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Journal articles on the topic 'Delayed Death Inhibitors'

Author: Grafiati

Published: 6 September 2023

Last updated: 31 July 2025

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1

Amberg-Johnson, Katherine, and Ellen Yeh. "Host Cell Metabolism Contributes to Delayed-Death Kinetics of Apicoplast Inhibitors inToxoplasma gondii." Antimicrobial Agents and Chemotherapy 63, no. 2 (2018): e01646-18. http://dx.doi.org/10.1128/aac.01646-18.

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ABSTRACTToxoplasma gondiiand related human parasites contain an essential plastid organelle called the apicoplast. Clinically used antibiotics and other inhibitors that disrupt apicoplast biogenesis cause a mysterious “delayed-death” phenotype in which parasite growth is unaffected during the first lytic cycle of inhibitor treatment but is severely inhibited in the second lytic cycle even after drug removal. Critical to understanding the complex downstream cellular effects of these drug classes are the timing of apicoplast loss during inhibitor treatment and how it relates to this peculiar gro

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Ramya, T. N. C., Satyendra Mishra, Krishanpal Karmodiya, Namita Surolia, and Avadhesha Surolia. "Inhibitors of Nonhousekeeping Functions of the Apicoplast Defy Delayed Death in Plasmodium falciparum." Antimicrobial Agents and Chemotherapy 51, no. 1 (2006): 307–16. http://dx.doi.org/10.1128/aac.00808-06.

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ABSTRACT Targeting of apicoplast replication and protein synthesis in the apicomplexan Toxoplasma gondii has conventionally been associated with the typical “delayed death” phenotype, characterized by the death of parasites only in the generation following drug intervention. We demonstrate that antibiotics like clindamycin, chloramphenicol, and tetracycline, inhibitors of prokaryotic protein synthesis, invoke the delayed death phenotype in Plasmodium falciparum, too, as evident from a specific reduction of apicoplast genome copy number. Interestingly, however, molecules like triclosan, cerulen

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Kindy, Mark S. "Inhibition of Tyrosine Phosphorylation Prevents Delayed Neuronal Death following Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 13, no. 3 (1993): 372–77. http://dx.doi.org/10.1038/jcbfm.1993.50.

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Protein tyrosine phosphorylation plays an important role in the regulation of neuronal function. We examined the effects of inhibition of tyrosine phosphorylation on ischemic neuronal damage in the CA1 region of the hippocampus. In the gerbil hippocampus, genistein and lavendustin A, tyrosine kinase inhibitors, were administered 30 min before initiation of 5-min ischemia and reperfusion. Both genistein and lavendustin A blocked tyrosine phosphorylation and prevented delayed neuronal death (DND). However, genistin, an inactive analogue of genistein, did not block DND. Genistein was dose-depende

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Weil, M., M. D. Jacobson, and M. C. Raff. "Are caspases involved in the death of cells with a transcriptionally inactive nucleus? Sperm and chicken erythrocytes." Journal of Cell Science 111, no. 18 (1998): 2707–15. http://dx.doi.org/10.1242/jcs.111.18.2707.

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We show that mouse sperm die spontaneously within 1–2 days in culture and that treatment with either staurosporine (STS) and cycloheximide (CHX) or a peptide caspase inhibitor does not accelerate or delay the cell death. Chicken erythrocytes, by contrast, are induced to die by either serum deprivation or treatment with STS and CHX, and embryonic erythrocytes are more sensitive than adult erythrocytes to both treatments. Although these erythrocyte deaths display a number of features that are characteristic of apoptosis, they are not blocked, or even delayed, by peptide caspase inhibitors, and m

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Jäckle, Tina, Cornelia Hasel, Ingo Melzner, S. Brüderlein, Peter M. Jehle, and Peter Möller. "Sustained hyposmotic stress induces cell death: apoptosis by defeat." American Journal of Physiology-Cell Physiology 281, no. 5 (2001): C1716—C1726. http://dx.doi.org/10.1152/ajpcell.2001.281.5.c1716.

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We describe sustained hyposmotic stress as a novel type of environmental condition enforcing apoptosis. In a dose- and time-dependent fashion, hyposmotic stress leads to a delayed type of apoptosis with considerable variations in constitutive sensitivity among different cell types. For example, after 48 h at 84 mosmol/l, the death rate ranged from 10.8 ± 0.7% in AsPc1 human pancreatic carcinoma cells to 72.0 ± 1.6% in HK-2 human kidney tubule cells. Caspase inhibitors rendered cells more resistant to hyposmolar stress; the caspase 3 inhibitor Ac-Asp-Glu-Val-aspartic acid aldehyde was the most

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Shishido, Yoshiyuki, Masayoshi Furushiro, Shuichi Tanabe, Shigenobu Shibata, Shusuke Hashimoto, and Teruo Yokokura. "Effects of prolyl endopeptidase inhibitors and neuropeptides on delayed neuronal death in rats." European Journal of Pharmacology 372, no. 2 (1999): 135–42. http://dx.doi.org/10.1016/s0014-2999(99)00185-5.

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Lewin, Matthew, José Gutiérrez, Stephen Samuel, et al. "Delayed Oral LY333013 Rescues Mice from Highly Neurotoxic, Lethal Doses of Papuan Taipan (Oxyuranus scutellatus) Venom." Toxins 10, no. 10 (2018): 380. http://dx.doi.org/10.3390/toxins10100380.

