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Journal articles on the topic 'Cellular control mechanisms'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 July 2024

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1

Reynolds, Noah M., Beth A. Lazazzera, and Michael Ibba. "Cellular mechanisms that control mistranslation." Nature Reviews Microbiology 8, no. 12 (November 16, 2010): 849–56. http://dx.doi.org/10.1038/nrmicro2472.

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2

Roath, Stuart. "Cellular Proteases and Control Mechanisms." Blood Coagulation & Fibrinolysis 2, no. 4 (August 1991): 575. http://dx.doi.org/10.1097/00001721-199108000-00010.

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3

Keeling, Jacob, Leonidas Tsiokas, and Dipak Maskey. "Cellular Mechanisms of Ciliary Length Control." Cells 5, no. 1 (January 29, 2016): 6. http://dx.doi.org/10.3390/cells5010006.

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4

Erne, P., E. Carafoli, C. van Breemen, and F. R. Bühler. "Update on Cellular Calcium Control Mechanisms." Journal of Cardiovascular Pharmacology 12, Supplement (1988): 1. http://dx.doi.org/10.1097/00005344-198800125-00001.

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5

Erne, P., E. Carafoli, C. van Breemen, and F. R. Bühler. "Update on Cellular Calcium Control Mechanisms." Journal of Cardiovascular Pharmacology 12 (1988): 1. http://dx.doi.org/10.1097/00005344-198806125-00001.

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6

Berridge, Michael J. "Calcium signal transduction and cellular control mechanisms." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1742, no. 1-3 (December 2004): 3–7. http://dx.doi.org/10.1016/j.bbamcr.2004.08.012.

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7

Deaton, Lewis E., and Sidney K. Pierce. "Introduction: Cellular volume regulation—mechanisms and control." Journal of Experimental Zoology 268, no. 2 (February 1, 1994): 77–79. http://dx.doi.org/10.1002/jez.1402680202.

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8

Andrews, Norma W., Patricia E. Almeida, and Matthias Corrotte. "Damage control: cellular mechanisms of plasma membrane repair." Trends in Cell Biology 24, no. 12 (December 2014): 734–42. http://dx.doi.org/10.1016/j.tcb.2014.07.008.

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9

Outeiro, Tiago Fleming, and Julie Tetzlaff. "Mechanisms of Disease II: Cellular Protein Quality Control." Seminars in Pediatric Neurology 14, no. 1 (March 2007): 15–25. http://dx.doi.org/10.1016/j.spen.2006.11.005.

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10

Billmann, GE. "Cellular Mechanisms for Ventricular Fibrillation." Physiology 7, no. 6 (December 1, 1992): 254–59. http://dx.doi.org/10.1152/physiologyonline.1992.7.6.254.

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Alterations in cardiac autonomic control cause changes in cytosolic second messenger concentrations. This may represent the cellular mechanism for malignant arrhythmias. In particular, cytosolic calcium elevations can alter cardiac impulse generation (oscillatory afterdepolarization) and impulse conduction (nonuniform repolarization), which alone or in combination could trigger ventricular fibrillation.

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11

Jadiya, Pooja, and Dhanendra Tomar. "Mitochondrial Protein Quality Control Mechanisms." Genes 11, no. 5 (May 18, 2020): 563. http://dx.doi.org/10.3390/genes11050563.

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Mitochondria serve as a hub for many cellular processes, including bioenergetics, metabolism, cellular signaling, redox balance, calcium homeostasis, and cell death. The mitochondrial proteome includes over a thousand proteins, encoded by both the mitochondrial and nuclear genomes. The majority (~99%) of proteins are nuclear encoded that are synthesized in the cytosol and subsequently imported into the mitochondria. Within the mitochondria, polypeptides fold and assemble into their native functional form. Mitochondria health and integrity depend on correct protein import, folding, and regulated turnover termed as mitochondrial protein quality control (MPQC). Failure to maintain these processes can cause mitochondrial dysfunction that leads to various pathophysiological outcomes and the commencement of diseases. Here, we summarize the current knowledge about the role of different MPQC regulatory systems such as mitochondrial chaperones, proteases, the ubiquitin-proteasome system, mitochondrial unfolded protein response, mitophagy, and mitochondria-derived vesicles in the maintenance of mitochondrial proteome and health. The proper understanding of mitochondrial protein quality control mechanisms will provide relevant insights to treat multiple human diseases.

