LIFE01200604005 Shri Somnath Ghosh - Homi Bhabha National ...

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CHAPTER 3 RESULTS (7.5±0.64) (Fig. 3.3.1.5) and the foci, although less in number were larger in size than gamma induced foci. Presence of BRCA1 foci in all cells irradiated after carbon irradiation indicates that BRCA1 might be the important player in response to complex DNA damage induced by high LET radiation. Fig.3.3.1.5 Phosphorylation of BRCA1 at 4h after exposure to 1Gy gamma or carbon irradiation in A549 cells. (A) Representative image showing p-BRCA1 foci 4 hours after irradiation. Each phospho-BRCA1 antibody was indirectly labeled with Molecular Probe 488 secondary antibody (green) and cells were mounted with ProLong Gold antifede with DAPI (blue). All images were captured using Carl Zeiss confocal microscope with the same exposure time. (B) Graph represents average numbers of foci per cell, percentage of cells showing the foci is marked above the bars. (C) Graph represents relative intensity of p-BRCA1 as determined by ImageJ software. At least 100 cells per experiment were analyzed from three independent experiments. Data represents means ± SD of three independent experiments. 151
CHAPTER 3 RESULTS 3.3.1.6 Activation of downstream effectors; Chk1 and Chk2 Activation of ATM, ATR and BRCA1 after DNA damage leads to the activation of further downstream components including Chk1 and Chk2. After activation in the nuclei, Chk1 and Chk2 move to cytoplasm. Phospho Chk1, the major target of ATR, was found to increase in nuclei of carbon-irradiated cells but not in gamma (Fig.6 A). Marginal activation of Chk2, the preferred substrate of ATM, was observed in the nucleus in all the cells irrespective of radiation quality (Fig.6 B). Many pChk2 foci were observed outside the nuclei of carbon irradiated cells unlike gamma-irradiated cells (Fig.6 C). 3.3.1.7 Activation of intracellular MAPKs, ERK and JNK ERK1/2 showed significant activation 1 hour after gamma irradiation and thereafter the increase was persistent till 4 hours (Fig.3.3.1.7a), while JNK did not show any activation after gamma irradiation (Fig.3.3.1.7b). Interestingly, after carbon irradiation the activation pattern of these kinases was exact opposite. ERK was not activated at all after carbon irradiation (Fig.3.3.1.7a) while JNK showed marginal activation at 15 minutes that remained so till 1 hour (Fig.3.3.1.7b). 3.3.1.8 Apoptosis At 4 hours after irradiation, morphological features of DAPI stained apoptotic nuclei were scored and many apoptotic nuclei were observed in cells irradiated with carbon ion but not in gamma irradiated cells (Fig. 3.3.1.8 A, B). Upregulation of Bax expression was also observed as early as 2 hours after carbon ion irradiation indicating apoptotic tendency of the cells (Fig. 3.3.1.8C). Gamma irradiated cells did not show any upregulation of Bax. 152
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RADIATION INDUCED SIGNALING IN MAMM
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DECLARATION I, hereby declare that
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CONTENTS Page No. SYNOPSIS………
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2.11 Measurement of NO production
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PREAMBLE SYNOPSIS Ionising radiatio
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SYNOPSIS Aims and Objectives: To St
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SYNOPSIS 2.6 Immunofluorescence sta
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SYNOPSIS ATM gene expression, which
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SYNOPSIS Percentage Survival 100 80
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SYNOPSIS Ratio of Rad52 to Actin Ra
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Relative Phosphorylation 45 40 35 3
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SYNOPSIS Fig. 3.3A Clonogenic Cell
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SYNOPSIS (A) Av No. of phospho BRCA
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SYNOPSIS Percentage Survival 120 10
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SYNOPSIS Fig.3.4B. Existance of cro
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SYNOPSIS Fig. 3.4EDNA damage in EL-
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SYNOPSIS subsequent cytotoxicity ca
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SYNOPSIS [4] Hall, E. J. Radiobiolo
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CHAPTER 1 INTRODUCTION INTRODUCTION
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CHAPTER 1 INTRODUCTION 15.8% 9.56%
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CHAPTER 1 INTRODUCTION far apart an
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CHAPTER 1 INTRODUCTION and are more
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CHAPTER 1 INTRODUCTION 1.3 DNA dama
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CHAPTER 1 INTRODUCTION associates w
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CHAPTER 1 INTRODUCTION are unable t
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CHAPTER 1 INTRODUCTION Perhaps one
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CHAPTER 1 INTRODUCTION occurs at DS
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CHAPTER 1 INTRODUCTION related prot
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CHAPTER 1 INTRODUCTION damage must
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CHAPTER 1 INTRODUCTION At the prese
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CHAPTER 1 INTRODUCTION predominant
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CHAPTER 1 INTRODUCTION provide a me
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CHAPTER 1 INTRODUCTION hypersensiti
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CHAPTER 1 INTRODUCTION cycle-specif