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There is an unmet need for economical snakebite therapies with long shelf lives that are effective even with delays in treatment. The orally bioavailable, heat-stable, secretory phospholipase A2 (sPLA2) inhibitor, LY333013, demonstrates antidotal characteristics for severe snakebite envenoming in both field and hospital use. A murine model of lethal envenoming by a Papuan taipan (Oxyuranus scutellatus) demonstrates that LY333013, even with delayed oral administration, improves the chances of survival. Furthermore, LY333013 improves the performance of antivenom even after it no longer reverses

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Duval, R., V. Bellet, S. Delebassée, and C. Bosgiraud. "Implication of caspases during maedi–visna virus-induced apoptosis." Journal of General Virology 83, no. 12 (2002): 3153–61. http://dx.doi.org/10.1099/0022-1317-83-12-3153.

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Maedi–visna virus (MVV) causes encephalitis, pneumonia and arthritis in sheep. In vitro, MVV infection and replication lead to strong cytopathic effects characterized by syncytia formation and subsequent cellular lysis. It was demonstrated previously that MVV infection in vitro induces cell death of sheep choroid plexus cells (SCPC) by a mechanism that can be associated with apoptotic cell death. Here, the relative implication of several caspases during acute infection with MVV is investigated by employing diverse in vitro and in situ strategies. It was demonstrated using specific pairs of cas

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Nakagomi, T., T. Sasaki, T. Kirino, et al. "Effect of cyclooxygenase and lipoxygenase inhibitors on delayed neuronal death in the gerbil hippocampus." Stroke 20, no. 7 (1989): 925–29. http://dx.doi.org/10.1161/01.str.20.7.925.

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10

STEFANELLI, Claudio, Francesca BONAVITA, Ivana STANIC', et al. "ATP depletion inhibits glucocorticoid-induced thymocyte apoptosis." Biochemical Journal 322, no. 3 (1997): 909–17. http://dx.doi.org/10.1042/bj3220909.

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In quiescent thymocytes, mitochondrial de-energization was not correlated to apoptotic death. In fact, thymocytes treated with oligomycin, a highly specific inhibitor of ATP synthase, alone or with atractyloside to block ATP translocation from the cytoplasm, were alive, even if their mitochondria were depolarized, as revealed by flow cytometry after Rhodamine 123 staining. Furthermore, oligomycin was a powerful inhibitor of apoptosis induced in rat thymocytes by dexamethasone and, to a lesser extent, by the calcium ionophore A23187 and etoposide, but was without effect when apoptosis was induc

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Schweber, Sarah J., Alicia G. Rodriguez-LaRocca, Valerie Calvert, et al. "Protein pathway activation mapping guided biomarker development to identify optimal combinations of MEK inhibitor with PI3K/mTOR pathway inhibitors for the treatment of triple-negative breast cancer." Journal of Clinical Oncology 31, no. 15_suppl (2013): 2612. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.2612.

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2612 Background: Activated MAPK and PI3K pathway signaling are associated with poor prognosis in triple negative breast cancer (TNBC). Although some TNBC cell models are sensitive to MEK inhibition, feedback activation of the PI3K pathway mediates resistance. Thus, suppression of both arms of the MAPK/PI3K/mTOR network is a rational approach to targeting TNBC. Here we explore the anti-tumor efficacy of combinations of MEK inhibitor with PI3K, AKT, or mTOR inhibitors with a focus on biomarker development. Methods: Combinations of the MEK inhibitor PD-0325901 with the PI3K inhibitor GDC-0941, AK

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Hilton, Genell D., Bogdan A. Stoica, Kimberly R. Byrnes, and Alan I. Faden. "Roscovitine Reduces Neuronal Loss, Glial Activation, and Neurologic Deficits after Brain Trauma." Journal of Cerebral Blood Flow & Metabolism 28, no. 11 (2008): 1845–59. http://dx.doi.org/10.1038/jcbfm.2008.75.

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Traumatic brain injury (TBI) causes both direct and delayed tissue damage. The latter is associated with secondary biochemical changes such as cell cycle activation, which leads to neuronal death, inflammation, and glial scarring. Flavopiridol—a cyclin-dependent kinase (CDK) inhibitor that is neither specific nor selective—is neuroprotective. To examine the role of more specific CDK inhibitors as potential neuroprotective agents, we studied the effects of roscovitine in TBI. Central administration of roscovitine 30 mins after injury resulted in significantly decreased lesion volume, as well as

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Fu, Shengya, Ting Wang, and Feng Xu. "Delayed immune thrombocytopenia after discontinuation of nivolumab therapy: A case report and literature review." Journal of Oncology Pharmacy Practice 27, no. 6 (2021): 1548–52. http://dx.doi.org/10.1177/1078155220981155.

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Introduction Nivolumab, a programmed death-1(PD-1) inhibitor antibody, have demonstrated anti-tumor activity for multiple malignancies. Such immune checkpoint inhibitors induce novel and distinctive adverse effects, which are collectively named immune-related adverse events. Immune-related adverse events can theoretically occur at any part of the body, including the haemopoietic system. Most immune-related adverse events developed within 10 weeks of receiving immunotherapy. Thus far, there is no report of immune thrombocytopenia as an immune-related adverse event developed after discontinuatio

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Ying, Weihai, Yongmei Chen, Conrad C. Alano, and Raymond A. Swanson. "Tricarboxylic Acid Cycle Substrates Prevent PARP-Mediated Death of Neurons and Astrocytes." Journal of Cerebral Blood Flow & Metabolism 22, no. 7 (2002): 774–79. http://dx.doi.org/10.1097/00004647-200207000-00002.

