君，已阅读到文档的结尾了呢~~
《细胞生物学》论述练习题及参考答案
扫扫二维码，随身浏览文档
手机或平板扫扫即可继续访问
《细胞生物学》论述练习题及参考答案
举报该文档为侵权文档。
举报该文档含有违规或不良信息。
反馈该文档无法正常浏览。
举报该文档为重复文档。
推荐理由：
将文档分享至：
分享完整地址
文档地址：
粘贴到BBS或博客
flash地址：
支持嵌入FLASH地址的网站使用
html代码：
&embed src='/DocinViewer--144.swf' width='100%' height='600' type=application/x-shockwave-flash ALLOWFULLSCREEN='true' ALLOWSCRIPTACCESS='always'&&/embed&
450px*300px480px*400px650px*490px
支持嵌入HTML代码的网站使用
您的内容已经提交成功
您所提交的内容需要审核后才能发布，请您等待！
3秒自动关闭窗口您现在的位置：&&>&&>&&>&正文
作者：xiyang
来源：生物谷
关键词：P53,抑癌基因,癌症治疗
近日，来自俄勒冈州立大学的科学家通过研究发现了一种遗传因子Grasp（Grp1-associated scaffold protein，Grp1相关支架蛋白），其可以帮助促进P53抑癌基因的功能并抑制癌症发生。研究者说，如果找到方法来维持或者增强这种遗传因子的作用，便可以为癌症治疗提供了一条重要的新途径。
相关研究论文发表在《光化学和光生物学科学》（Photochemical and Photobiological Sciences）杂志上，作者是来自俄勒冈州立大学和俄勒冈健康与科学大学的研究团队。
P53基因涉及到损伤DNA的修复，如果细胞损伤太严重，P53基因会引发，以防癌变。P53基因的失活与很多我们所知的癌症有关，特别是皮肤癌，食道癌，结肠癌，胰腺癌，肺癌，子宫癌，以及头与颈癌症。
本文研究的第一作者，马克-雷德教授说，DNA突变在我们人体内很容易发生，比如暴露在日光下几分钟就有可能引发基因突变。P53基因和其他的一些抑癌基因就会被激活从而修复DNA损伤，如果损伤太严重不能被修复，P53会引发细胞凋亡。如果这些抑癌基因正常运作，就可以预防癌症形成。但是P53基因有时会失活从而引发癌症。现在一些癌症治疗的途径就是基于刺激或激活P53蛋白来正常工作。
这项最新研究中，研究者发现，Grasp基因可以明显影响P53基因的正常功能。当Grasp没有充分表达时，进入细胞核完成修复或损伤细胞功能的蛋白质就会在其发挥功能之前从细胞核释放出来。
“Grasp，P19胚胎肿瘤细胞中维甲酸诱导基因的产物，主要表达在小鼠的脑部、心脏和肺部等部位。我们发现如果进行强烈的紫外诱导作用，也会在小鼠的皮肤细胞中发现Grasp转化子。”研究者写道，“Grasp-小鼠实验中发现剧烈地紫外暴露后，细胞增殖缓慢，细胞凋零循环也变得迟钝。免疫组织化学分析揭示，经过紫外诱变处理的Grasp-小鼠，P53蛋白在细胞核内的存在时间明显减少。通过以上实验现象，研究者们推断Grasp的生理作用是在紫外照射后通过减少P53引发的细胞凋亡反应来控制皮肤内的稳态。”
“这样看来Grasp的主要功能是在损伤的皮肤细胞的细胞核周围形成一个类似光环，起一个塞子的作用，使P53在细胞核内直至发挥其功能为止。”雷德博士强调，“如果可以找到一种药物增强Grasp的功能，也许会增强P53抑癌基因的作用，同时给我们提供了一条新路径来维持肿瘤抑制因子使其发挥正常作用。”（）
原英文报道：
Scientists at Oregon State University say they have discovered a genetic function that helps the p53 tumor suppressor gene carry out its function and prevent cancer. Finding ways to maintain or increase the effectiveness of the gene in question―Grp1-associated scaffold protein， or Grasp―could offer an important new avenue for human cancer therapies， according to the researchers.
The study (“Grp1-associated scaffold protein regulates skin homeostasis after ultraviolet irradiation”) was published in Photochemical and Photobiological Sciences by researchers from OSU and Oregon Health & Science University.
