日期:
2020 年 — 2026 年
2020
2021
2022
2023
2024
2025
2026
影响因子:

Visualization and quantification of rDNA instabilities in mammalian cells and mouse models.

哺乳动物细胞和鼠模型中rDNA不稳定性可视化和定量分析。

Zhu Xiaolu, Jiang Wenxia, Wu Wei, Lee Brian J, Menolfi Demis, Tubbs Anthony, Cupo Olivia M, Malkovskiy Eli, Nester Mattie, Wang Xiaobin S, Sims Peter A, Lin Chyuan-Sheng V, Symington Lorraine, Nussenzweig Andre, McStay Brian, Zha Shan

Inactive Parp2 causes Tp53-dependent lethal anemia by blocking replication-associated nick ligation in erythroblasts

Parp2 失活会通过阻断成红细胞中与复制相关的切口连接,导致 Tp53 依赖性致死性贫血。

Xiaohui Lin ,Dipika Gupta ,Alina Vaitsiankova ,Seema Khattri Bhandari ,Kay Sze Karina Leung ,Demis Menolfi ,Brian J Lee ,Helen R Russell ,Steven Gershik ,Xiaoyu Huang ,Wei Gu ,Peter J McKinnon ,Françoise Dantzer ,Eli Rothenberg ,Alan E Tomkinson ,Shan Zha

Asymmetric distribution of parental H3K9me3 in S phase silences L1 elements

亲本 H3K9me3 在 S 期的不对称分布使 L1 元件沉默

Zhiming Li #, Shoufu Duan #, Xu Hua, Xiaowei Xu, Yinglu Li, Demis Menolfi, Hui Zhou, Chao Lu, Shan Zha, Stephen P Goff, Zhiguo Zhang

ATR kinase supports normal proliferation in the early S phase by preventing replication resource exhaustion

ATR激酶通过防止复制资源耗尽来支持早期S期的正常增殖。

Demis Menolfi ,Brian J Lee ,Hanwen Zhang ,Wenxia Jiang ,Nicole E Bowen ,Yunyue Wang ,Junfei Zhao ,Antony Holmes ,Steven Gershik ,Raul Rabadan ,Baek Kim ,Shan Zha

Smc5/6 functions with Sgs1-Top3-Rmi1 to complete chromosome replication at natural pause sites

Smc5/6 与 Sgs1-Top3-Rmi1 协同作用,在天然暂停位点完成染色体复制。

Sumedha Agashe ,Chinnu Rose Joseph # ,Teresa Anne Clarisse Reyes # ,Demis Menolfi ,Michele Giannattasio ,Anja Waizenegger ,Barnabas Szakal # ,Dana Branzei

The Cancer-Associated ATM R3008H Mutation Reveals the Link between ATM Activation and Its Exchange

与癌症相关的ATM R3008H突变揭示了ATM激活及其交换之间的联系

Maja Milanovic ,Lisa Sprinzen ,Demis Menolfi ,Ji-Hoon Lee ,Kenta Yamamoto ,Yang Li ,Brian J Lee ,Jun Xu ,Verna M Estes ,Dong Wang ,Peter J Mckinnon ,Tanya T Paull ,Shan Zha

DNA damage-induced phosphorylation of CtIP at a conserved ATM/ATR site T855 promotes lymphomagenesis in mice.

DNA损伤诱导的CtIP在保守的ATM/ATR位点T855的磷酸化促进小鼠淋巴瘤的发生

Wang Xiaobin S, Menolfi Demis, Wu-Baer Foon, Fangazio Marco, Meyer Stefanie N, Shao Zhengping, Wang Yunyue, Zhu Yimeng, Lee Brian J, Estes Verna M, Cupo Olivia M, Gautier Jean, Pasqualucci Laura, Dalla-Favera Riccardo, Baer Richard, Zha Shan

FATC Domain Deletion Compromises ATM Protein Stability, Blocks Lymphocyte Development, and Promotes Lymphomagenesis

FATC结构域缺失会损害ATM蛋白的稳定性,阻碍淋巴细胞发育,并促进淋巴瘤的发生

Maja Milanovic ,Zhengping Shao ,Verna M Estes ,Xiaobin S Wang ,Demis Menolfi ,Xiaohui Lin ,Brian J Lee ,Jun Xu ,Olivia M Cupo ,Dong Wang ,Shan Zha

ATM, ATR and DNA-PKcs kinases-the lessons from the mouse models: inhibition ≠ deletion

ATM、ATR 和 DNA-PKcs 激酶——来自小鼠模型的启示:抑制≠删除

Menolfi, Demis; Zha, Shan

Kinase-dead ATR differs from ATR loss by limiting the dynamic exchange of ATR and RPA

激酶失活 ATR 与 ATR 丢失的区别在于,它限制了 ATR 和 RPA 的动态交换

Demis Menolfi, Wenxia Jiang, Brian J Lee, Tatiana Moiseeva, Zhengping Shao, Verna Estes, Mark G Frattini, Christopher J Bakkenist, Shan Zha