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The DNA repair enzyme, poly(ADP-ribose) polymerase-1 (PARP1), contributes to cell death during ischemia/reperfusion when extensively activated by DNA damage. The cell death resulting from PARP1 activation is linked to NAD+ depletion and energy failure, but the intervening steps are not well understood. Because glycolysis requires cytosolic NAD+, the authors tested whether PARP1 activation impairs glycolytic flux and whether substrates that bypass glycolysis can rescue cells after PARP1 activation. PARP1 was activated in mouse cortical astrocyte and astrocyte-neuron cocultures with the DNA alky

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White, Michael G., Osama Saleh, Doris Nonner, Ellen F. Barrett, Carlos T. Moraes, and John N. Barrett. "Mitochondrial dysfunction induced by heat stress in cultured rat CNS neurons." Journal of Neurophysiology 108, no. 8 (2012): 2203–14. http://dx.doi.org/10.1152/jn.00638.2011.

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Previous work demonstrated that hyperthermia (43°C for 2 h) results in delayed, apoptotic-like death in striatal neuronal cultures. We investigated early changes in mitochondrial function induced by this heat stress. Partial depolarization of the mitochondrial membrane potential (ΔΨm) began about 1 h after the onset of hyperthermia and increased as the stress continued. When the heat stress ended, there was a partial recovery of ΔΨm, followed hours later by a progressive, irreversible depolarization of ΔΨm. During the heat stress, O2 consumption initially increased but after 20–30 min began a

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Finnegan, Ryan Michael. "Abstract P1-13-02: Autophagy inhibition and senolytics to improve the response to fulvestrant + palbociclib in ER positive breast cancer." Cancer Research 82, no. 4_Supplement (2022): P1–13–02—P1–13–02. http://dx.doi.org/10.1158/1538-7445.sabcs21-p1-13-02.

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Abstract While anti-estrogens or aromatase inhibitors in combination with cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitors are the current standard of care for estrogen receptor-positive (ER+) Her-2 negative metastatic breast cancer, relapse after remission continues to be a serious limitation to the effectiveness of these therapies. Although these combination therapies prolong progression-free survival compared to endocrine therapy alone, the growth-arrested state of residual tumor cells is clearly transient. Tumor cells that escape what might be considered a dormant or quiescent state and

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Endres, Matthias, Shobu Namura, Masao Shimizu-Sasamata, et al. "Attenuation of Delayed Neuronal Death after Mild Focal Ischemia in Mice by Inhibition of the Caspase Family." Journal of Cerebral Blood Flow & Metabolism 18, no. 3 (1998): 238–47. http://dx.doi.org/10.1097/00004647-199803000-00002.

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Inhibitors of apoptosis and of excitotoxic cell death reduce brain damage after transient and permanent middle cerebral artery occlusion. We compared the neuroprotective effects of two caspase family inhibitors with the N-methyl-d-aspartate receptor antagonist (+)-MK-801 hydrogen maleate (MK-801) in a newly characterized cycloheximidesensitive murine model of transient middle cerebral artery occlusion (30 minutes) in which apoptotic cell death is prominent. Ischemic infarction, undetected by 2,3,5-triphenyltetrazolium chloride staining at 24-hour reperfusion, featured prominently in the striat

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Puyal, Julien, Anne Vaslin, Vincent Mottier, and Peter G. H. Clarke. "Postischemic treatment of neonatal cerebral ischemia should target autophagy." Annals of Neurology 66, no. 3 (2009): 378–89. https://doi.org/10.1002/ana.21714.

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OBJECTIVE: To evaluate the contributions of autophagic, necrotic, and apoptotic cell death mechanisms after neonatal cerebral ischemia and hence define the most appropriate neuroprotective approach for postischemic therapy. METHODS: Rats were exposed to transient focal cerebral ischemia on postnatal day 12. Some rats were treated by postischemic administration of pan-caspase or autophagy inhibitors. The ischemic brain tissue was studied histologically, biochemically, and ultrastructurally for autophagic, apoptotic, and necrotic markers. RESULTS: Lysosomal and autophagic activities were increas

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Tikhonova, Olga A., Dmitry S. Druzhinin, Evgenia S. Druzhinina, and Maria А. Rukosueva. "Chronic Inflammatory Demyelinating Polyneuropathy Induced by Immune Checkpoint Inhibitors: Case Reports." Annals of Clinical and Experimental Neurology 18, no. 1 (2024): 98–104. http://dx.doi.org/10.54101/acen.2024.1.11.

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Neurological immune-related adverse events (irAE) are rare but potentially fatal complications associated with the use of immune checkpoint inhibitors (ICI). Recently, there has been a trend towards an increase in the incidence of these cases. We present two case reports of demyelinating polyneuropathy in patients with skin melanoma treated with pembrolizumab or nivolumab. Unawareness of neurological irAE induced by ICI leads to delayed diagnosis and medical treatment, and this may result in persistent neurological deficit or even patients’ death. Neurological irAEs include myasthenia gr

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Erkkila, Krista, Sauli Kyttanen, Marten Wikstrom, et al. "Regulation of human male germ cell death by modulators of ATP production." American Journal of Physiology-Endocrinology and Metabolism 290, no. 6 (2006): E1145—E1154. http://dx.doi.org/10.1152/ajpendo.00142.2005.