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12

Feodorova, Yana N., and Victoria S. Sarafian. "Psychological Stress – Cellular and Molecular Mechanisms." Folia Medica 54, no. 3 (September 1, 2012): 5–13. http://dx.doi.org/10.2478/v10153-011-0091-9.

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ABSTRACT Pathophysiological regulation of the stress response involves a number of complex interactions at the organismal, cellular and molecular levels. A salient feature of the stress response is the activation of the hypothalamic-pituitaryadrenal axis. Molecular studies of this phenomenon have found a number of genes which are differentially expressed in stressed individuals and control subjects. The transcription factor NF-κB controls many of these genes, which is evidence of the key role it plays in the cellular stress response. Stress upregulates a number of genes such as the transcription factor genes that control cell growth, chromatin structure, cell cycle activation and enzymes involved in the biosynthesis of nucleic acids and proteins. The genes that are down-regulated in stress are cell cycle inhibitors, apoptosis related genes, antiproliferative cytokines and Apo J, the NF-κB inhibitor. Post-traumatic stress disorder (PTSD) is an anxiety disorder which develops as a reaction to an extreme traumatic event but only in a small proportion of the population. It is still unknown what molecular mechanisms trigger its progression. Both genetic and epigenetic factors play a role in this condition. Although the environmental component is necessary for developing PTSD, it has been suggested that 30% of the variance in PTSD symptoms could be attributed to genetic influences. Utilizing genome wide association studies, it would be possible to identify new genes involved in PTSD development and elucidate the molecular pathways which are dysregulated. This will facilitate the identification of novel biomarkers that may help in PTSD diagnosis and treatment.

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13

Alapan, Yunus, Oncay Yasa, Berk Yigit, I. Ceren Yasa, Pelin Erkoc, and Metin Sitti. "Microrobotics and Microorganisms: Biohybrid Autonomous Cellular Robots." Annual Review of Control, Robotics, and Autonomous Systems 2, no. 1 (May 3, 2019): 205–30. http://dx.doi.org/10.1146/annurev-control-053018-023803.

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Biohybrid microrobots, composed of a living organism integrated with an artificial carrier, offer great advantages for the miniaturization of devices with onboard actuation, sensing, and control functionalities and can perform multiple tasks, including manipulation, cargo delivery, and targeting, at nano- and microscales. Over the past decade, various microorganisms and artificial carriers have been integrated to develop unique biohybrid microrobots that can swim or crawl inside the body, in order to overcome the challenges encountered by the current cargo delivery systems. Here, we first focus on the locomotion mechanisms of microorganisms at the microscale, crucial criteria for the selection of biohybrid microrobot components, and the integration of the selected artificial and biological components using various physical and chemical techniques. We then critically review biohybrid microrobots that have been designed and used to perform specific tasks in vivo. Finally, we discuss key challenges, including fabrication efficiency, swarm manipulation, in vivo imaging, and immunogenicity, that should be overcome before biohybrid microrobots transition to clinical use.

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14

Mohanraj, Karthik, Urszula Nowicka, and Agnieszka Chacinska. "Mitochondrial control of cellular protein homeostasis." Biochemical Journal 477, no. 16 (August 26, 2020): 3033–54. http://dx.doi.org/10.1042/bcj20190654.

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Mitochondria are involved in several vital functions of the eukaryotic cell. The majority of mitochondrial proteins are coded by nuclear DNA. Constant import of proteins from the cytosol is a prerequisite for the efficient functioning of the organelle. The protein import into mitochondria is mediated by diverse import pathways and is continuously under watch by quality control systems. However, it is often challenged by both internal and external factors, such as oxidative stress or energy shortage. The impaired protein import and biogenesis leads to the accumulation of mitochondrial precursor proteins in the cytosol and activates several stress response pathways. These defense mechanisms engage a network of processes involving transcription, translation, and protein clearance to restore cellular protein homeostasis. In this review, we provide a comprehensive analysis of various factors and processes contributing to mitochondrial stress caused by protein biogenesis failure and summarize the recovery mechanisms employed by the cell.

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15

Jackson, F. R., A. J. Schroeder, M. A. Roberts, G. P. McNeil, K. Kume, and B. Akten. "Cellular and molecular mechanisms of circadian control in insects." Journal of Insect Physiology 47, no. 8 (July 2001): 833–42. http://dx.doi.org/10.1016/s0022-1910(01)00056-7.

