS) was triggered in a subset of mouse hepatocytes, whi

132 ion can lead to oncogene-induced senescence (OIS), a barrier to cellular transformation.

133 growth arrest, oncogene-induced senescence (OIS), and apoptosis of immature thymocytes.

134 ytes experience oncogene-induced senescence (OIS), growth arrest and apoptosis.

135 During oncogene-induced senescence (OIS), heterochromatin is lost from the nuclear periphery

136 Oncogene-induced senescence (OIS), the proliferative arrest engaged in response to pe

137 cient to escape oncogene-induced senescence (OIS), thereby facilitating oncogenic cell transformation

138 ce Hsf1 affects oncogene-induced senescence (OIS), these findings suggest that Hsf1 affects tumor ini

139 cence, known as oncogene-induced senescence (OIS)-a putative autonomous tumor-suppressive mechanism.

140 by suppressing oncogene-induced senescence (OIS).

141 ansformation is oncogene-induced senescence (OIS).

142 nsformation and oncogene-induced senescence (OIS).

143 eplicative, and oncogene-induced senescence (OIS).

144 cells can enter oncogene-induced senescence (OIS).

145 nt regulator of oncogene-induced senescence (OIS).

146 mately triggers oncogene-induced senescence (OIS).

147 ce (RS) or upon oncogene-induced senescence (OIS).

148 suppression of oncogene-induced senescence (OIS).

149 or dysfunction [oncogene-induced senescence (OIS)].

150 assigned to a lean, obese insulin sensitive (OIS), or obese insulin resistant (OIR) group.

151 such as optical imaging of intrinsic signal (OIS) and single-unit electrophysiology.

152 BV-based fMRI with optical intrinsic signal (OIS) imaging, a technique that identifies sites of incre

153 with the method of optical intrinsic signal (OIS) imaging.

154 Optical imaging of intrinsic signals (OIS) offers perhaps the best combination of spatial cove

155 As SIPS/OIS bypass is a prerequisite for the immortalization of

156 oncogene-induced premature senescence (SIPS/OIS), mediated via the p16-Rb and/or ARF-p53-p21 tumour-

157 , and are therefore useful for studying SIPS/OIS bypass in isolation.

158 lls from small rodents possess only the SIPS/OIS barrier, and are therefore useful for studying SIPS/

159 An optical impedance spectroscopy (OIS) technique based on a single-mode electro-active-int

160 nt, the use of an optimum internal standard (OIS) at a concentration close to that of the analyte sig

161 Intermediate "sub-OIS" states may play a critical role in tumor initiation

162 visual loss due to ocular ischemic syndrome (OIS) with BCCAO.

163 eneral concepts of ocular ischemic syndrome (OIS), and present current scientific developments in del

164 artery occlusion, ocular ischemic syndrome (OIS), non-arteritic anterior ischemic optic neuropathy (

165 Above all, we show here that OIS with single-mode EA-IOW's provide strong analytical

166 hallmark of advanced tumors indicating that OIS serves a critical tumor-suppressive function.

167 We propose that OIS in melanocytes is accompanied by an antigen presenta

168 Recent studies suggest that OIS is associated with a significant risk of cerebrovasc

169 inical precancerous lesions; 2) suggest that OIS is targetable; and 3) propose the utilization of sen

170 The OIS response to ipsilateral central pad stimulation was

171 tor designed to act mainly to antagonize the OIS process to accelerate tumorigenesis.

172 Thus, the OIS engaged after dysregulated RAS expression provides a

173 This OIS-specific configuration brings active genes located i

174 ticular, when restricted to life-threatening OIS, the proportion of events varied from 5% to 27% amon

175 Thus, OIS with BCCAO was diagnosed.

176 Therefore, in addition to OIS, Hsf1 regulates the HuR-HIF-1 pathway, thus affectin

177 f the visual cortex, an area inaccessible to OIS imaging.

178 V) does not induce tumours, in part owing to OIS-driven immune clearance(3).

179 al distinct hepatocyte clusters with typical OIS or progenitor-like features, corresponding to high a

180 Cells undergoing OIS express a wide variety of secreted factors that affe

181 Cells undergoing OIS secrete multiple CXCR2-binding chemokines in a progr

182 as increased in tumor transplants undergoing OIS.

183 In vitro, OIS melanocytes activate T-cell proliferation.

184 so exhibited significant although 75% weaker OIS activation in response to stimulation of the ipsilat

185 gest that Hsf1 affects tumor initiation when OIS plays a role.

186 -AION, 203 with CRAO, 127 with BRAO, 80 with OIS and 52 with AF.

187 s induce expression of genes associated with OIS, growth arrest and p53-dependent apoptosis.

188 vation in area 3b previously identified with OIS as neural correlates of the "funneling illusion." Th