ライフサイエンスコーパス: OIS

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

2 OIS is characterized by a stable proliferation arrest an

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

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

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

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

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

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

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

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

11 tivation may represent a mechanism to bypass OIS.

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

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

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

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

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

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

18 he levels of these DNA repair factors during OIS.

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

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

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

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

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

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

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

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

27 reas ectopic expression of hTERT facilitated OIS escape.

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

29 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%

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

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

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

33 CNA1 in the cytoplasm and caused escape from OIS.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

57 ole of deoxyribonucleotides in regulation of OIS.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 ansformation is oncogene-induced senescence (OIS).

96 nsformation and oncogene-induced senescence (OIS).

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

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

99 mately triggers oncogene-induced senescence (OIS).

100 suppression of oncogene-induced senescence (OIS).

101 by suppressing oncogene-induced senescence (OIS).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

118 The OIS response to ipsilateral central pad stimulation was

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

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

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

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

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

124 as increased in tumor transplants undergoing OIS.

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

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

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

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

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

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