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Showing 1-12 of 12 results for "114666" within Papers
Leonid Anikin et al.
International journal of molecular sciences, 23(3) (2022-02-16)
Aminoacridines, used for decades as antiseptic and antiparasitic agents, are prospective candidates for therapeutic repurposing and new drug development. Although the mechanisms behind their biological effects are not fully elucidated, they are most often attributed to the acridines' ability to
Anna L Koessinger et al.
Cell death and differentiation, 29(10), 2089-2104 (2022-04-28)
Glioblastoma (GBM) is the most prevalent malignant primary brain tumour in adults. GBM typically has a poor prognosis, mainly due to a lack of effective treatment options leading to tumour persistence or recurrence. We investigated the therapeutic potential of targeting
Florian J Bock et al.
Nature communications, 12(1), 6572-6572 (2021-11-14)
Damaged or superfluous cells are typically eliminated by apoptosis. Although apoptosis is a cell-autonomous process, apoptotic cells communicate with their environment in different ways. Here we describe a mechanism whereby cells under apoptotic stress can promote survival of neighbouring cells.
Martha M Monick et al.
Journal of immunology (Baltimore, Md. : 1950), 177(3), 1636-1645 (2006-07-20)
Human alveolar macrophages, central to immune responses in the lung, are unique in that they have an extended life span in contrast to precursor monocytes. We have shown previously that the ERK MAPK (ERK) pathway is constitutively active in human
Yuan Zhang et al.
Redox biology, 69, 103005-103005 (2023-12-28)
Major depressive disorder (MDD) is a devastating condition. Although progress has been made in the past seven decades, patients with MDD continue to receive an inadequate treatment, primarily due to the late onset of first-line antidepressant drugs and to their
Sarah V Schweighofer et al.
Cell death and differentiation, 31(4), 469-478 (2024-03-20)
One hallmark of apoptosis is the oligomerization of BAX and BAK to form a pore in the mitochondrial outer membrane, which mediates the release of pro-apoptotic intermembrane space proteins into the cytosol. Cells overexpressing BAX or BAK fusion proteins are
Victor L Bass et al.
Molecular systems biology, 17(7), e10127-e10127 (2021-07-22)
Cell-to-cell heterogeneity is a feature of the tumor necrosis factor (TNF)-stimulated inflammatory response mediated by the transcription factor NF-κB, motivating an exploration of the underlying sources of this noise. Here, we combined single-transcript measurements with computational models to study transcriptional
Yu Zhou et al.
iScience, 27(2), 108822-108822 (2024-02-02)
Alternative polyadenylation (APA) is an important post-transcriptional regulatory mechanism and is involved in many diseases, but its function and mechanism in regulating pancreatic cancer (PC) pathogenesis remain unclear. In this study, we found that the 3' UTR shortening of MZT1
Edward J Morris et al.
Cell reports, 30(11), 3605-3615 (2020-03-19)
Multiple cancer-related genes both promote and paradoxically suppress growth initiation, depending on the cell context. We discover an explanation for how this occurs for one such protein, Stat3, based on asymmetric cell division. Here, we show that Stat3, by Stathmin/PLK-1
Janaki N Sudhakar et al.
Biology of the cell, 106(10), 359-376 (2014-07-25)
During the initiation of cell death, mitochondrial protein, apoptosis-inducing factor (AIF), is transported to the nucleus. The mechanism of AIF nuclear translocation, however, is not clear. After protein synthesis, the AIF is originally targetted to the mitochondria, and the nuclear
Azam Asgarihafshejani et al.
iScience, 25(5), 104259-104259 (2022-05-07)
Hippocampal somatostatin (SOM) cells are dendrite-projecting inhibitory interneurons. CA1 SOM cells receive major excitatory inputs from pyramidal cells (PC-SOM synapses) which show mGluR1a- and mTORC1-mediated long-term potentiation (LTP). PC-SOM synapse LTP contributes to CA1 network metaplasticity and memory consolidation, but
Viana Manrique-Suárez et al.
Proteins, 89(11), 1508-1521 (2021-07-06)
Tumor necrosis factor-alpha (TNFα) inhibitors could prevent neurological disorders systemically, but their design generally relies on molecules unable to cross the blood-brain barrier (BBB). This research was aimed to design and characterize a novel TNFα inhibitor based on the angiopeptide-2
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