Results 61 to 70 of about 172,662 (343)

Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine

Molecular Oncology, EarlyView.
The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu, Jianlei Zhao, Aaban Asfar Azmi, Avanti Gupte, Jenna Thibodeau, Shuang Liu, Jinli Yang, Guan Wang, Holly Edwards, Lisa A. Polin, Juiwanna Kushner, Sijana H. Dzinic, Kathryn White, Julie Boerner, Maik Hüttemann, Jay Yang, Yue Wang, Jeffrey W. Taub, Yubin Ge   +18 more
wiley   +1 more source

Engineering a DYRK1B R102C mutation: insights into metabolic syndrome pathogenesis through lentiviral gene delivery [PDF]

Medical Laboratory Journal
Background: A rare heterozygous DYRK1B mutation (R102C) recently linked to a familial form of metabolic syndrome prompted this study to introduce the R102C mutation into the mouse DYRK1B gene, utilizing recombinant lentiviruses for long-term gene ...
Afrooz Daneshparvar, Iman Jamhiri, Vahid Razban, Jafar Fallahi, Nasrin Hamidizadeh, Behnam Moghtaderi, Mehdi Dianatpour   +6 more
doaj  

Adaptaquin is selectively toxic to glioma stem cells through disruption of iron and cholesterol metabolism

Molecular Oncology, EarlyView.
Adaptaquin selectively kills glioma stem cells while sparing differentiated brain cells. Transcriptomic and proteomic analyses show Adaptaquin disrupts iron and cholesterol homeostasis, with iron chelation amplifying cytotoxicity via cholesterol depletion, mitochondrial dysfunction, and elevated reactive oxygen species.
Adrien M. Vaquié, Davod R. Shah, Eliane E. S. Brechbühl, Michael McNicholas, Zhaoyang Xu, John H. Stockley, Laura Morcom, Diana Gold Diaz, Gemma C. Girdler, Rachel V. Seear, Gabriel Balmus, Rajiv R. Ratan, Harry Bulstrode, James A. Nathan, Manav Pathania, Kevin M. Brindle, David H. Rowitch   +16 more
wiley   +1 more source

Preparation for a first-in-man lentivirus trial in patients with cystic fibrosis

Thorax, 2016
We have recently shown that non-viral gene therapy can stabilise the decline of lung function in patients with cystic fibrosis (CF). However, the effect was modest, and more potent gene transfer agents are still required.
E. W. Alton, J. Beekman, A. Boyd, June Brand, Marianne S. Carlon, M. Connolly, M. Chan, S. Conlon, H. Davidson, Jane C. Davies, L. Davies, J. Dekkers, A. Doherty, S. Gea‐Sorlí, D. Gill, U. Griesenbach, M. Hasegawa, T. Higgins, T. Hironaka, L. Hyndman, G. McLachlan, M. Inoue, S. Hyde, J. Innes, Toby M. Maher, C. Moran, C. Meng, Michael C. Paul-Smith, I. Pringle, K. Pytel, A. Rodriguez-Martinez, A. Schmidt, B. Stevenson, S. Sumner-Jones, R. Toshner, S. Tsugumine, M. Wasowicz, Jie Zhu   +37 more
semanticscholar   +1 more source

Dual targeting of RET and SRC synergizes in RET fusion‐positive cancer cells

Molecular Oncology, EarlyView.
Despite the strong activity of selective RET tyrosine kinase inhibitors (TKIs), resistance of RET fusion‐positive (RET+) lung cancer and thyroid cancer frequently occurs and is mainly driven by RET‐independent bypass mechanisms. Son et al. show that SRC TKIs significantly inhibit PAK and AKT survival signaling and enhance the efficacy of RET TKIs in ...
Juhyeon Son, Lily L. Remsing Rix, Bin Fang, Eric A. Welsh, Nicole V. Bremer, Valentina Foglizzo, Paola Roa, Nickole Sigcha‐Coello, Yi Liao, Eric B. Haura, Alexander Drilon, John M. Koomen, Emiliano Cocco, Uwe Rix   +13 more
wiley   +1 more source

DDX3X induces mesenchymal transition of endothelial cells by disrupting BMPR2 signaling

FEBS Open Bio, EarlyView.
Elevated DDX3X expression led to downregulation of BMPR2, a key regulator of endothelial homeostasis and function. Our co‐immunoprecipitation assays further demonstrated a molecular interaction between DDX3X and BMPR2. Notably, DDX3X promoted lysosomal degradation of BMPR2, thereby impairing its downstream signaling and facilitating endothelial‐to ...
Yu Zhang, Jing Wang, De‐Hui Qian, Yang‐Fan Lv, Tian‐Le Cheng, Da‐Peng Wang, Jing Zhang, Ye Fan   +7 more
wiley   +1 more source

Reducing neuroinflammation by delivery of IL‐10 encoding lentivirus from multiple‐channel bridges

Bioengineering & Translational Medicine, 2016
The spinal cord is unable to regenerate after injury largely due to growth‐inhibition by an inflammatory response to the injury that fails to resolve, resulting in secondary damage and cell death.
Daniel J Margul, Jonghyuck Park, R. M. Boehler, Dominique R. Smith, Mitchell A. Johnson, D. McCreedy, Ting He, Aishani Ataliwala, Todor V. Kukushliev, Jesse Liang, Alireza Sohrabi, A. Goodman, Christopher M. Walthers, L. Shea, S. Seidlits   +14 more
semanticscholar   +1 more source

Automated FRAP microscopy for high‐throughput analysis of protein dynamics in chromatin organization and transcription

FEBS Open Bio, EarlyView.
RoboMic is an automated confocal microscopy pipeline for high‐throughput functional imaging in living cells. Demonstrated with fluorescence recovery after photobleaching (FRAP), it integrates AI‐driven nuclear segmentation, ROI selection, bleaching, and analysis.
Selçuk Yavuz, Bart Geverts, Johan A. Slotman, Andrea Sacchetti, Stefan Prekovic, Martin E. van Royen, Adriaan B. Houtsmuller   +6 more
wiley   +1 more source

A Distinct Subset of Highly Proliferative and Lentiviral Vector (LV)-Transducible NK Cells Define a Readily Engineered Subset for Adoptive Cellular Therapy

Frontiers in Immunology, 2019
Genetic engineering is an important tool for redirecting the function of various types of immune cells and their use for therapeutic purpose. Although NK cells have many beneficial therapeutic features, genetic engineering of immune cells for targeted ...
Rafijul Bari, Markus Granzin, Kam Sze Tsang, Andre Roy, Winfried Krueger, Rimas Orentas, Dina Schneider, Rita Pfeifer, Nina Moeker, Els Verhoeyen, Els Verhoeyen, Boro Dropulic, Wing Leung   +12 more
doaj   +1 more source

Restriction of lentivirus in monkeys [PDF]

Proceedings of the National Academy of Sciences, 2002
Retroviruses are able to cross species barriers and have done so many times throughout evolution. Perhaps as a consequence, dominant mechanisms have arisen to block infection by murine retroviruses in mice (restriction factor Fv1) and humans (restriction factor Ref1), as well as in other mammals.
Caroline, Besnier, Yasuhiro, Takeuchi, Greg, Towers   +2 more
openaire   +2 more sources