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16

Brecht, Michael, Valery Grinevich, Tae-Eun Jin, Troy Margrie, and Pavel Osten. "Cellular mechanisms of motor control in the vibrissal system." Pflügers Archiv - European Journal of Physiology 453, no. 3 (May 31, 2006): 269–81. http://dx.doi.org/10.1007/s00424-006-0101-6.

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17

Stein, C. "Immune mechanisms in pain control." Journal of Neurochemistry 85 (May 8, 2003): 12. http://dx.doi.org/10.1046/j.1471-4159.85.s2.12_1.x.

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18

Case, R. M. "Cellular mechanisms of control and secretion in the exocrine pancreas." Current Opinion in Gastroenterology 6, no. 5 (October 1990): 731–38. http://dx.doi.org/10.1097/00001574-199010000-00013.

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19

Zuñiga, Joaquin, Diana Torres-García, Teresa Santos-Mendoza, Tatiana S. Rodriguez-Reyna, Julio Granados, and Edmond J. Yunis. "Cellular and Humoral Mechanisms Involved in the Control of Tuberculosis." Clinical and Developmental Immunology 2012 (2012): 1–18. http://dx.doi.org/10.1155/2012/193923.

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Mycobacterium tuberculosis(Mtb) infection is a major international public health problem. One-third of the world's population is thought to have latent tuberculosis, a condition where individuals are infected by the intracellular bacteria without active disease but are at risk for reactivation, if their immune system fails. Here, we discuss the role of nonspecific inflammatory responses mediated by cytokines and chemokines induced by interaction of innate receptors expressed in macrophages and dendritic cells (DCs). We also review current information regarding the importance of several cytokines including IL-17/IL-23 in the development of protective cellular and antibody-mediated protective responses against Mtb and their influence in containment of the infection. Finally, in this paper, emphasis is placed on the mechanisms of failure of Mtb control, including the immune dysregulation induced by the treatment with biological drugs in different autoimmune diseases. Further functional studies, focused on the mechanisms involved in the early host-Mtb interactions and the interplay between host innate and acquired immunity against Mtb, may be helpful to improve the understanding of protective responses in the lung and in the development of novel therapeutic and prophylactic tools in TB.

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20

Jean, André. "Brain Stem Control of Swallowing: Neuronal Network and Cellular Mechanisms." Physiological Reviews 81, no. 2 (April 1, 2001): 929–69. http://dx.doi.org/10.1152/physrev.2001.81.2.929.

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Swallowing movements are produced by a central pattern generator located in the medulla oblongata. It has been established on the basis of microelectrode recordings that the swallowing network includes two main groups of neurons. One group is located within the dorsal medulla and contains the generator neurons involved in triggering, shaping, and timing the sequential or rhythmic swallowing pattern. Interestingly, these generator neurons are situated within a primary sensory relay, that is, the nucleus tractus solitarii. The second group is located in the ventrolateral medulla and contains switching neurons, which distribute the swallowing drive to the various pools of motoneurons involved in swallowing. This review focuses on the brain stem mechanisms underlying the generation of sequential and rhythmic swallowing movements. It analyzes the neuronal circuitry, the cellular properties of neurons, and the neurotransmitters possibly involved, as well as the peripheral and central inputs which shape the output of the network appropriately so that the swallowing movements correspond to the bolus to be swallowed. The mechanisms possibly involved in pattern generation and the possible flexibility of the swallowing central pattern generator are discussed.

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21

Pilowsky, Paul M. "Central mechanisms of cardiovascular control — cellular, molecular and integrative aspects." Autonomic Neuroscience 98, no. 1-2 (June 2002): 1. http://dx.doi.org/10.1016/s1566-0702(02)00019-x.

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22

Ermolaeva, Maria A., Alexander Dakhovnik, and Björn Schumacher. "Quality control mechanisms in cellular and systemic DNA damage responses." Ageing Research Reviews 23 (September 2015): 3–11. http://dx.doi.org/10.1016/j.arr.2014.12.009.

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23

Kampinga, Harm H., Matthias P. Mayer, and Axel Mogk. "Protein quality control: from mechanism to disease." Cell Stress and Chaperones 24, no. 6 (November 2019): 1013–26. http://dx.doi.org/10.1007/s12192-019-01040-9.

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Abstract The cellular protein quality control machinery with its central constituents of chaperones and proteases is vital to maintain protein homeostasis under physiological conditions and to protect against acute stress conditions. Imbalances in protein homeostasis also are keys to a plethora of genetic and acquired, often age-related, diseases as well as aging in general. At the EMBO Workshop, speakers covered all major aspects of cellular protein quality control, from basic mechanisms at the molecular, cellular, and organismal level to medical translation. In this report, the highlights of the meeting will be summarized.

