文献库，生知库 | 链接生命科学的每一步

The NAE inhibitor pevonedistat interacts with the HDAC inhibitor belinostat to target AML cells by disrupting the DDR.

NAE 抑制剂 pevonedistat 与 HDAC 抑制剂 belinostat 相互作用，通过破坏 DDR 来靶向 AML 细胞

doi:10.1182/blood-2015-06-653717

Zhou Liang, Chen Shuang, Zhang Yu, Kmieciak Maciej, Leng Yun, Li Lihong, Lin Hui, Rizzo Kathryn A, Dumur Catherine I, Ferreira-Gonzalez Andrea, Rahmani Mohamed, Povirk Lawrence, Chalasani Sri, Berger Allison J, Dai Yun, Grant Steven

细胞生物学

发表日期：2016

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Tumor Cell Recovery from Senescence Induced by Radiation with PARP Inhibition

PARP抑制剂诱导肿瘤细胞从辐射诱导的衰老中恢复

期刊:Radiation Research

影响因子:2.7

doi:10.1667/RR14437.1

Gewirtz, David A; Alotaibi, Moureq; Yakovlev, Vasily A; Povirk, Lawrence F

Senescence

发表日期：2016

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Correction: Mutation of the BRCA1 SQ-cluster results in aberrant mitosis, reduced homologous recombination, and a compensatory increase in non-homologous end joining

更正：BRCA1 SQ 簇的突变会导致异常有丝分裂、同源重组减少以及非同源末端连接的代偿性增加。

期刊:Oncotarget

影响因子:

doi:10.18632/oncotarget.11846

Beckta, Jason M; Dever, Seth M; Gnawali, Nisha; Khalil, Ashraf; Sule, Amrita; Golding, Sarah E; Rosenberg, Elizabeth; Narayanan, Aarthi; Kehn-Hall, Kylene; Xu, Bo; Povirk, Lawrence F; Valerie, Kristoffer

BRCA1

发表日期：2016

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Mutation of the BRCA1 SQ-cluster results in aberrant mitosis, reduced homologous recombination, and a compensatory increase in non-homologous end joining

BRCA1 SQ 簇的突变会导致异常有丝分裂、同源重组减少以及非同源末端连接的代偿性增加。

期刊:Oncotarget

影响因子:

doi:10.18632/oncotarget.4876

BRCA1

发表日期：2015

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Involvement of p53 in the repair of DNA double strand breaks: multifaceted Roles of p53 in homologous recombination repair (HRR) and non-homologous end joining (NHEJ)

p53参与DNA双链断裂修复：p53在同源重组修复（HRR）和非同源末端连接（NHEJ）中的多方面作用

期刊:Sub-Cellular Biochemistry

影响因子:

doi:10.1007/978-94-017-9211-0_17

Menon, Vijay; Povirk, Lawrence

发表日期：2014

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Restoration of G1 chemo/radioresistance and double-strand-break repair proficiency by wild-type but not endonuclease-deficient Artemis.

野生型 Artemis 可恢复 G1 化疗/放疗抗性和双链断裂修复能力，但内切酶缺陷型 Artemis 则不能

期刊:Nucleic Acids Research

影响因子:13.1

doi:10.1093/nar/gkr257

Mohapatra Susovan, Kawahara Misako, Khan Imran S, Yannone Steven M, Povirk Lawrence F

免疫/内分泌

发表日期：2011

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Improved ATM kinase inhibitor KU-60019 radiosensitizes glioma cells, compromises insulin, AKT and ERK prosurvival signaling, and inhibits migration and invasion

改良型ATM激酶抑制剂KU-60019可增强胶质瘤细胞的放射敏感性，抑制胰岛素、AKT和ERK促生存信号通路，并抑制细胞迁移和侵袭。

期刊:Molecular Cancer Therapeutics

影响因子:5.5

doi:10.1158/1535-7163.MCT-09-0519

Golding, Sarah E; Rosenberg, Elizabeth; Valerie, Nicholas; Hussaini, Isa; Frigerio, Mark; Cockcroft, Xiaoling F; Chong, Wei Yee; Hummersone, Marc; Rigoreau, Laurent; Menear, Keith A; O'Connor, Mark J; Povirk, Lawrence F; van Meter, Timothy; Valerie, Kristoffer

Pro-survival AKT and ERK signaling from EGFR and mutant EGFRvIII enhances DNA double-strand break repair in human glioma cells

EGFR及其突变体EGFRvIII激活的促生存AKT和ERK信号通路可增强人胶质瘤细胞中DNA双链断裂的修复。

期刊:Cancer Biology & Therapy

影响因子:4.6

doi:10.4161/cbt.8.8.7927

Golding, Sarah E; Morgan, Rhiannon N; Adams, Bret R; Hawkins, Amy J; Povirk, Lawrence F; Valerie, Kristoffer

Tyrosyl-DNA phosphodiesterases: rescuing the genome from the risks of relaxation

酪氨酰-DNA磷酸二酯酶：拯救基因组免受放松带来的风险

The NAE inhibitor pevonedistat interacts with the HDAC inhibitor belinostat to target AML cells by disrupting the DDR.

NAE 抑制剂 pevonedistat 与 HDAC 抑制剂 belinostat 相互作用，通过破坏 DDR 来靶向 AML 细胞

Tumor Cell Recovery from Senescence Induced by Radiation with PARP Inhibition

PARP抑制剂诱导肿瘤细胞从辐射诱导的衰老中恢复

Correction: Mutation of the BRCA1 SQ-cluster results in aberrant mitosis, reduced homologous recombination, and a compensatory increase in non-homologous end joining

更正：BRCA1 SQ 簇的突变会导致异常有丝分裂、同源重组减少以及非同源末端连接的代偿性增加。

Mutation of the BRCA1 SQ-cluster results in aberrant mitosis, reduced homologous recombination, and a compensatory increase in non-homologous end joining

BRCA1 SQ 簇的突变会导致异常有丝分裂、同源重组减少以及非同源末端连接的代偿性增加。

Involvement of p53 in the repair of DNA double strand breaks: multifaceted Roles of p53 in homologous recombination repair (HRR) and non-homologous end joining (NHEJ)

p53参与DNA双链断裂修复：p53在同源重组修复（HRR）和非同源末端连接（NHEJ）中的多方面作用

Restoration of G1 chemo/radioresistance and double-strand-break repair proficiency by wild-type but not endonuclease-deficient Artemis.

野生型 Artemis 可恢复 G1 化疗/放疗抗性和双链断裂修复能力，但内切酶缺陷型 Artemis 则不能

Improved ATM kinase inhibitor KU-60019 radiosensitizes glioma cells, compromises insulin, AKT and ERK prosurvival signaling, and inhibits migration and invasion

改良型ATM激酶抑制剂KU-60019可增强胶质瘤细胞的放射敏感性，抑制胰岛素、AKT和ERK促生存信号通路，并抑制细胞迁移和侵袭。

Pro-survival AKT and ERK signaling from EGFR and mutant EGFRvIII enhances DNA double-strand break repair in human glioma cells

EGFR及其突变体EGFRvIII激活的促生存AKT和ERK信号通路可增强人胶质瘤细胞中DNA双链断裂的修复。