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Signalling Pathways, Tumour Necrosis Factor, Chromatin Remodelling, Epigenetics, Tumour Suppressive, Oncogenic Process, Lagging Strand, Eukaryotic Cells, Cancer Cell Growth, Lesion Specific are some points this exam paper.
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Page 1 of 2 Semester 2 Examinations 2011/ Exam Code(s) 4BY Exam(s) Module Code(s) BG41 5 Module(s) Molecular and Cellular Biology Paper No. 1 Repeat Paper External Examiner(s) Prof. M. J. R. Stark Internal Examiner(s) Dr A. Gorman, Dr L. Byrnes, Prof N. Lowndes, Dr H.-P. Nasheuer, Dr M. Carty, Prof R. Lahue, Prof A. Samali Instructions: Answer three questions. Please start each answer with a new answer book and clearly indicate the number on the front. All questions carry equal marks. Duration 3 hours No. of Pages 2 Discipline(s) Biochemistry Course Co-ordinator(s) Dr. Andrew Flaus Requirements : MCQ Release to Library: Yes x No Handout Statistical/ Log Tables Cambridge Tables Graph Paper Log Graph Paper Other Materials
Page 2 of 2 BG415 Molecular and Cellular Biology Time allowed: Three Hours Write on three of the following topics. Please start each answer with a new answer book and clearly indicate the number on the front.
1. Using diagrams to illustrate your answer, describe the signalling pathways that are activated downstream of the tumour necrosis factor (TNF) receptor. 2. Discuss the roles of non-coding RNAs and chromatin remodelling in epigenetics. 3. The DNA damage response is tumour suppressive. Discuss this statement with respect to the oncogenic process. 4. The replication of the lagging strand creates multiple challenges to eukaryotic cells. Discuss the differences of the leading and lagging strand DNA synthesis and how telomeres can regulate cancer cell growth. 5. Answer EITHER part (a) OR part (b) OR part (c) of the following question: a. ‘Excision repair involves the use of lesion-specific DNA damage recognition proteins, and sequence information from the undamaged strand, to maintain genome stability and prevent cancer.’ Discuss this statement with reference to nucleotide excision repair. OR b. Describe what is necroptosis and how it is initiated and regulated at the molecular level. OR c. Answer both parts of this question: i) Compare and contrast ‘forward genetic’ and ‘reverse genetic’ screens in mice. (70% of marks) ii) Choose any one specific mouse model that was discussed in the Mutagenesis lectures and summarize a key experiment that helped reveal gene function. (30% of marks)