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24

Atkinson, Stuart P., and W. Nicol Keith. "Epigenetic control of cellular senescence in disease: opportunities for therapeutic intervention." Expert Reviews in Molecular Medicine 9, no. 7 (March 2007): 1–26. http://dx.doi.org/10.1017/s1462399407000269.

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AbstractUnderstanding how senescence is established and maintained is an important area of study both for normal cell physiology and in tumourigenesis. Modifications to N-terminal tails of histone proteins, which can lead to chromatin remodelling, appear to be key to the regulation of the senescence phenotype. Epigenetic mechanisms such as modification of histone proteins have been shown to be sufficient to regulate gene expression levels and specific gene promoters can become epigenetically altered at senescence. This suggests that epigenetic mechanisms are important in senescence and further suggests epigenetic deregulation could play an important role in the bypass of senescence and the acquisition of a tumourigenic phenotype. Tumour suppressor proteins and cellular senescence are intimately linked and such proteins are now known to regulate gene expression through chromatin remodelling, again suggesting a link between chromatin modification and cellular senescence. Telomere dynamics and the expression of the telomerase genes are also both implicitly linked to senescence and tumourigenesis, and epigenetic deregulation of the telomerase gene promoters has been identified as a possible mechanism for the activation of telomere maintenance mechanisms in cancer. Recent studies have also suggested that epigenetic deregulation in stem cells could play an important role in carcinogenesis, and new models have been suggested for the attainment of tumourigenesis and bypass of senescence. Overall, proper regulation of the chromatin environment is suggested to have an important role in the senescence pathway, such that its deregulation could lead to tumourigenesis.

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25

Blinova, S. A., F. S. Oripov, and F. M. Khamidova. "Cellular and molecular mechanisms of pulmonary malformations." Genes & Cells 16, no. 1 (March 15, 2021): 24–28. http://dx.doi.org/10.23868/202104003.

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Until now, the cellular and molecular mechanisms of the development of lung defects remain a poorly studied area of pulmonology. In the occurrence of anomalies in the airways of the lungs, a change in the expression of proteins that control early lung morphogenesis in normal conditions (proteins FGF, TGF, SHH, WNT) was established. Along with this, bronchial markers and markers of type 2 alveolocytes play a certain role in the occurrence of lung defects. A number of congenital malformations are caused by improper formation of the airways, which may be associated with the influence of various soluble factors, receptors, transcription factors and microRNAs. The possible role of the pulmonary neuroendocrine system (apudocytes and neuroepithelial bodies) in the pathogenesis and pathobiology of childhood lung diseases, including congenital lung diseases, is discussed.

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26

WADA, Kei. "Study of Structural Basis for Molecular Mechanisms of Cellular Redox Control." Nihon Kessho Gakkaishi 63, no. 2 (May 31, 2021): 105–12. http://dx.doi.org/10.5940/jcrsj.63.105.

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27

Ying, Kai er, Wenguang Feng, Wei-Zhong Ying, and Paul W. Sanders. "Cellular antioxidant mechanisms control immunoglobulin light chain-mediated proximal tubule injury." Free Radical Biology and Medicine 171 (August 2021): 80–90. http://dx.doi.org/10.1016/j.freeradbiomed.2021.05.011.

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28

Kordon, Claude. "Neural mechanisms involved in pituitary control." Neurochemistry International 7, no. 6 (January 1985): 917–25. http://dx.doi.org/10.1016/0197-0186(85)90140-8.

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29

Smith, C. M., D. Lans, and D. A. Weisblat. "Cellular mechanisms of epiboly in leech embryos." Development 122, no. 6 (June 1, 1996): 1885–94. http://dx.doi.org/10.1242/dev.122.6.1885.

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Gastrulation in leech embryos is dominated by the epibolic movements of two tissues: germinal bands, composed of segmental precursor cells, and an overlying epithelium that is part of a provisional integument. During gastrulation, the germinal bands move over the surface of the embryo and coalesce along the prospective ventral midline. Concurrently, the epithelium spreads to cover the embryo. We have begun to analyze the mechanisms involved in gastrulation in the leech by assessing the independent contributions of the epithelium and the germinal bands to these cell movements. Here we describe cellular events during epiboly in normal embryos and in embryos perturbed by either reducing the number of cells in the epithelium, or by preventing the formation of the germinal bands, or both. These experiments indicate that both the germinal bands and the epithelium are able to undergo epibolic movements independently, although each is required for the other to behave as in control embryos.

