Going ape as an approach to cancer therapeutics.
Going ape as an approach to cancer therapeutics.
复制标题
DOI：
10.1089/ars.2008.2218
复制
发表时间：
2009-03
影响因子：
6.6
通讯作者：
Kelley MR
中科院分区：
文献类型：
--
作者：
Bapat A;Fishel ML;Kelley MR
DNA碱基切除修复（BER）途径修复由内源性和外源性试剂（包括化疗剂）引起的烷基化和氧化DNA损伤。在去除受损的碱基AP核酸内切酶1（Ape 1）后，该途径的关键组分切割脱碱基位点以促进修复。Ape 1是一种多功能蛋白质，不仅在DNA修复中发挥作用，而且还作为还原-氧化因子发挥作用，在文献中称为Ref-1，以增加参与不同生长信号传导途径的几种转录因子的DNA结合能力。Ape 1水平升高与化疗耐药性、预后不良和生存不良有关。使用RNA干扰和反义寡核苷酸技术减少癌细胞和肿瘤中Ape 1蛋白的量可使哺乳动物肿瘤细胞对各种实验室和化疗药物敏感。因此，选择性抑制Ape 1的DNA修复活性是开发新的癌症治疗方法的有希望的途径。
The DNA base excision repair (BER) pathway repairs alkylation and oxidative DNA damage caused by endogenous and exogenous agents, including chemotherapeutic agents. Upon removal of the damaged base AP endonuclease 1 (Ape1), a critical component of the pathway cleaves the abasic site to facilitate repair. Ape1 is a multifunctional protein which plays a role not only in DNA repair but it also functions as a reduction-oxidation factor, known as Ref-1 in the literature, to increase the DNA binding ability of several transcription factors involved in different growth signaling pathways. Elevated levels of Ape1 have been linked to resistance to chemotherapy, poor prognosis, and poor survival. Reducing the amount of Ape1 protein in cancer cells and tumors using RNA interference and anti-sense oligonucleotide technology sensitizes mammalian tumor cells to a variety of laboratory and chemotherapeutic agents. Therefore, selective inhibition of Ape1's DNA repair activity is a promising avenue to develop novel cancer therapeutics.
登录
查看更多内容
影响因子：
11.5
作者：
Bobola, MS;Finn, LS;Silber, JR
通讯作者：
Silber, JR
影响因子：
4.8
作者：
Chou, KM;Kukhanova, M;Cheng, YC
通讯作者：
Cheng, YC
影响因子：
14.9
作者：
Chattopadhyay R;Wiederhold L;Szczesny B;Boldogh I;Hazra TK;Izumi T;Mitra S
通讯作者：
Mitra S
影响因子：
56.9
作者：
ABATE, C;PATEL, L;CURRAN, T
通讯作者：
CURRAN, T
影响因子：
14.9
作者：
CHEN, DS;HERMAN, T;DEMPLE, B
通讯作者：
DEMPLE, B