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The understanding of testicular physiology, pathology, and male fertility issues requires knowledge of male germ cell death and energy production. Here, we induced human male germ cell apoptosis (detected by Southern blot analysis of DNA fragmentation, TUNEL, activation of caspases-3 and -9, and electron microscopy) by incubating seminiferous tubule segments under hormone- and serum-free conditions. Inhibitors of complexes I to IV of mitochondrial respiration, exposure to anoxia, and inhibition of F0F1-ATPase (with oligomycin) decreased the ATP levels (analyzed by HPLC) and suppressed apoptosi

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Kohno, Keiji, Shinsuke Ohta, Shigeru Furuta, Kanehisa Kohno, Yoshiaki Kumon, and Saburo Sakaki. "Intraventricular administration of nitric oxide synthase inhibitors prevents delayed neuronal death in gerbil hippocampal CA 1 neurons." Neuroscience Letters 199, no. 1 (1995): 65–68. http://dx.doi.org/10.1016/0304-3940(95)12018-y.

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Koponen, Susanna, Gundars Goldsteins, Riitta Keinänen та Jari Koistinaho. "Induction of Protein Kinase Cδ Subspecies in Neurons and Microglia after Transient Global Brain Ischemia". Journal of Cerebral Blood Flow & Metabolism 20, № 1 (2000): 93–102. http://dx.doi.org/10.1097/00004647-200001000-00013.

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The delayed death of CA1 neurons after global brain ischemia is associated with induction of apoptosis genes and is inhibited by protein synthesis inhibitors, suggesting that the degeneration of CA1 pyramidal neurons is an active process that requires new gene expression. The transient global ischemia model has been extensively used to identify enzymes and other proteins underlying delayed neuronal cell death. The expression of protein kinase C (PKC) subspecies after 20 minutes of global brain ischemia produced by a four-vessel occlusion model in the rat was studied. From the multiple PKC subs

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Seifrtová, M., R. Havelek, M. Chmelařová, et al. "The Effect of ATM and ERK1/2 Inhibition on Mitoxantrone-Induced Cell Death of Leukaemic Cells." Folia Biologica 57, no. 2 (2011): 74–81. http://dx.doi.org/10.14712/fb2011057020074.

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The relationship between signal pathways MEK1/2-ERK1/2 and ATM-p53 in the response to DNA damage is not well understood. The aim of our study was to investigate the effect of mitoxantrone and two protein kinase inhibitors – caffeine (inhibitor of ATM kinase) and U0126 (inhibitor of MEK1/2 kinase) – on MOLT-4 and Jurkat leukaemic cell lines. In this work we show that the inhibition of MEK1/2 is associated with an increased mortality of cells after mitoxantrone treatment. Inhibition of ATM by caffeine delayed mitoxantrone-induced cell death in MOLT-4 cells. Mitoxantrone itself induced cell-cycle

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Dawson, T. L., G. J. Gores, A. L. Nieminen, B. Herman, and J. J. Lemasters. "Mitochondria as a source of reactive oxygen species during reductive stress in rat hepatocytes." American Journal of Physiology-Cell Physiology 264, no. 4 (1993): C961—C967. http://dx.doi.org/10.1152/ajpcell.1993.264.4.c961.

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Cell killing, oxygen consumption, and hydroperoxide formation were determined in rat hepatocytes after glycolytic and respiratory inhibition. These conditions model the ATP depletion and reductive stress of anoxia (“chemical hypoxia”). Glycolysis was inhibited with iodoacetate, and mitochondrial electron transfer was blocked with sodium azide, cyanide, or myxothiazol. Cell killing, hydroperoxide formation, and inhibitor-insensitive oxygen consumption were greater after azide than after myxothiazol or cyanide. Desferrioxamine, an inhibitor of iron-catalyzed hydroxyl radical formation, delayed c

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Hutson, Thomas E., Frank Xiaoqing Liu, Shivani Pandya, et al. "Clinical impact of early progression among patients (Pts) with metastatic renal cell carcinoma (mRCC) treated with tyrosine kinase inhibitors (TKIs) in first-line (1L) setting: IMPACT RCC real-world study." Journal of Clinical Oncology 38, no. 15_suppl (2020): e17079-e17079. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e17079.

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e17079 Background: Previous research has indicated a high burden of illness among mRCC pts who progressed to second line (2L) systemic therapy, suggesting benefits to delaying 1L progression. This study examined the clinical impact of early vs delayed disease progression among mRCC pts treated with 1L TKI monotherapies followed by 2L therapy in the US Veterans Health Administration (VHA) database. Methods: Newly diagnosed mRCC pts treated with 1L TKIs followed by 2L therapy were identified between OCT2013-MAR2018 within the VHA database (1L start date = index date). Eligible pts were required

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Yan, Jie, Alexander Günter, Soumyaparna Das, et al. "Inherited Retinal Degeneration: PARP-Dependent Activation of Calpain Requires CNG Channel Activity." Biomolecules 12, no. 3 (2022): 455. http://dx.doi.org/10.3390/biom12030455.