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Abramov, Andrey Y., and Plamena R. Angelova. "Cellular mechanisms of complex I-associated pathology." Biochemical Society Transactions 47, no. 6 (November 26, 2019): 1963–69. http://dx.doi.org/10.1042/bst20191042.

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Mitochondria control vitally important functions in cells, including energy production, cell signalling and regulation of cell death. Considering this, any alteration in mitochondrial metabolism would lead to cellular dysfunction and the development of a disease. A large proportion of disorders associated with mitochondria are induced by mutations or chemical inhibition of the mitochondrial complex I — the entry point to the electron transport chain. Subunits of the enzyme NADH: ubiquinone oxidoreductase, are encoded by both nuclear and mitochondrial DNA and mutations in these genes lead to cardio and muscular pathologies and diseases of the central nervous system. Despite such a clear involvement of complex I deficiency in numerous disorders, the molecular and cellular mechanisms leading to the development of pathology are not very clear. In this review, we summarise how lack of activity of complex I could differentially change mitochondrial and cellular functions and how these changes could lead to a pathology, following discrete routes.

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31

Richards, Roy J., Lisa C. Masek, and Roger F. R. Brown. "Biochemical and Cellular Mechanisms of Pulmonary Fibrosis." Toxicologic Pathology 19, no. 4_part_1 (November 1991): 526–39. http://dx.doi.org/10.1177/0192623391019004-118.

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This review summarizes the manner in which a variety of agents may induce fibrogenic reactions in the lung. The extent of reaction is dependent on dose, time scale of exposure, and chemical reactivity. The regime of multiple dosing with chemicals or gases with recovery periods is important in disease progression. The means by which biochemists and histopathologists assess fibrosis, the advantages and disadvantages of each of the methods as related to subjectivity, quantitation, and speed of analysis are compared. The mechanisms which control the step from fibrogenesis (a potentially reversible reaction) to fibrosis (irreversible) may be linked to the maturation of collagen, calcification, or the formation of cross-linked protein masses. Attention is given to hydroxylysine cross-links in newly formed “fibrotic” collagen but focusses on γ-glutamyl-∊-lysyl cross-links formed by calcium-dependent transglutaminases. It is suggested that these enzymes, released by replacement epithelial cells, could be responsible for the formation of stabilized protein masses in the lung, thus contributing to a progressive fibrosis.

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32

Wood, Shona H. "How can a binary switch within the pars tuberalis control seasonal timing of reproduction?" Journal of Endocrinology 239, no. 1 (October 2018): R13—R25. http://dx.doi.org/10.1530/joe-18-0177.

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Life in seasonally changing environments is challenging. Biological systems have to not only respond directly to the environment, but also schedule life history events in anticipation of seasonal changes. The cellular and molecular basis of how these events are scheduled is unknown. Cellular decision-making processes in response to signals above certain thresholds regularly occur i.e. cellular fate determination, apoptosis and firing of action potentials. Binary switches, the result of cellular decision-making processes, are defined as a change in phenotype between two stable states. A recent study presents evidence of a binary switch operating in the pars tuberalis (PT) of the pituitary, seemingly timing seasonal reproduction in sheep. Though, how a binary switch would allow for anticipation of seasonal environmental changes, not just direct responsiveness, is unclear. The purpose of this review is to assess the evidence for a binary switching mechanism timing seasonal reproduction and to hypothesize how a binary switch would allow biological processes to be timed over weeks to years. I draw parallels with mechanisms used in development, cell fate determination and seasonal timing in plants. I propose that the adult PT is a plastic tissue, showing a seasonal cycle of cellular differentiation, and that the underlying processes are likely to be epigenetic. Therefore, considering the mechanisms behind adult cellular plasticity offers a framework to hypothesize how a long-term timer functions within the PT.

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33

Kay, John. "Cellular proteases and control mechanisms, UCLA Symposia on molecular and cellular biology, new series, volume 104." FEBS Letters 275, no. 1-2 (November 26, 1990): 240–41. http://dx.doi.org/10.1016/0014-5793(90)81483-5.

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34

Gu, Yeun-Hwa, Takenori Yamashita, Tota Inoue, Jin-Ho Song, and Ki-Mun Kang. "Cellular and Molecular Level Mechanisms against Electrochemical Cancer Therapy." Journal of Pathogens 2019 (April 14, 2019): 1–11. http://dx.doi.org/10.1155/2019/3431674.

