Results 91 to 100 of about 514,126 (359)

The roles of apoptosis, autophagy and unfolded protein response in arbovirus, influenza virus, and HIV infections

Virulence, 2019
Virus infection induces different cellular responses in infected cells. These include cellular stress responses like autophagy and unfolded protein response (UPR).
Parvaneh Mehrbod, Sudharsana R. Ande, Javad Alizadeh, Shahrzad Rahimizadeh, Aryana Shariati, Hadis Malek, Mohammad Hashemi, Kathleen K. M. Glover, Affan A. Sher, Kevin M. Coombs, Saeid Ghavami   +10 more
doaj   +1 more source

The Barley Apoptosis Suppressor Homologue Bax Inhibitor-1 Compromises Nonhost Penetration Resistance of Barley to the Inappropriate Pathogen Blumeria graminis f. sp. tritici

Molecular Plant-Microbe Interactions, 2004
BAX inhibitor-1 (BI-1) proteins have been characterized as suppressors of programmed cell death in mammals and plants. The barley BI-1 is a suppressor of nonspecific background resistance and mlo-mediated penetration resistance to the biotrophic fungal ...
Ruth Eichmann, Holger Schultheiss, Karl-Heinz Kogel, Ralph Hückelhoven   +3 more
doaj   +1 more source

Caspase-3 Is Required for DNA Fragmentation and Morphological Changes Associated with Apoptosis*

Journal of Biological Chemistry, 1998
Interleukin 1β-converting enzyme-like proteases (caspases) are crucial components of cell death pathways. Among the caspases identified, caspase-3 stands out because it is commonly activated by numerous death signals and cleaves a variety of important ...
R. Jänicke, M. L. Sprengart, M. R. Wati, A. Porter   +3 more
semanticscholar   +1 more source

A caspase for stress

The Journal of Cell Biology, 2004
Stress in the endoplasmic reticulum (ER)—caused by anything from ischemia to expression of mutant proteins—triggers several responses. Cells slow translation, produce more chaperones, degrade more unfolded proteins, and as a last resort, induce apoptosis. Hitomi et al. (page 347) identify caspase-4 as a critical component of the pathway leading from ER
openaire   +2 more sources

PYCR1 inhibition in bone marrow stromal cells enhances bortezomib sensitivity in multiple myeloma cells by altering their metabolism

Molecular Oncology, EarlyView.
This study investigated how PYCR1 inhibition in bone marrow stromal cells (BMSCs) indirectly affects multiple myeloma (MM) cell metabolism and viability. Culturing MM cells in conditioned medium from PYCR1‐silenced BMSCs impaired oxidative phosphorylation and increased sensitivity to bortezomib.
Inge Oudaert, Lauren van den Broecke, Osman Aksoy, Judith Lind, Sonia Vallet, Arne Van der Vreken, Gamze Ates, Ann Massie, Ken Maes, Kim De Veirman, Elke De Bruyne, Karin Vanderkerken, Klaus Podar, Eline Menu   +13 more
wiley   +1 more source

Defining Characteristics of Types I and II Apoptotic Cells in Response to TRAIL

Neoplasia: An International Journal for Oncology Research, 2002
Type I cells have been defined to be independent of mitochondria for the induction of Fas death receptormediated apoptosis, whereas Type II cells are mitochondria-dependent.
Nesrin Özören, Wafik S. El-Deiry
doaj   +1 more source

Caspase-1 inhibition alleviates cognitive impairment and neuropathology in an Alzheimer’s disease mouse model

Nature Communications, 2018
Alzheimer's disease (AD) is an intractable progressive neurodegenerative disease characterized by cognitive decline and dementia. An inflammatory neurodegenerative pathway, involving Caspase-1 activation, is associated with human age-dependent cognitive ...
Joseph Flores, Anastasia Noël, B. Foveau, Jeffrey Lynham, Clotilde Lecrux, A. LeBlanc   +5 more
semanticscholar   +1 more source

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

A synthetic benzoxazine dimer derivative targets c‐Myc to inhibit colorectal cancer progression

Molecular Oncology, EarlyView.
Benzoxazine dimer derivatives bind to the bHLH‐LZ region of c‐Myc, disrupting c‐Myc/MAX complexes, which are evaluated from SAR analysis. This increases ubiquitination and reduces cellular c‐Myc. Impairing DNA repair mechanisms is shown through proteomic analysis.
Nicharat Sriratanasak, Bodee Nutho, Worawat Wattanathana, Narumon Phaonakrop, Bunnatut Panasawatwong, Katharina Erlenbach‐Wuensch, Sittiruk Roytrakul, Regine Schneider‐Stock, Pithi Chanvorachote   +8 more
wiley   +1 more source

Ordering the Cytochrome c–initiated Caspase Cascade: Hierarchical Activation of Caspases-2, -3, -6, -7, -8, and -10 in a Caspase-9–dependent Manner

Journal of Cell Biology, 1999
Exit of cytochrome c from mitochondria into the cytosol has been implicated as an important step in apoptosis. In the cytosol, cytochrome c binds to the CED-4 homologue, Apaf-1, thereby triggering Apaf-1–mediated activation of caspase-9.
E. Slee, M. Harte, R. Kluck, B. Wolf, C. Casiano, D. Newmeyer, Hong-Gang Wang, John Calvin Reed, D. Nicholson, E. Alnemri, D. Green, Seamus J. Martin   +11 more
semanticscholar   +1 more source