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Inherited retinal degenerations (IRDs) are a group of blinding diseases, typically involving a progressive loss of photoreceptors. The IRD pathology is often based on an accumulation of cGMP in photoreceptors and associated with the excessive activation of calpain and poly (ADP-ribose) polymerase (PARP). Inhibitors of calpain or PARP have shown promise in preventing photoreceptor cell death, yet the relationship between these enzymes remains unclear. To explore this further, organotypic retinal explant cultures derived from wild-type and IRD-mutant mice were treated with inhibitors specific fo

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Shinzawa, Koei, and Yoshihide Tsujimoto. "PLA2 activity is required for nuclear shrinkage in caspase-independent cell death." Journal of Cell Biology 163, no. 6 (2003): 1219–30. http://dx.doi.org/10.1083/jcb.200306159.

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Apoptosis is defined on the basis of morphological changes like nuclear fragmentation and chromatin condensation, which are dependent on caspases. Many forms of caspase-independent cell death have been reported, but the mechanisms are still poorly understood. We found that hypoxic cell death was independent of caspases and was associated with significant nuclear shrinkage. Neither Bcl-2 nor Apaf-1 deficiency prevented hypoxic nuclear shrinkage. To understand the molecular mechanism of the nuclear shrinkage, we developed an in vitro system using permeabilized cells, which allowed us to purify a

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Péron, Julien, Alexandre Lambert, Stephane Munier, et al. "Assessing Long-Term Survival Benefits of Immune Checkpoint Inhibitors Using the Net Survival Benefit." JNCI: Journal of the National Cancer Institute 111, no. 11 (2019): 1186–91. http://dx.doi.org/10.1093/jnci/djz030.

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Abstract Background The treatment effect in survival analysis is commonly quantified as the hazard ratio, and tested statistically using the standard log-rank test. Modern anticancer immunotherapies are successful in a proportion of patients who remain alive even after a long-term follow-up. This new phenomenon induces a nonproportionality of the underlying hazards of death. Methods The properties of the net survival benefit were illustrated using the dataset from a trial evaluating ipilimumab in metastatic melanoma. The net survival benefit was then investigated through simulated datasets und

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Zhang, Yunhong, Xiaochun Zhang, Tae S. Park, and Jeffrey M. Gidday. "Cerebral Endothelial Cell Apoptosis after Ischemia—Reperfusion: Role of PARP Activation and AIF Translocation." Journal of Cerebral Blood Flow & Metabolism 25, no. 7 (2005): 868–77. http://dx.doi.org/10.1038/sj.jcbfm.9600081.

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Cerebral ischemia-reperfusion leads to vascular dysfunction characterized by endothelial cell injury or death. In the present study, we used an in vitro model to elucidate mechanisms of human brain microvascular endothelial cell (HBMEC) injury after episodic ischemia-reperfusion. Near-confluent HBMEC cultures were exposed to intermittent hypoxia-reoxygenation (HX/RO) and, at different recovery time points, cell viability was assessed by the MTT assay, apoptotic death by fluorescence microscopy of terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate-biotin nick end lab

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Bommareddy, Praveen K., Salvatore Aspromonte, Andrew Zloza, Samuel D. Rabkin, and Howard L. Kaufman. "MEK inhibition enhances oncolytic virus immunotherapy through increased tumor cell killing and T cell activation." Science Translational Medicine 10, no. 471 (2018): eaau0417. http://dx.doi.org/10.1126/scitranslmed.aau0417.

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Melanoma is an aggressive cutaneous malignancy, but advances over the past decade have resulted in multiple new therapeutic options, including molecularly targeted therapy, immunotherapy, and oncolytic virus therapy. Talimogene laherparepvec (T-VEC) is a herpes simplex type 1 oncolytic virus, and trametinib is a MEK inhibitor approved for treatment of melanoma. Therapeutic responses with T-VEC are often limited, and BRAF/MEK inhibition is complicated by drug resistance. We observed that the combination of T-VEC and trametinib resulted in enhanced melanoma cell death in vitro. Further, combinat

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Vucic, D., S. Seshagiri, and L. K. Miller. "Characterization of reaper- and FADD-induced apoptosis in a lepidopteran cell line." Molecular and Cellular Biology 17, no. 2 (1997): 667–76. http://dx.doi.org/10.1128/mcb.17.2.667.

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Expression of the reaper gene (rpr) correlates with the initiation of apoptosis in Drosophila melanogaster. Transient expression of rpr in the lepidopteran SF-21 cell line induced apoptosis displaying nuclear condensation and fragmentation, oligonucleosomal ladder formation, cell surface blebbing, and apoptotic body formation. Inhibitors of ICE-family proteases p35 and crmA, as well as members of the iap class of genes, Op-iap and D-iap2, but not bcl-2 family members, blocked rpr-induced apoptosis. Mutational analysis of rpr provided no support for the proposed sequence similarity of Reaper an

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Burdova, Kamila, Radka Storchova, Matous Palek, and Libor Macurek. "WIP1 Promotes Homologous Recombination and Modulates Sensitivity to PARP Inhibitors." Cells 8, no. 10 (2019): 1258. http://dx.doi.org/10.3390/cells8101258.

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Genotoxic stress triggers a combined action of DNA repair and cell cycle checkpoint pathways. Protein phosphatase 2C delta (referred to as WIP1) is involved in timely inactivation of DNA damage response by suppressing function of p53 and other targets at chromatin. Here we show that WIP1 promotes DNA repair through homologous recombination. Loss or inhibition of WIP1 delayed disappearance of the ionizing radiation-induced 53BP1 foci in S/G2 cells and promoted cell death. We identify breast cancer associated protein 1 (BRCA1) as interactor and substrate of WIP1 and demonstrate that WIP1 activit

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Liu, Yongqing, Pengbo Hu, Liang Xu, et al. "Current Progress on Predictive Biomarkers for Response to Immune Checkpoint Inhibitors in Gastric Cancer: How to Maximize the Immunotherapeutic Benefit?" Cancers 15, no. 8 (2023): 2273. http://dx.doi.org/10.3390/cancers15082273.

