Results 121 to 130 of about 526,953 (308)

HIV-1 Vif Triggers Cell Cycle Arrest by Degrading Cellular PPP2R5 Phospho-regulators

Cell Reports, 2019
Summary: HIV-1 Vif hijacks a cellular ubiquitin ligase complex to degrade antiviral APOBEC3 enzymes and PP2A phosphatase regulators (PPP2R5A–E). APOBEC3 counteraction is essential for viral pathogenesis.
Daniel J. Salamango, Terumasa Ikeda, Seyed Arad Moghadasi, Jiayi Wang, Jennifer L. McCann, Artur A. Serebrenik, Diako Ebrahimi, Matthew C. Jarvis, William L. Brown, Reuben S. Harris   +9 more
doaj   +1 more source

Romidepsin Induces G2/M Phase Arrest and Apoptosis in Cholangiocarcinoma Cells

Technology in Cancer Research & Treatment, 2020
Background: Cholangiocarcinoma (CCA) is an extremely intractable malignancy since most patients are already in an advanced stage when firstly discovered. CCA needs more effective treatment, especially for advanced cases.
Pihong Li MD, Luguang Liu MD, Xiangguo Dang MD, Xingsong Tian MD   +3 more
doaj   +1 more source

Unanticipated differences between α- and γ-diaminobutyric acid-linked hairpin polyamide-alkylator conjugates [PDF]

, 2006
Hairpin polyamide–chlorambucil conjugates containing an {alpha}-diaminobutyric acid ({alpha}-DABA) turn moiety are compared to their constitutional isomers containing the well-characterized {gamma}-DABA turn.
Chou, C. James, Dervan, Peter B., Farkas, Michelle E., Gottesfeld, Joel M., Tsai, Sherry M.   +4 more
core   +4 more sources

Cell‐cycle‐specific lesion evolution rather than inhibition of double‐strand‐break repair underpins cisplatin radiosensitization

Molecular Oncology, EarlyView.
We analyze cisplatin–DNA adducts (CDAs) and double‐strand breaks (DSBs) in a cell‐cycle‐dependent manner. We find that CDAs form similarly across all cell cycle phases. DSBs arise only in S‐phase. CDAs might not directly impair DSB repair, but S‐phase DSB lesions evolve in the presence of CDAs and disrupt repair in G2, also causing radiosensitization ...
Ye Qiu, Xixi Lin, Emil Mladenov, Veronika Mladenova, Jürgen Thomale, Ali Sak, Yao Wang, Yunxuan Deng, Eleni Gkika, Martin Stuschke, George Iliakis   +10 more
wiley   +1 more source

Cytotoxic activities and effects of atractylodin and β-eudesmol on the cell cycle arrest and apoptosis on cholangiocarcinoma cell line

Journal of Pharmacological Sciences, 2018
Cholangiocarcinoma (CCA) is the cancer of bile duct with high mortality rate particularly in Thailand. The clinical efficacy of the standard chemotherapeutics remains unsatisfactory, and therefore, discovery and development of the new alternative drugs ...
Kanawut Kotawong, Wanna Chaijaroenkul, Phunuch Muhamad, Kesara Na-Bangchang   +3 more
doaj   +1 more source

Cyclin D-Cdk4,6 Drives Cell-Cycle Progression via the Retinoblastoma Protein's C-Terminal Helix. [PDF]

, 2019
The cyclin-dependent kinases Cdk4 and Cdk6 form complexes with D-type cyclins to drive cell proliferation. A well-known target of cyclin D-Cdk4,6 is the retinoblastoma protein Rb, which inhibits cell-cycle progression until its inactivation by ...
Cristea, Sandra, Kõivomägi, Mardo, Rubin, Seth M, Sage, Julien, Skotheim, Jan M, Tambo, Carrie S, Topacio, Benjamin R, Xie, Shicong, Zatulovskiy, Evgeny   +8 more
core  

Regulation of DNA damage responses and cell cycle progression by hMOB2. [PDF]

, 2015
Mps one binder proteins (MOBs) are conserved regulators of essential signalling pathways. Biochemically, human MOB2 (hMOB2) can inhibit NDR kinases by competing with hMOB1 for binding to NDRs.
Alexander Hergovich, Avruch, Bakkenist, Bothos, Bouwman, Campbell, Cerami, Colaluca, Cook, Cornils, Cotta-Ramusino, Debnath, Fang, Franken, Geng, Gomez-Martinez, Gudjonsson, Harvey, He, Henderson, Hergovich, Hergovich, Hergovich, Hergovich, Hergovich, Hergovich, Hergovich, Holohan, Hotz, Jackson, Johnson, Kanu, Kastan, Kim, Kim, Kitagawa, Kohler, Kruse, Lai, Lily Hoa, Lim, Lin, Lindahl, Ling, Liu, Loewer, Mark O'Driscoll, Marta Gomez, Meitinger, Neelam Panchal, Nishio, Olive, Polo, Purvis, Ramazan Gundogdu, Rupnik, Sartori, Shiloh, Staley, Stracker, Stracker, Stumpf, Tang, Theunissen, Uziel, Valenti Gomez, van de Wetering, Vichalkovski, Waltes, Williams, Yazdi   +70 more
core   +1 more source

Longitudinal circulating tumor DNA profiling in patients with advanced endometrial cancer using an off‐the‐shelf targeted NGS panel

Molecular Oncology, EarlyView.
Intratumour heterogeneity complicates precision management of advanced endometrial cancer. Circulating tumor DNA (ctDNA) offers a minimally invasive strategy to capture tumor evolution and therapeutic resistance. Here, we compare tumor‐agnostic NGS with tumor‐informed ddPCR, outlining their relative sensitivity, concordance, and clinical implications ...
Carlos Casas‐Arozamena, Karin Teien Lande, Eva Diaz, Ana Vilar, Juan Cueva, Efigenia Arias, Victoria Sampayo, Alicia Abalo, Nerea González, Eva Colás, Antonio Gil‐Moreno, Miguel Abal, Gema Moreno‐Bueno, Therese Sørlie, Kristina Lindemann, Laura Muinelo‐Romay   +15 more
wiley   +1 more source

Proteasome inhibitor, ixazomib prevents topoisomerase‐I degradation and reverses irinotecan resistance in colorectal cancer

Molecular Oncology, EarlyView.
Ixazomib inhibits proteasome‐mediated degradation of topoisomerase I induced by irinotecan, thereby restoring drug sensitivity and promoting tumor cell death in colorectal cancer. Irinotecan, a topoisomerase I (topoI) inhibitor, is widely used for colorectal cancer, but resistance remains a major clinical challenge.
Yuho Ebata, Koji Ando, Hirofumi Hasuda, Koshi Mimori, Elizabeth C. Unan, Siddhartha Pulukuri, Aahana Tiku, Allison Berger, Eiji Oki, Ajit Bharti, Tomoharu Yoshizumi   +10 more
wiley   +1 more source

Growth inhibitory effect and Chk1-dependent signaling involved in G2/M arrest on human gastric cancer cells induced by diallyl disulfide

Brazilian Journal of Medical and Biological Research, 2010
Diallyl disulfide (DADS) inhibits growth and induces cell cycle G2/M arrest in human gastric cancer MGC803 cells. In this study, 15 mg/L DADS exerted similar effects on growth and cell cycle arrest in human gastric cancer BGC823 cells.
H. Ling, L. Wen, X.X. Ji, Y.L. Tang, J. He, H. Tan, H. Xia, J.G. Zhou, Q. Su   +8 more
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