scholarly journals Molecular basis of disregulation of programmed lymphocytes’ death in chronic viral infection

2006 ◽  
Vol 5 (2) ◽  
pp. 23-34
Author(s):  
V. V. Novitsky ◽  
N. V. Ryazantseva ◽  
O. B. Zhoukova
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Viral Infection ◽  
Immune Cells ◽  
Molecular Basis ◽  
Molecular Mechanisms ◽  
Recent Literature ◽  
Chronic Viral Infection ◽  
Persistent Viruses

The review analyses information from recent literature and results of the authors’ own investigations concerning imbalance of programmed cell death in forming chronic viral infection. Molecular mechanisms of apoptosis modulation of immune cells by persistent viruses are discussed in the article.

scholarly journals Prostaglandin E2 and programmed cell death 1 signaling coordinately impair CTL function and survival during chronic viral infection

2015 ◽  
Vol 21 (4) ◽  
pp. 327-334 ◽  
Author(s):  
Jonathan H Chen ◽  
Curtis J Perry ◽  
Yao-Chen Tsui ◽  
Matthew M Staron ◽  
Ian A Parish ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Viral Infection ◽  
Prostaglandin E2 ◽  
Chronic Viral Infection ◽  
Programmed Cell Death 1

scholarly journals Conformational states of the cytoprotective protein Bcl-xL

2020 ◽  
Author(s):  
P. Ryzhov ◽  
Y. Tian ◽  
Y. Yao ◽  
A. A. Bobkov ◽  
W. Im ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Molecular Basis ◽  
Molecular Mechanisms ◽  
Md Simulations ◽  
Water Soluble ◽  
Titration Calorimetry ◽  
Intracellular Membranes ◽  
Intrinsically Disordered ◽  
Disordered Loop

ABSTRACTBcl-xL is a major inhibitor of apoptosis, a fundamental homeostatic process of programmed cell death that is highly conserved across evolution. Because it plays prominent roles in cancer, Bcl-xL is a major target for anti-cancer therapy and for studies aimed at understanding its structure and activity. While Bcl-xL is active primarily at intracellular membranes, most studies have focused on soluble forms of the protein lacking both the membrane-anchoring C-terminal tail and the intrinsically disordered loop, and this has resulted in a fragmented view of the protein’s biological activity. Here we describe how these segments affect the protein’s conformation and ligand binding activity in both its soluble and membrane-anchored states. The combined data from nuclear magnetic resonance (NMR) spectroscopy, molecular dynamics (MD) simulations, and isothermal titration calorimetry (ITC) provide information about the molecular basis for the protein’s functionality and a view of its complex molecular mechanisms.SIGNIFICANCEThe human protein Bcl-xL is a key regulator of programmed cell death in health and disease. Structural studies, important for understating the molecular basis for its functions, have advanced primarily by deleting both the long disordered loop that regulates its activity and the C-terminal tail that anchors the protein to intracellular membranes Here we describe the preparation and conformations of full-length Bcl-xL in both its water-soluble and membrane-anchored states. The study provides new biophysical insights about Bcl-xL and its greater Bcl-2 protein family.

scholarly journals Progress in understanding the role of lncRNA in programmed cell death

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Na Jiang ◽  
Xiaoyu Zhang ◽  
Xuejun Gu ◽  
Xiaozhuang Li ◽  
Lei Shang
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Molecular Mechanisms ◽  
Membrane Receptors ◽  
Gene Expressions ◽  
Apoptosis Pathway ◽  
Stem Cell Pluripotency ◽  
Extrinsic Apoptosis ◽  
Related Proteins ◽  
Cycle Regulation

AbstractLong non-coding RNAs (lncRNAs) are transcripts longer than 200 nucleotides but not translated into proteins. LncRNAs regulate gene expressions at multiple levels, such as chromatin, transcription, and post-transcription. Further, lncRNAs participate in various biological processes such as cell differentiation, cell cycle regulation, and maintenance of stem cell pluripotency. We have previously reported that lncRNAs are closely related to programmed cell death (PCD), which includes apoptosis, autophagy, necroptosis, and ferroptosis. Overexpression of lncRNA can suppress the extrinsic apoptosis pathway by downregulating of membrane receptors and protect tumor cells by inhibiting the expression of necroptosis-related proteins. Some lncRNAs can also act as competitive endogenous RNA to prevent oxidation, thereby inhibiting ferroptosis, while some are known to activate autophagy. The relationship between lncRNA and PCD has promising implications in clinical research, and reports have highlighted this relationship in various cancers such as non-small cell lung cancer and gastric cancer. This review systematically summarizes the advances in the understanding of the molecular mechanisms through which lncRNAs impact PCD.