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Gastric cancer is the fifth most prevalent cancer and the fourth leading cause of cancer death globally. Delayed diagnosis and pronounced histological and molecular variations increase the complexity and challenge of treatment. Pharmacotherapy, which for a long time was systemic chemotherapy based on 5-fluorouracil, is the mainstay of management for advanced gastric cancer. Trastuzumab and programmed cell death 1 (PD-1) inhibitors have altered the therapeutic landscape, contributing to noticeably prolonged survivorship in patients with metastatic gastric cancer. However, research has revealed

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Khaskheli, Allah Jurio, Muharam Ali, Muhammad Ibrahim Khaskheli, Niaz Ahmed Wahocho, Shahla Baloch, and Juang Hong Li. "Senescence Associated Genes Modulating Programmed Cell Death in Plant Leaves." Journal of Applied Research in Plant Sciences 6, no. 1 (2025): 48–55. https://doi.org/10.38211/joarps.2025.06.312.

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The aim of this study was to evaluate the effects of various promoters and inhibitors of leaf senescence in Rosa hybrida by applying different concentrations of plant hormones under controlled tissue culture conditions. The study sought to identify hormonal treatments that can delay or accelerate senescence, with the goal of improving the postharvest quality and longevity of rose foliage. The plants were grown by tissue culture techniques, which were free from disease. Regenerated plants with well-defined leaves, were infiltrated with hormones and the untreated plant leaves used as control. Af

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Vogel, Peter, Herman v. d. Putten, Erik Popp, et al. "Improved Resuscitation after Cardiac Arrest in Rats Expressing the Baculovirus Caspase Inhibitor Protein p35 in Central Neurons." Anesthesiology 99, no. 1 (2003): 112–21. http://dx.doi.org/10.1097/00000542-200307000-00020.

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Background Global cerebral ischemia is associated with delayed neuronal death. Given the role of caspases in apoptosis, caspase inhibitors may provide neuronal protection after cardiac arrest. To this end, the authors generated a transgenic rat line expressing baculovirus p35, a broad-spectrum caspase inhibitor, in central neurons. Its effects were evaluated on neuronal cell death and outcome after global cerebral ischemia. Methods Global cerebral ischemia was induced by cardiocirculatory arrest. After 6 min, animals were resuscitated by controlled ventilation, extrathoracic cardiac massage, e

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Zehnle, Patricia M. A., Ying Wu, Naile Koleci, Sheila Bohler, and Miriam Erlacher. "Lentivirus-Mediated BCL-XL Overexpression Inhibits Stem Cell Apoptosis during Ex Vivo Expansion and Provides Competitive Advantage Following Xenotransplantation." International Journal of Molecular Sciences 25, no. 7 (2024): 4105. http://dx.doi.org/10.3390/ijms25074105.

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Hematopoietic reconstitution after hematopoietic stem cell transplantation (HSCT) is influenced by the number of transplanted cells. However, under certain conditions donor cell counts are limited and impair clinical outcome. Hematopoietic stem and progenitor cell (HSPC) expansion prior to HSCT is a widely used method to achieve higher donor cell counts and minimize transplantation-related risks such as graft failure or delayed engraftment. Still, expansion in a non-physiological environment can trigger cell death mechanisms and hence counteract the desired effect. We have shown earlier that d

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Neuendorff, Nina Rosa. "Therapie-assoziierte myeloische Neoplasien: Woran bei Blutbildveränderungen unter Therapie mit PARP-Inhibitoren gedacht werden sollte." Kompass Onkologie 9, no. 1 (2022): 20–21. http://dx.doi.org/10.1159/000522397.

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<b>Background:</b> Poly(ADP-ribose) polymerase (PARP) inhibitors have shown efficacy and acceptable safety in a range of neoplasms, particularly in ovarian cancers. However, some concerns have emerged regarding rare and delayed adverse events including cases of myelodysplastic syndrome and acute myeloid leukaemia, for which data are scarce. The aim of this study was to estimate the risk of myelodysplastic syndrome and acute myeloid leukaemia related to PARP inhibitors, via a systematic review and safety meta-analysis, and to describe clinical features of PARP inhibitor-related myel

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Ellis, Leigh, Michael Bots, Ralph K. Lindemann, et al. "The histone deacetylase inhibitors LAQ824 and LBH589 do not require death receptor signaling or a functional apoptosome to mediate tumor cell death or therapeutic efficacy." Blood 114, no. 2 (2009): 380–93. http://dx.doi.org/10.1182/blood-2008-10-182758.

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Abstract LAQ824 and LBH589 (panobinostat) are histone deacetylase inhibitors (HDACi) developed as cancer therapeutics and we have used the Eμ-myc lymphoma model to identify the molecular events required for their antitumor effects. Induction of tumor cell death was necessary for these agents to mediate therapeutic responses in vivo and both HDACi engaged the intrinsic apoptotic cascade that did not require p53. Death receptor pathway blockade had no effect on the therapeutic activities of LAQ824 and LBH589; however, overexpression of Bcl-2 or Bcl-XL protected lymphoma cells from HDACi-induced

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Smith, M. W., P. C. Phelps, and B. F. Trump. "Injury-induced changes in cytosolic Ca2+ in individual rabbit proximal tubule cells." American Journal of Physiology-Renal Physiology 262, no. 4 (1992): F647—F655. http://dx.doi.org/10.1152/ajprenal.1992.262.4.f647.