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Electrochemical treatment (ECT) is a promising new way to induce tumor regression by flowing direct current into the cancer tissue. ECT was applied to different kinds of tumors in clinical studies and showed good results. In addition, basic research has almost not been done in the field of evaluation of efficacy, dose-response, and cytotoxicity. Therefore, the objective is to study the cellular mechanism in the antitumor effect of ECT and to contribute data of basic research of ECT. In the cell-level study, tumor cells (Sarcoma-180, Scc-7, Ehrlich Carcinoma) were studied using ICR mice and C3H mice. In the study group, pH values of control, 10mA × 150secs, 10mA × 300secs, and 10mA × 600secs groups were measured five times each. In histological level studies, ECT was performed on tumors inoculated on the upper part of the right foot of C3H mice. In each group, mice were sacrificed by cervical dislocation 6, 12, and 24 hrs after ECT treatment, and tumors were removed. The excised tumor was fixed in tissue with 10% formalin, and HE staining and apoptosis antibody staining were carried out from the obtained tissue section and observation. In the study at the cellular level, statistically significant differences were observed in all ECT groups in Sarcoma in the tumor growth measurement study compared with the control group. Statistically significant differences were also observed in Scc-7 in all ECT groups compared to the control group. In the intratumoral pH measurement study, there was a statistically significant difference between the anode and the cathode in each group compared to the control group. In the examination at the histological level, microscopic observation of a slide stained with apoptosis antibody with a magnification of 400 times showed that 6hrs after ECT it was stronger and then decreased. By performing ECT, a weak current flows in the living body. As a result, changes in tissue pH, generation of gas, etc. occur. In this study, it was also confirmed that the intratumor pH value becomes strongly acidic on the anode side and strongly alkaline on the cathode side. In addition, this study confirmed the occurrence of gas during treatment of ECT. Changes in the pH and the like cause changes in the environment in the cell, denaturation of proteins, apoptosis, and necrosis. In this study, a significant increase in apoptosis was confirmed in each ECT group compared to the control group. Treatment effects by ECT were also observed in tumor growth measurement studies and tumor weight measurement studies. From these research results, ECT is considered to be effective as a tumor treatment method.

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Wang, Yang, and Goran Stjepanovic. "AMBRA1: Orchestrating Cell Cycle Control and Autophagy for Cellular Homeostasis." Journal of Cancer Immunology 6, no. 1 (2024): 44–50. http://dx.doi.org/10.33696/cancerimmunol.6.083.

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The Activating Molecule in Beclin-1-Regulated Autophagy (AMBRA1) is a scaffold protein involved in many cellular processes, including autophagy, apoptosis, cell growth and development. AMBRA1 functions as a substrate receptor of the DDB1-Cullin4-RBX1 ubiquitin E3 ligase complex that plays key roles in autophagy and the cell cycle regulatory network. Considering the crucial role of AMBRA1 in cellular homeostasis, structural and functional studies are important for understanding the mechanisms that coordinate these cell responses. Autophagy defects and impaired AMBRA1 function may contribute to the pathogenesis of several diseases, including cancer and neurodegenerative disorders. As a result, targeting AMBRA1 has gained interest as a potential therapeutic strategy. Due to the intrinsic disorder of AMBRA1, its structure has not been fully elucidated. A report by Liu et al., provided new insights into the structure and function of AMBRA1 [1]. This mini-review aims to summarize the DDB1-AMBRA1 complex structure and regulatory mechanism and discuss future research directions.

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36

Winters, Bryony Laura, and Christopher Walter Vaughan. "Mechanisms of endocannabinoid control of synaptic plasticity." Neuropharmacology 197 (October 2021): 108736. http://dx.doi.org/10.1016/j.neuropharm.2021.108736.

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37

Hoppe, Thorsten, and Ehud Cohen. "Organismal Protein Homeostasis Mechanisms." Genetics 215, no. 4 (August 2020): 889–901. http://dx.doi.org/10.1534/genetics.120.301283.

