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Förslaget inkom 2008-02-26

Gene Regulation by p73

OBS! ANSÖKNINGSTIDEN FÖR DETTA EXJOBB HAR LÖPT UT.
The project focuses on the transcription factor p73. The p73 protein was discovered in 1997 as a member of the p53 family. However, while the function of p53 as a tumor suppressor is well known, the role for p73 in tumorigenesis has, since its discovery, been debated. This is mainly due to the P73 gene giving rise to a complex pattern of antagonizing isoforms. There are two main classes of isoforms, so called TA and ?N. In most cases, the TA (for transactivation) isoforms works as tumor suppressor proteins, able to induce apoptosis (cell death) upon different stimuli. The ?N isoforms, on the other hand, can protect cells from dying and are regarded as potential oncogenes. In addition, the P73 gene can give rise to a range of different C-terminal isoforms, each one with their own specific properties.
p73 could be a potential therapeutic target as depicted by:
• p73 deficient mice display neurological and immunological defects
• ?Np73 expression can give rise to malignant transformation and tumor growth
• p73 is able to induce phosphorylation of tau, a salient feature of Alzheimer’s disease

This specific project focuses on the role of p73 as a transcription factor, and how the various domains of the protein affect the transcriptional activity differentially on promoters of target genes. It also takes into account the possible effect of other proteins on the transcriptional activity of p73.
We are studying the activity of p73 using
• Chromatin immunoprecipitation (ChIP)
• Immunoprecipitation (IP)
• Luciferase gene reporter assay
• Reverse Transcriptase-PCR
• Immunocytochemistry
• Other relevant methods.

Are you interested in participating, please contact: Ulrika.Nyman@ki.se, 08-524 87 554

Division of Toxicology, Institute for Environmental Medicine (IMM), KI Solna
Supervisors: docent Bertrand Joseph and PhD-student Ulrika Nyman


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