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Cell injury was studied in cultured rabbit proximal tubular epithelial cells using digital-imaging fluorescent microscopy to relate changes in cytosolic Ca2+ ([Ca2+]i) to bleb formation and cell death. Fura-2-loaded cells were treated in normal (1.37 mM) and low (less than 5 microM) extracellular Ca2+ ([Ca2+]e) with 1) inhibitors of glycolysis (iodoacetate) and/or mitochondrial oxidation (KCN), 2) thiol-modifying reagents (N-ethylmaleimide, p-chloromercuribenzene, and p-chloromercuribenzene sulfonate), and 3) Ca2+ ionophore (ionomycin). All three types of injury produced both [Ca2+]e-independe

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Tan, Chia Jie, Connor Willis, Trang Au, et al. "Abstract PO1-16-07: Patient Characteristics and Treatment Sequencing Among HER2-low Metastatic Breast Cancer Patients with Rapid vs. Delayed Progression on First-line Endocrine Therapy." Cancer Research 84, no. 9_Supplement (2024): PO1–16–07—PO1–16–07. http://dx.doi.org/10.1158/1538-7445.sabcs23-po1-16-07.

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Abstract Background Patients with HER2-low (IHC 1+ or 2+ and negative ISH) and hormone-receptor positive (HR+) metastatic breast cancer (mBC) who rapidly progress on first-line (1L) endocrine therapy may experience different treatment pathways than those with delayed progression. The goal of this multisite study is to describe the characteristics, treatment patterns and outcomes of these patients with rapid vs. delayed progression. Methods This was a retrospective cohort study of HER2-low, HR+, mBC patients who received 1L endocrine-based treatment regimen at the Huntsman Cancer Institute, Mof

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Fryknäs, Mårten, Linda Rickardson, Malin Wickström, et al. "Phenotype-Based Screening of Mechanistically Annotated Compounds in Combination with Gene Expression and Pathway Analysis Identifies Candidate Drug Targets in a Human Squamous Carcinoma Cell Model." Journal of Biomolecular Screening 11, no. 5 (2006): 457–68. http://dx.doi.org/10.1177/1087057106288048.

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The squamous cell carcinoma HeLa cell line and an epithelial cell line hTERT-RPE with a nonmalignant phenotype were interrogated for HeLa cell selectivity in response to 1267 annotated compounds representing 56 pharmacological classes. Selective cytotoxic activity was observed for 14 of these compounds dominated by cyclic adenosine monophosphate (cAMP) selective phosphodiesterase (PDE) inhibitors, which tended to span a representation of the chemical descriptor space of the library. The PDE inhibitors induced delayed cell death with features compatible with classical apoptosis. The PDE inhibit

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Fazer-Posorske, Casey, Anna Schwecke, Lisa Kottschade, and Katharine Price. "Navigating skin toxicity in the era of immunotherapy." Journal of Dermatology for Physician Assistants 19, no. 2 (2025): 11–17. https://doi.org/10.1097/jdpa.0000000000000053.

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Immunotherapy continues to revolutionize cancer treatment, instilling optimism and enhancing prognoses across diverse malignancies. Immune checkpoint inhibitors (ICIs), including cytotoxic T lymphocyte–associated-protein 4 (CTLA-4), programmed death receptor 1 (PD-1), programmed death ligand 1 (PD-L1), and lymphocyte activation gene 3 (LAG-3) represent a paradigm shift. However, these transformative therapies introduce immune-related adverse events (irAEs), distinct from conventional cancer treatments, with delayed onset and potential persistence. While most cutaneous irAEs are mild, severe to

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Tissawak, Amanda, Yarden Rosin, Shirly Katz Galay, et al. "A chaperonin complex regulates organelle proteostasis in malaria parasites." PLOS Pathogens 21, no. 7 (2025): e1013275. https://doi.org/10.1371/journal.ppat.1013275.

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The apicoplast of Plasmodium parasites serves as a metabolic hub that synthesize essential biomolecules. Like other endosymbiotic organelles, 90% of the apicoplast proteome is encoded by the cell nucleus and transported to the organelle. Evidence suggests that the apicoplast has minimal control over the synthesis of its proteome and therefore it is unclear how organelle proteostasis is regulated. Here, we identified and investigated a large and conserved chaperonin (CPN) complex with a previously unknown function. Using genetic tools, we demonstrated that ablation of the apicoplast CPN60 subun

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Pediaditakis, Peter, Jae-Sung Kim, Lihua He, Xun Zhang, Lee M. Graves, and John J. Lemasters. "Inhibition of the mitochondrial permeability transition by protein kinase A in rat liver mitochondria and hepatocytes." Biochemical Journal 431, no. 3 (2010): 411–21. http://dx.doi.org/10.1042/bj20091741.