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Sustaining a healthy proteome is a lifelong challenge for each individual cell of an organism. However, protein homeostasis or proteostasis is constantly jeopardized since damaged proteins accumulate under proteotoxic stress that originates from ever-changing metabolic, environmental, and pathological conditions. Proteostasis is achieved via a conserved network of quality control pathways that orchestrate the biogenesis of correctly folded proteins, prevent proteins from misfolding, and remove potentially harmful proteins by selective degradation. Nevertheless, the proteostasis network has a limited capacity and its collapse deteriorates cellular functionality and organismal viability, causing metabolic, oncological, or neurodegenerative disorders. While cell-autonomous quality control mechanisms have been described intensely, recent work on Caenorhabditis elegans has demonstrated the systemic coordination of proteostasis between distinct tissues of an organism. These findings indicate the existence of intricately balanced proteostasis networks important for integration and maintenance of the organismal proteome, opening a new door to define novel therapeutic targets for protein aggregation diseases. Here, we provide an overview of individual protein quality control pathways and the systemic coordination between central proteostatic nodes. We further provide insights into the dynamic regulation of cellular and organismal proteostasis mechanisms that integrate environmental and metabolic changes. The use of C. elegans as a model has pioneered our understanding of conserved quality control mechanisms important to safeguard the organismal proteome in health and disease.

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38

Hendricks, Matthew R., and Jennifer M. Bomberger. "Who's really in control: microbial regulation of protein trafficking in the epithelium." American Journal of Physiology-Cell Physiology 306, no. 3 (February 1, 2014): C187—C197. http://dx.doi.org/10.1152/ajpcell.00277.2013.

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Due to evolutionary pressure, there are many complex interactions at the interface between pathogens and eukaryotic host cells wherein host cells attempt to clear invading microorganisms and pathogens counter these mechanisms to colonize and invade host tissues. One striking observation from studies focused on this interface is that pathogens have multiple mechanisms to modulate and disrupt normal cellular physiology to establish replication niches and avoid clearance. The precision by which pathogens exert their effects on host cells makes them excellent tools to answer questions about cell physiology of eukaryotic cells. Furthermore, an understanding of these mechanisms at the host-pathogen interface will benefit our understanding of how pathogens cause disease. In this review, we describe a few examples of how pathogens disrupt normal cellular physiology and protein trafficking at epithelial cell barriers to underscore how pathogens modulate cellular processes to cause disease and how this knowledge has been utilized to learn about cellular physiology.

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39

Schreiber, Joyce M., Erik Limpens, and Jeroen de Keijzer. "Distributing Plant Developmental Regulatory Proteins via Plasmodesmata." Plants 13, no. 5 (February 28, 2024): 684. http://dx.doi.org/10.3390/plants13050684.

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During plant development, mobile proteins, including transcription factors, abundantly serve as messengers between cells to activate transcriptional signaling cascades in distal tissues. These proteins travel from cell to cell via nanoscopic tunnels in the cell wall known as plasmodesmata. Cellular control over this intercellular movement can occur at two likely interdependent levels. It involves regulation at the level of plasmodesmata density and structure as well as at the level of the cargo proteins that traverse these tunnels. In this review, we cover the dynamics of plasmodesmata formation and structure in a developmental context together with recent insights into the mechanisms that may control these aspects. Furthermore, we explore the processes involved in cargo-specific mechanisms that control the transport of proteins via plasmodesmata. Instead of a one-fits-all mechanism, a pluriform repertoire of mechanisms is encountered that controls the intercellular transport of proteins via plasmodesmata to control plant development.

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Murer, Heini, Nati Hernando, Ian Forster, and Jürg Biber. "Proximal Tubular Phosphate Reabsorption: Molecular Mechanisms." Physiological Reviews 80, no. 4 (January 10, 2000): 1373–409. http://dx.doi.org/10.1152/physrev.2000.80.4.1373.

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Renal proximal tubular reabsorption of Pi is a key element in overall Pi homeostasis, and it involves a secondary active Pi transport mechanism. Among the molecularly identified sodium-phosphate (Na/Pi) cotransport systems a brush-border membrane type IIa Na-Pi cotransporter is the key player in proximal tubular Pi reabsorption. Physiological and pathophysiological alterations in renal Pi reabsorption are related to altered brush-border membrane expression/content of the type IIa Na-Picotransporter. Complex membrane retrieval/insertion mechanisms are involved in modulating transporter content in the brush-border membrane. In a tissue culture model (OK cells) expressing intrinsically the type IIa Na-Pi cotransporter, the cellular cascades involved in “physiological/pathophysiological” control of Pi reabsorption have been explored. As this cell model offers a “proximal tubular” environment, it is useful for characterization (in heterologous expression studies) of the cellular/molecular requirements for transport regulation. Finally, the oocyte expression system has permitted a thorough characterization of the transport characteristics and of structure/function relationships. Thus the cloning of the type IIa Na-Pi cotransporter (in 1993) provided the tools to study renal brush-border membrane Na-Pi cotransport function/regulation at the cellular/molecular level as well as at the organ level and led to an understanding of cellular mechanisms involved in control of proximal tubular Pi handling and, thus, of overall Pihomeostasis.