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CHAPTER 1 INTRODUCTION 1.4 Overview
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CHAPTER 1 INTRODUCTION 1.4.1 Radiat
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CHAPTER 1 INTRODUCTION interaction
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CHAPTER 1 INTRODUCTION p90S6 kinase
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CHAPTER 1 INTRODUCTION CD4 (formerl
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CHAPTER 1 INTRODUCTION unrepaired d
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CHAPTER 1 INTRODUCTION well to the
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CHAPTER 1 INTRODUCTION 1.6 Radiatio
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CHAPTER 1 INTRODUCTION becomes pote
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CHAPTER 2 MATERIALS AND METHODS MAT
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CHAPTER 2 MATERIALS AND METHODS 2.2
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CHAPTER 2 MATERIALS AND METHODS res
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CHAPTER 2 MATERIALS AND METHODS Arr
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CHAPTER 2 MATERIALS AND METHODS PBS
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CHAPTER 2 MATERIALS AND METHODS the
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CHAPTER 2 MATERIALS AND METHODS 2.1
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CHAPTER 3 RESULTS RESULTS 93
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CHAPTER 3 RESULTS fractionated regi
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CHAPTER 3 RESULTS On comparison of
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CHAPTER 3 RESULTS Table 3.1.2A List
Page 110 and 111: CHAPTER 3 RESULTS 80 NM_002185 IL7R
Page 112 and 113: CHAPTER 3 RESULTS SAA2 149 AU134977
Page 114 and 115: CHAPTER 3 RESULTS 221 LOC643167 RNA
Page 116 and 117: CHAPTER 3 RESULTS 299 BF244402 FBXO
Page 118 and 119: CHAPTER 3 RESULTS CDK4) 57 AU152107
Page 120 and 121: CHAPTER 3 RESULTS 134 AL045793 METT
Page 122 and 123: CHAPTER 3 RESULTS 58 AF237813 ABAT
Page 124 and 125: CHAPTER 3 RESULTS 127 AI809749 ORMD
Page 126 and 127: CHAPTER 3 RESULTS 31 BE615699 UNC84
Page 128 and 129: CHAPTER 3 RESULTS 47 AF026303 SULT1
Page 130 and 131: CHAPTER 3 RESULTS 117 BF062193 CYor
Page 132 and 133: CHAPTER 3 RESULTS 187 AL036662 ---
Page 134 and 135: CHAPTER 3 RESULTS 52 AV686514 EMP2
Page 136 and 137: CHAPTER 3 RESULTS exposed to 10 Gy
Page 138 and 139: CHAPTER 3 RESULTS Fig.3.1.4 Gene ex
Page 140 and 141: CHAPTER 3 RESULTS Fig. 3.1.6 Radiat
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Page 144 and 145: CHAPTER 3 RESULTS 3.1.9 Stabilizati
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Page 148 and 149: CHAPTER 3 RESULTS whereas only the
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Page 156 and 157: CHAPTER 3 RESULTS Fig.3.3.1.2 Forma
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Page 170 and 171: CHAPTER 3 RESULTS 3.3.2.3 Radiation
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Page 178 and 179: CHAPTER 3 RESULTS PMA stimulated U9
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Page 190 and 191: CHAPTER 3 RESULTS Fig.3.4.4b DNA da
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CHAPTER 4 DISCUSSION Thus unlike th
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CHAPTER 4 DISCUSSION different from
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CHAPTER 4 DISCUSSION upregulates ma
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CHAPTER 4 DISCUSSION Numerous studi
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CHAPTER 4 DISCUSSION inhibition of
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CHAPTER 4 DISCUSSION The survival o
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CHAPTER 5 REFERENCES [1] Khan, F. T
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CHAPTER 5 REFERENCES [19] Woo, R. A
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CHAPTER 5 REFERENCES [35] Nghiem, P
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CHAPTER 5 REFERENCES [52] McKay, B.
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CHAPTER 5 REFERENCES [69] Cary, R.
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CHAPTER 5 REFERENCES [84] Uziel, T.
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CHAPTER 5 REFERENCES [98] Liu, Y.;
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CHAPTER 5 REFERENCES [111] Fei, P.;
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CHAPTER 5 REFERENCES [127] Frank, K
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CHAPTER 5 REFERENCES [141] Pierce,
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CHAPTER 5 REFERENCES [156] Roots, R
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CHAPTER 5 REFERENCES [171] Xia, Z.;
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CHAPTER 5 REFERENCES (MAP) kinase c
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CHAPTER 5 REFERENCES phosphorylatio
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CHAPTER 5 REFERENCES [211] Anderson
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CHAPTER 5 REFERENCES [229] Konca, K
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CHAPTER 5 REFERENCES [245] Kastan,
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CHAPTER 5 REFERENCES [261] Miralbel
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CHAPTER 5 REFERENCES [278] Weizman,
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CHAPTER 5 REFERENCES [294] Zhou, H.
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PUBLICATIONS AND PRESENTATIONS Publ
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Mutation Research 729 (2012) 61-72
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S. Ghosh, M. Krishna / Mutation Res
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Cancer Invest Downloaded from infor
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