The p53 gene is involved in repair of DNA damage and， if the damage is too great， causing a mutated cell to die before it can cause further problems， up to and including cancer. Dysfunction of p53 genetic pathways have been linked to more than half of all known cancers， particularly skin， esophageal， colon， pancreatic， lung， ovarian， and head and neck cancers.
“DNA mutations occur constantly in our bodies just by ordinary stresses， something as simple as exposure to sunlight for a few seconds，” explained Mark Leid， Ph.D.， professor of pharmacology and associate dean for research in the OSU College of Pharmacy， and one of the lead authors on this study. “Just as constantly， the p53 gene and other tumor suppressors are activated to repair that damage. And in cases where the damage is too severe to be repaired， p53 will cause apoptosis of the mutated cell. Almost all of the time， when they are working right， these processes prevent the formation of cancers.”
But the activity and function of p53 can sometimes decline or fail， Dr. Leid said， and allow development of cancer. Promising approaches to cancer therapy are now based on activating or stimulating the p53 protein to do its job.
The new study has found that the Grasp gene is significantly involved in maintaining the proper function of p53. When Grasp is not being adequately expressed， the p53 protein that has entered the cell nucleus to either repair or destroy the cell comes back out of the nucleus before its work is finished.
“Grp1-associated scaffold protein (Grasp)， the product of a retinoic acid-induced gene in P19 embryonal carcinoma cells， is expressed primarily in brain， heart， and lung of the mouse. We report herein that Grasp transcripts are also found in mouse skin in which the Grasp gene is robustly induced following acute ultraviolet-B (UVB) exposure，” write the investigators. “Grasp/ mice were found to exhibit delayed epidermal proliferation and a blunted apoptotic response after acute UVB exposure. Immunohistochemical analyses revealed that the nuclear residence time of the tumor suppressor protein p53 was reduced in Grasp/mice after UVB exposure. Taken together， our results suggest that a physiological role of Grasp may be to regulate skin homeostasis after UVB exposure， potentially by influencing p53-mediated apoptotic responses in skin.”
“It appears that a primary function of Grasp is to form sort of a halo around the nucleus of a damaged skin cell， and act as kind of a plug to keep the p53 cell inside the nucleus until its work is done，” noted Dr. Leid. “A drug that could enhance Grasp function might also help enhance the p53 function， and give us a different way to keep this important tumor suppressor working the way that it is supposed to.”
(责任编辑：lilizhao)
小编提示：87%用户都在上阅读，扫描立刻下载!
您还可以这样阅读微信扫一扫，体验新式阅读
打开微信扫描二维码 生物谷微信账号：bioonnews 我们提供多种阅读途径供您选择，随时随地掌握医药生物领域最新资讯。
立足行业，提供求职招聘，中高端人才搜索，人才培训及对接等服务 Ta的文章
欢迎行业评论、发现、小道消息、官方爆料、采访约稿
订阅我们的资讯
关注我们新浪微博
中国的市场的确存在很大的隐患，干细胞行业是个专业性要求较高的行业
个体化医疗是未来医学研究与应用的趋势，而个体化治疗的关键在基于生物分子标志物的诊疗策略
中国疫苗市场的巨大潜力，吸引了世界排名最领先的跨国疫苗制造巨头前来淘金。细胞生物学!!!_图文_百度文库
两大类热门资源免费畅读
续费一年阅读会员，立省24元！
细胞生物学!!!
上传于||文档简介
&&分​子​细​胞​生​物​学​考​试
阅读已结束，如果下载本文需要使用3下载券
想免费下载本文？
定制HR最喜欢的简历
下载文档到电脑，查找使用更方便
还剩4页未读，继续阅读
定制HR最喜欢的简历
你可能喜欢中国海洋大学生命学院2014考的四个大题_百度文库
两大类热门资源免费畅读
续费一年阅读会员，立省24元！
中国海洋大学生命学院2014考的四个大题
上传于||文档简介
&&21春​季​学​期​于​苗​苗​老​师​的​课​考​的​四​个​大​题
阅读已结束，如果下载本文需要使用2下载券
想免费下载本文？
定制HR最喜欢的简历
你可能喜欢