scholarly journals Mutations in the Parkinson’s Disease-Associated PARK2 Gene Are Accompanied by Imbalance in Programmed Cell Death Systems

Acta Naturae ◽  
2015 ◽  
Vol 7 (4) ◽  
pp. 146-149 ◽  
Author(s):  
E. V. Konovalova ◽  
O. M. Lopacheva ◽  
I. A. Grivennikov ◽  
O. S. Lebedeva ◽  
E. В. Dashinimaev ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Dopaminergic Neurons ◽  
Molecular Mechanisms ◽  
Disease Patient ◽  
Parkinsons Disease ◽  
Leading Role ◽  
Midbrain Dopaminergic Neurons ◽  
Induced Pluripotent ◽  
Apoptotic Factors

Parkinsons disease is caused by the degeneration of midbrain dopaminergic neurons. A rare recessive form of the disease may be caused by a mutation in the PARK2 gene, whose product, Parkin, controls mitophagy and programmed cell death. The level of pro- and anti-apoptotic factors of the Bcl-2 family was determined in dopaminergic neurons derived from the induced pluripotent stem cells of a healthy donor and a Parkinsons disease patient bearing PARK2 mutations. Western blotting was used to study the ratios of Bax, Bak, Bcl-2, Bcl-XL, and Bcl-W proteins. The pro-apoptotic Bak protein level in PARK2-neurons was shown to be two times lower than that in healthy cells. In contrast, the expression of the anti-apoptotic factors Bcl-XL, Bcl-W, and Bcl-2 was statistically significantly higher in the mutant cells compared to healthy dopaminergic neurons. These results indicate that PARK2 mutations are accompanied by an imbalance in programmed cell death systems in which non-apoptotic molecular mechanisms play the leading role.

scholarly journals The nitrogen-fixing symbiotic cyanobacterium, Nostoc punctiforme can regulate plant programmed cell death

2020 ◽  
Author(s):  
Samuel P. Belton ◽  
Paul F. McCabe ◽  
Carl K. Y. Ng
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Molecular Mechanisms ◽  
Differential Regulation ◽  
Nitrogen Fixing ◽  
Nostoc Punctiforme ◽  
Transcriptional Reprogramming ◽  
Cell Growth And Differentiation ◽  
Transcriptome Resource ◽  
Developmental Signalling

AbstractCyanobacteria such as Nostoc spp. can form nitrogen-fixing symbioses with a broad range of plant species. Unlike other plant-bacteria symbioses, little is understood about the immunological and developmental signalling events induced by Nostoc cyanobionts (symbiotic cyanobacteria). Here, we used suspension cell cultures to elucidate the early molecular mechanisms underpinning the association between cyanobionts and plants by studying the effects of conditioned medium (CM) from Nostoc punctiforme cultures on plant programmed cell death (PCD), a typical immune response activated during incompatible interactions. We showed that N. punctiforme-CM could suppress PCD induced by a temperature stress. Interestingly, this was preceded by significant transcriptional reprogramming, as evidenced by the differential regulation of a network of defence-associated genes, as well as genes implicated in regulating cell growth and differentiation. This work is the first to show that cyanobionts can regulate PCD in plants and provides a valuable transcriptome resource for the early immunological and developmental signalling events elicited by Nostoc cyanobionts.

Programmed Cell Death in Plants: Insights Into developmental and Stress-Induced Cell Death

2021 ◽  
Vol 22 ◽  
Author(s):  
Heba T. Ebeed ◽  
Ahmed A. El-helely
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Plant Development ◽  
Molecular Basis ◽  
Stress Conditions ◽  
Similar Form ◽  
Cellular Homeostasis ◽  
Endogenous Factors ◽  
Selective Elimination

: Programmed cell death (PCD) is a fundamental genetically controlled process in most organisms. PCD is responsible for the selective elimination of damaged or unwanted cells and organs to maintain cellular homeostasis during the organ’s development under normal conditions as well as during defense or adaptation to stressful conditions. PCD pathways have been extensively studied in animals. In plants, studies focusing on understanding the pathways of PCD have advanced significantly. However, the knowledge about the molecular basis of PCD is still very limited. Some PCD pathways that have been discovered in animals are not present in plants or found with a similar form. PCD in plants is developmentally controlled (by endogenous factors) to function in organ development and differentiations as well as environmentally induced (by exogenous stimuli) to help the plant in surviving under stress conditions. Here, we present a review of the role of PCD in plant development and explore different examples of stress-induced PCD as well as highlight the main differences between the plant and animal PCD.

