| Summary: | 碩士 === 國防醫學院 === 生物化學研究所 === 91 === p53 tumor suppressor is one of the most important proteins in regulating cell growth and protect cell from malignant transformation. In about half of tumors, p53 is inactivated or mutatede. In normal cell, the level of p53 is maintained in a low concentration by protein degradation. In response to stress (including DNA damage, hypoxia or ionic radiation) p53 can be activated and consequently the activated p53 is responsible for cell cycle arrest, apoptosis or DNA repair.
Pip, p53-interacting protein, is a ring finger-containing protein and was cloned and identified as a p53 binding protein in our laboratory. After the initial characterization, we demonstrated that Pip interacts with p53 both in vitro and in vivo. In our laboratory, we used adenoviral expression system to overexpress p53 and pip protein after infected cell line. In this overexpression condition, we would like to know how pip affects p53’s biological activities such as cell cycle arrest and apoptosis in several different experimental settings.
From the data in my thesis, pip’s functions are listed as following eight points: (1) pip significantly reduces fragmented chromosome DNAs. (2) pip’s inhibitory effect for sub-G1 formation is strictly p53-dependent. (3) pip slightly reduces the formation of fragmented DNAs and increases the number of condensed chromosomal DNAs. (4) pip reduces the scale of apoptotic chromosome degradation. (5) pip does not affect the activity of several key caspases in apoptotic pathway. (6) pip does not change p53-induced cell membrane modification. (7) pip does not affect the apoptosis derived from cells at G2/M phases. (8) pip causes G2/M arrest in p53 dependent manner.
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