LIFE01200604005 Shri Somnath Ghosh - Homi Bhabha National ...

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SYNOPSIS (A) Av No. of phospho BRCA1 Foci per cell 22 20 18 16 14 12 10 8 6 4 2 0 -2 55% Gamma Con 1 Gy 100% Carbon (B) Relative phosphorylation of BRCA 3.0 2.5 2.0 1.5 1.0 0.5 0.0 Gamma Con 1Gy Carbon Fig. 3.3E Phosphorylation of BRCA1 at 4h after exposure to 1 Gy gamma or carbon irradiation in A 549 cells. (A) Graph represents average numbers of foci per cell, percentage of cells showing the foci is marked above the bars. (B) Graph represents relative phosphorylation of 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. (A) Relative intensity of pChk1 2.5 2.0 1.5 1.0 0.5 Con 1Gy (C) Relative intensity of Chk2 2.5 2.0 1.5 1.0 0.5 Con 1Gy 0.0 Gamma Carbon 0.0 Gamma Carbon Control 1Gy (B) p-Chk2 (Gamma) p-Chk2 (Carbon) Fig.3.3F Phosphorylation of Chk1 and Chk2 at 4h after exposure to 1 Gy gamma or carbon irradiation in A 549 cells. (A) Graph represents relative phosphorylation of Chk1 as determined by ImageJ software (B) Representative image showing phosphorylation and foci formation of Chk2 shown by “arrow” between 1Gy carbon beam and 1Gy γ-radiation. Each phospho-Chk2 antibody was indirectly labeled with Molecular Probe 488 secondary antibody (green). All images were captured using Carl Zeiss confocal microscope with the same exposure time (C) Graph represents relative phosphorylation of Chk2 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. 17
SYNOPSIS Relative phosphorylation 1.5 1.0 0.5 0.0 (A) pERK(gamma) pERK(carbon) Con 0.1 0.5 1 2 3 4 6 Time after irradiation (hrs) Relative phosphorylation (B) 1.5 1.0 0.5 0.0 pJNK(gamma) pJNK(carbon) Con 0.1 0.5 1 2 3 4 6 Time after irradiation (Hrs) Carbon Gamma Con 10 30 1 2 3 4 6 Lane Con 10 30 1 2 3 4 6 pERK pJNK Fig.3.3G Phosphorylation of ERK (pERK) and JNK (pJNK) in A549 cells cells at different time periods (hours) after exposure to 1 Gy dose of gamma or carbon ion irradiation. Treated and untreated cells were immunoblotted and detected using antiphospho 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. (A) 30 Control 1Gy Gamma 1Gy Carbon (B) % Apoptotic Nuclei at 4h 25 20 15 10 5 0 Con Gamma Carbon 1 Gy Con 2h 3h 4h 6h (C) Bax Lane Fig.3.3H Apoptosis in carbon irradiated A549 cells. Panel A, Apoptotic nuclei of A549 cells were visualized and quantified by using DAPI staining, 4 hours after carbon or gamma irradiation (1Gy). Panel B, The percentage of cells with apoptotic nuclei are represented as graph. At least 100 cells per experiment were analyzed from three independent experiments. Panel C, Representative immunoblot image depicting upregulation of Bax, observed at various time periods (2, 3, 4 and 6 hours) after carbon irradiation (1 Gy). 18
Page 1: RADIATION INDUCED SIGNALING IN MAMM
Page 4 and 5: DECLARATION I, hereby declare that
Page 6 and 7: CONTENTS Page No. SYNOPSIS………
Page 8 and 9: 2.11 Measurement of NO production
Page 10 and 11: PREAMBLE SYNOPSIS Ionising radiatio
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Page 16 and 17: SYNOPSIS ATM gene expression, which
Page 18 and 19: SYNOPSIS Percentage Survival 100 80
Page 20 and 21: SYNOPSIS Ratio of Rad52 to Actin Ra
Page 22 and 23: Relative Phosphorylation 45 40 35 3
Page 24 and 25: SYNOPSIS Fig. 3.3A Clonogenic Cell
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Page 30 and 31: SYNOPSIS Fig.3.4B. Existance of cro
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Page 36 and 37: SYNOPSIS [4] Hall, E. J. Radiobiolo
Page 38 and 39: CHAPTER 1 INTRODUCTION INTRODUCTION
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Page 42 and 43: CHAPTER 1 INTRODUCTION far apart an
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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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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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Cancer Invest Downloaded from infor
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