LIFE01200604005 Shri Somnath Ghosh - Homi Bhabha National ...

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16 S. <strong>Ghosh</strong> et al. / Mutation Research 716 (2011) 10–19 Fig. 6. Phosphorylation of Chk1 and Chk2 at 4 h after exposure to 1 Gy -rays or carbon irradiation in A549 cells. (A) Representative image showing p-Chk1 4 h after irradiation. Graph represents relative phosphorylation of Chk1 as determined by ImageJ software. (B) Representative image showing p-Chk2 4 h after irradiation. Graph represents relative phosphorylation of Chk2 as determined by ImageJ software. Each phospho-Chk1 or phospho-Chk2 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. At least 100 cells per experiment were analyzed from three independent experiments. Data represents means ± SD of three independent experiments. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of the article.) high LET ions. Presence of ATM foci in only half of carbon irradiated cells while BRCA1 foci in all the cells also suggest that BRCA1 is associated with different proteins and may not require activated ATM. Further study on co-localization experiment for BRCA1 with ATM by immunofluorescence would provide better understanding of repair responses elicited by low and high LET radiations. Number of Chk2 foci, another important regulator of HRR, also did not seem to parallel ATM foci. This, along with the fact that the survival of the cells is only 20% (Fig. 1) and many apoptotic nuclei are present at 4 h (Fig. 8) indicates that these macromolecular complexes containing BRCA1 may be involved in apoptotic responses after a complex damage to the DNA. Recent studies suggest multifunctional nature of BRCA1 in maintaining genome integrity. It has been shown to play an important role in apoptosis and cell cycle control and does so by associating in distinct protein complexes [37]. However, further studies on BRCA1 and apoptosis again need to be experimentally addressed. The cytoplasmic MAPK pathways, ERK and JNK, that feed into and are fed upon by DNA damage repair signaling also play an equally important role in deciding the fate of the irradiated cell. Reactive oxygen species generated after -rays irradiation has been thought to be one of the mechanisms for early activation of these kinases [18]. ATM has been shown to enhance repair via activation of ERK pathway [35] and inhibition of JNK [21]. Observed activation of ERK (Fig. 7A) but not JNK (Fig. 7B) in -rays irradiated cells indicated the dominance of pro-survival pathways.
S. <strong>Ghosh</strong> et al. / Mutation Research 716 (2011) 10–19 17 Fig. 7. Phosphorylation of ERK (pERK) and JNK (pJNK) in A549 cells at different time periods (h) after exposure to 1 Gy dose of -rays or carbon ion irradiation. Treated and untreated cells were immunoblotted and detected using anti-phospho ERK (panel A) or anti phospho JNK (panel B). One representative image of three independent experiments is shown here. Bar graph represents the relative pERK (panel A) and pJNK (panel B) band intensities plotted against time. The intensities of pERK/pJNK were obtained after dividing them with the respective loading control intensities and have been normalized for comparison. Data represents means ± SEM of three independent experiments. Fig. 8. Apoptosis in carbon irradiated A549 cells. (A) Apoptotic nuclei of A549 cells were visualized and quantified by using DAPI staining, 4 h after carbon or -rays irradiation (1 Gy). (B) Graph showing the percentage of cells with apoptotic nuclei. At least 100 cells per experiment were analyzed from three independent experiments. (C) Representative immunoblot image depicting upregulation of Bax, observed at various time periods (2, 3, 4 and 6 h) after carbon irradiation (1 Gy).
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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
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CHAPTER 3 RESULTS 80 NM_002185 IL7R
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CHAPTER 3 RESULTS SAA2 149 AU134977
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CHAPTER 3 RESULTS 221 LOC643167 RNA
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CHAPTER 3 RESULTS 299 BF244402 FBXO
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CHAPTER 3 RESULTS CDK4) 57 AU152107
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CHAPTER 3 RESULTS 134 AL045793 METT
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CHAPTER 3 RESULTS 58 AF237813 ABAT
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CHAPTER 3 RESULTS 127 AI809749 ORMD
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CHAPTER 3 RESULTS 31 BE615699 UNC84
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CHAPTER 3 RESULTS 47 AF026303 SULT1
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CHAPTER 3 RESULTS 117 BF062193 CYor
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CHAPTER 3 RESULTS 187 AL036662 ---
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CHAPTER 3 RESULTS 52 AV686514 EMP2
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CHAPTER 3 RESULTS exposed to 10 Gy
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CHAPTER 3 RESULTS Fig.3.1.4 Gene ex
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CHAPTER 3 RESULTS Fig. 3.1.6 Radiat
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CHAPTER 3 RESULTS Fig. 3.1.7 Transl
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CHAPTER 3 RESULTS 3.1.9 Stabilizati
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CHAPTER 3 RESULTS 23±1.5% (Fig. 3.
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CHAPTER 3 RESULTS whereas only the
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CHAPTER 3 RESULTS with equal doses
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CHAPTER 3 RESULTS Fig.3.3.1.2 Forma
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CHAPTER 3 RESULTS Fig.3.3.1.3 Phosp
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CHAPTER 3 RESULTS (7.5±0.64) (Fig.
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CHAPTER 3 RESULTS Fig.3.3.1.7b Phos
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CHAPTER 3 RESULTS 3.3.2 Oxygen beam
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CHAPTER 3 RESULTS in all the cells.
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CHAPTER 3 RESULTS 3.3.2.3 Radiation
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CHAPTER 3 RESULTS Fig.3.3.2.7 Apopt
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CHAPTER 3 RESULTS PMA stimulated U9
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CHAPTER 3 RESULTS Fig.3.4.2. Exista
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CHAPTER 3 RESULTS up-regulation of
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CHAPTER 3 RESULTS Fig.3.4.3.2 NO pr
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CHAPTER 3 RESULTS 3.4.3.4 Apoptotic
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CHAPTER 3 RESULTS 3.4.4 Bystander e
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CHAPTER 3 RESULTS Fig.3.4.4b DNA da
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CHAPTER 3 RESULTS Fig.3.4.5a Gene e
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CHAPTER 4 DISCUSSION DISCUSSION 185
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CHAPTER 4 DISCUSSION directly expos
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CHAPTER 4 DISCUSSION dose is delive
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CHAPTER 4 DISCUSSION A clear cause
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CHAPTER 4 DISCUSSION 4.2 Proton bea
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CHAPTER 4 DISCUSSION Although the e
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CHAPTER 4 DISCUSSION Similar number
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CHAPTER 4 DISCUSSION the mechanism
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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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