2010-08-012024-05-15https://scholars.lib.ntu.edu.tw/handle/123456789/661890摘要：我們先前的研究顯示人類p29蛋白屬於與染色質結合的蛋白質，細胞若轉殖p29的短鏈 siRNA會造成進行DNA複製的細胞減少，利用紫外光照射已轉殖p29短鏈 siRNA的細胞，結果會降低ATM與Chk1的磷酸化，推測缺少p29蛋白的細胞無法完成DNA複製的先期準備工作，因而減少ATM與Chk1的磷酸化，顯示p29與ATM的活化有關；我們與國家動物中心合作已建立mp29基因轉殖鼠，為了探討mp29基因轉殖鼠是否能補救ATM基因剔除鼠不孕的現象，我們將mp29基因轉殖鼠與ATM基因剔除鼠交配，觀察子代精虫發育情形並研究其可能機制。<br> Abstract: Our previous data demonstrated that the phosphorylation of ATM kinase at S1981 was suppressed in p29-depleted HeLa cells with UV irradiation (Cancer Res. 66, 8484-8491, 2006), suggesting a functional relevance between p29 and ATM. Recently, we generated mp29 transgenic mice and preliminary results showed that these mp29 overexpressed mice are less sensitive to UV irradiation compared with wild-type mice. Here, we would like to investigate whether mp29 overexpression could rescue the prophase-I arrest characteristic of Atm-deficient spermatocytes.p29transgenic micegene-trapp29transgenic micegene-trap