scholarly journals Long-term depression: a cell biological view

2014 ◽  
Vol 369 (1633) ◽  
pp. 20130138 ◽  
Author(s):  
Morgan Sheng ◽  
Ali Ertürk
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Dendritic Spines ◽  
Crucial Role ◽  
Molecular Mechanisms ◽  
Signalling Pathways ◽  
Long Term Depression ◽  
A Cell ◽  
Biological Programme

Recent studies of the molecular mechanisms of long-term depression (LTD) suggest a crucial role for the signalling pathways of apoptosis (programmed cell death) in the weakening and elimination of synapses and dendritic spines. With this backdrop, we suggest that LTD can be considered as the electrophysiological aspect of a larger cell biological programme of synapse involution, which uses localized apoptotic mechanisms to sculpt synapses and circuits without causing cell death.

scholarly journals Unveiling the immune infiltrate modulation in cancer and response to immunotherapy by MIXTURE—an enhanced deconvolution method

2020 ◽  
Author(s):  
Elmer A Fernández ◽  
Yamil D Mahmoud ◽  
Florencia Veigas ◽  
Darío Rocha ◽  
Matías Miranda ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Immune Cells ◽  
Immune Cell ◽  
Immune Escape ◽  
Intratumor Heterogeneity ◽  
Support Vector ◽  
Tumor Immune Escape ◽  
Immune Infiltrate ◽  
Tumor Biopsies

Abstract The accurate quantification of tumor-infiltrating immune cells turns crucial to uncover their role in tumor immune escape, to determine patient prognosis and to predict response to immune checkpoint blockade. Current state-of-the-art methods that quantify immune cells from tumor biopsies using gene expression data apply computational deconvolution methods that present multicollinearity and estimation errors resulting in the overestimation or underestimation of the diversity of infiltrating immune cells and their quantity. To overcome such limitations, we developed MIXTURE, a new ν-support vector regression-based noise constrained recursive feature selection algorithm based on validated immune cell molecular signatures. MIXTURE provides increased robustness to cell type identification and proportion estimation, outperforms the current methods, and is available to the wider scientific community. We applied MIXTURE to transcriptomic data from tumor biopsies and found relevant novel associations between the components of the immune infiltrate and molecular subtypes, tumor driver biomarkers, tumor mutational burden, microsatellite instability, intratumor heterogeneity, cytolytic score, programmed cell death ligand 1 expression, patients’ survival and response to anti-cytotoxic T-lymphocyte-associated antigen 4 and anti-programmed cell death protein 1 immunotherapy.

scholarly journals The Immune Landscape of Thyroid Cancer in the Context of Immune Checkpoint Inhibition

2019 ◽  
Vol 20 (16) ◽  
pp. 3934 ◽  
Author(s):  
Gilda Varricchi ◽  
Stefania Loffredo ◽  
Giancarlo Marone ◽  
Luca Modestino ◽  
Poupak Fallahi ◽  
...  
Keyword(s):  
Cell Death ◽  
Thyroid Cancer ◽  
Programmed Cell Death ◽  
Immune Cells ◽  
Immune Checkpoint ◽  
Checkpoint Inhibitors ◽  
Lymphatic Vessels ◽  
The United States ◽  
Immune Checkpoints ◽  
Antitumor Effects

Immune cells play critical roles in tumor prevention as well as initiation and progression. However, immune-resistant cancer cells can evade the immune system and proceed to form tumors. The normal microenvironment (immune cells, fibroblasts, blood and lymphatic vessels, and interstitial extracellular matrix (ECM)) maintains tissue homeostasis and prevents tumor initiation. Inflammatory mediators, reactive oxygen species, cytokines, and chemokines from an altered microenvironment promote tumor growth. During the last decade, thyroid cancer, the most frequent cancer of the endocrine system, has emerged as the fifth most incident cancer in the United States (USA), and its incidence is steadily growing. Inflammation has long been associated with thyroid cancer, raising critical questions about the role of immune cells in its pathogenesis. A plethora of immune cells and their mediators are present in the thyroid cancer ecosystem. Monoclonal antibodies (mAbs) targeting immune checkpoints, such as mAbs anti-cytotoxic T lymphocyte antigen 4 (anti-CTLA-4) and anti-programmed cell death protein-1/programmed cell death ligand-1 (anti-PD-1/PD-L1), have revolutionized the treatment of many malignancies, but they induce thyroid dysfunction in up to 10% of patients, presumably by enhancing autoimmunity. Combination strategies involving immune checkpoint inhibitors (ICIs) with tyrosine kinase (TK) or serine/threonine protein kinase B-raf (BRAF) inhibitors are showing considerable promise in the treatment of advanced thyroid cancer. This review illustrates how different immune cells contribute to thyroid cancer development and the rationale for the antitumor effects of ICIs in combination with BRAF/TK inhibitors.

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