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NO and cGMP administered at reperfusion after ischaemia prevent injury to hepatocytes mediated by the MPT (mitochondrial permeability transition). To characterize further the mechanism of protection, the ability of hepatic cytosol in combination with cyclic nucleotides to delay onset of the calcium-induced MPT was evaluated in isolated rat liver mitochondria. Liver cytosol plus cGMP or cAMP dose-dependently inhibited the MPT, required ATP hydrolysis for inhibition and did not inhibit mitochondrial calcium uptake. Specific peptide inhibitors for PKA (protein kinase A), but not PKG (protein kina

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Gray, Jonathan J., Philip E. Bickler, Christian S. Fahlman, Xinhua Zhan, and Jennifer A. Schuyler. "Isoflurane Neuroprotection in Hypoxic Hippocampal Slice Cultures Involves Increases in Intracellular Ca2+and Mitogen-activated Protein Kinases." Anesthesiology 102, no. 3 (2005): 606–15. http://dx.doi.org/10.1097/00000542-200503000-00020.

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Background The volatile anesthetic isoflurane reduces acute and delayed neuron death in vitro models of brain ischemia, an action that the authors hypothesize is related to moderate increases in intracellular calcium concentration ([Ca2+]i). Specifically, the authors propose that during hypoxia, moderate increases in [Ca2+]i in the presence of isoflurane stimulates the Ca2+-dependent phosphorylation of members of the mitogen-activated protein kinase (MAP) kinase Ras-Raf-MEK-ERK pathway that are critical for neuroprotective signaling and suppression of apoptosis. Methods Death of CA1, CA3, and

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Dudek, F. Edward, and Philip A. Williams. "Does Neuroprotection Prevent Epileptogenesis?" Epilepsy Currents 3, no. 2 (2003): 68–69. http://dx.doi.org/10.1111/j.1535-7597.2003.03213.x.

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Delayed Sclerosis, Neuroprotection, and Limbic Epileptogenesis After Status Epilepticus in the Rat Ebert U, Brandt C, Loscher W Epilepsia 2002;43(suppl 5):86–95 Purpose Hippocampal sclerosis and massive neurodegeneration in other parts of the limbic system are considered hallmarks of temporal lobe epilepsy. With the rat model of kainate-induced status epilepticus, we sought to determine if limbic sclerosis after an excitotoxic insult follows a delayed type of neurodegeneration and is thus accessible to neuroprotective intervention after the insult. Effective pharmacologic neuroprotection after

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Wang, Tzu-Fei, and Marc Carrier. "Immune Checkpoint Inhibitors-Associated Thrombosis: Incidence, Risk Factors and Management." Current Oncology 30, no. 3 (2023): 3032–46. http://dx.doi.org/10.3390/curroncol30030230.

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Immune checkpoint inhibitors (ICIs) target programmed cell death (PD) 1 receptor and its ligand PD-L1, and have become an integral part of treatment regimens in many cancers including lung cancer, renal cell carcinoma, melanoma, and more. Cancer is associated with a significantly increased risk of venous thromboembolism compared to non-cancer patients, and the risks increase further with anticancer therapies including ICIs. Cancer-associated thrombosis can lead to hospitalizations, delayed cancer treatment, and mortality. While thrombosis was not reported as a major complication in initial cli

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Anderson, Jeffrey L., Kirk U. Knowlton, J. Brent Muhlestein, Tami L. Bair, Viet T. Le, and Benjamin D. Horne. "Evaluation of TReatment With Angiotensin Converting Enzyme Inhibitors and the Risk of Lung Cancer: ERACER—An Observational Cohort Study." Journal of Cardiovascular Pharmacology and Therapeutics 26, no. 4 (2021): 321–27. http://dx.doi.org/10.1177/1074248420987054.

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Introduction: Angiotensin converting enzyme inhibitors (ACEIs) are widely prescribed medications. A recent British study reported a 14% increased risk of lung cancer with ACEI versus angiotensin receptor blocker (ARB) prescriptions, and risk increased with longer use. We sought to validate this observation. Methods: We searched the Intermountain Enterprise Data Warehouse from 1996 to 2018 for patients newly treated with an ACEI or an ARB and with ≥1 year’s follow-up or to incident lung cancer or death. Unadjusted and adjusted hazard ratios (HRs) for lung cancer and for lung cancer or all-cause

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Katchanov, Juri, Christoph Harms, Karen Gertz, et al. "Mild Cerebral Ischemia Induces Loss of Cyclin-Dependent Kinase Inhibitors and Activation of Cell Cycle Machinery before Delayed Neuronal Cell Death." Journal of Neuroscience 21, no. 14 (2001): 5045–53. http://dx.doi.org/10.1523/jneurosci.21-14-05045.2001.

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Xu, Fangling, Xiaodong Liang, Robert B. Tesh, and Shu-Yuan Xiao. "Characterization of cell-death pathways in Punta Toro virus-induced hepatocyte injury." Journal of General Virology 89, no. 9 (2008): 2175–81. http://dx.doi.org/10.1099/vir.0.2008/001644-0.

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Punta Toro virus (PTV; genus Phlebovirus, family Bunyaviridae) causes apoptosis of hepatocytes in vivo in experimentally infected hamsters and in vitro in cultured HepG2 cells. Screening for expression of apoptosis-related genes has shown alterations in the genes for tumour necrosis factor-α (TNF-α) and the TNF receptor family. This study examined the roles of the TNF receptor-related extrinsic pathway and the Bcl-2 family-associated mitochondrial pathway in PTV-induced cell death. The effects of caspase inhibitors (caspIs) and TNF on cellular viability, virus replication, and morphological an

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