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Sukhbaatar, Nyamdelger, and Thomas Weichhart. "Iron Regulation: Macrophages in Control." Pharmaceuticals 11, no. 4 (December 14, 2018): 137. http://dx.doi.org/10.3390/ph11040137.

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Macrophages are sentinel cells of the innate immune system and have important functions in development, tissue homeostasis, and immunity. These phylogenetically ancient cells also developed a variety of mechanisms to control erythropoiesis and the handling of iron. Red pulp macrophages in the spleen, Kupffer cells in the liver, and central nurse macrophages in the bone marrow ensure a coordinated metabolism of iron to support erythropoiesis. Phagocytosis of senescent red blood cells by macrophages in the spleen and the liver provide a continuous delivery of recycled iron under steady-state conditions and during anemic stress. Central nurse macrophages in the bone marrow utilize this iron and provide a cellular scaffold and niche to promote differentiation of erythroblasts. This review focuses on the role of the distinct macrophage populations that contribute to efficient iron metabolism and highlight important cellular and systemic mechanisms involved in iron-regulating processes.

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Druker, Jimena, James W. Wilson, Fraser Child, Dilem Shakir, Temitope Fasanya, and Sonia Rocha. "Role of Hypoxia in the Control of the Cell Cycle." International Journal of Molecular Sciences 22, no. 9 (May 5, 2021): 4874. http://dx.doi.org/10.3390/ijms22094874.

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The cell cycle is an important cellular process whereby the cell attempts to replicate its genome in an error-free manner. As such, mechanisms must exist for the cell cycle to respond to stress signals such as those elicited by hypoxia or reduced oxygen availability. This review focuses on the role of transcriptional and post-transcriptional mechanisms initiated in hypoxia that interface with cell cycle control. In addition, we discuss how the cell cycle can alter the hypoxia response. Overall, the cellular response to hypoxia and the cell cycle are linked through a variety of mechanisms, allowing cells to respond to hypoxia in a manner that ensures survival and minimal errors throughout cell division.

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Cherepantsev, A. S. "The Mechanism of the Fault Genesis and Synchronization in the Dissipative Cellular Model of Earthquakes." Nelineinaya Dinamika 18, no. 1 (2022): 43–59. http://dx.doi.org/10.20537/nd220103.

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This paper is concerned with the study of the patterns of the behavior of coupling elements in the OFC model, which describes the statistical regularities of the seismic regime. It is shown that there are two different modes of synchronous drop formation, simulating an earthquake. Both mechanisms are determined by the capture of a neighboring element and the subsequent synchronization of the drops. This process forms a stable drop of a larger size. The first mechanism is typical for the initial stage of the system’s evolution toward a steady self-organized critical state. In this case, the capture is determined by different rates of input of energy into the elements in near-boundary regions of the lattice. The second mechanism is based on an increase in the number of cluster boundary elements and, accordingly, an increase in the probability of capture and synchronization of neighboring external elements. The theoretical values of the parameter of the cluster size growth rate presented in this work are in good agreement with the calculated values.

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Chertok, V. M., A. E. Kotsyuba, and I. A. Khramova. "Mechanisms and regulatory factors of endometrial neovascularization." Pacific Medical Journal, no. 4 (January 6, 2022): 26–33. http://dx.doi.org/10.34215/1609-1175-2021-4-26-33.

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Cellular-molecular mechanisms and factors, regulating uterus vascularization are also a focal point ensuring reproduction processes. In the process of angiogenesis endothelium expresses a number of receptors of growth factors and ligands which control main stages of the cellular makeup during vascular walls formation process. It in turn supports proliferation and reparation of the endometrium during menstrual cycle and prepares for the implantation and placentation.

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Liu, T. "Cortical Mechanisms of Feature-based Attentional Control." Cerebral Cortex 13, no. 12 (December 1, 2003): 1334–43. http://dx.doi.org/10.1093/cercor/bhg080.

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Crozier, Stephen J., Thomas C. Vary, Scot R. Kimball, and Leonard S. Jefferson. "Cellular energy status modulates translational control mechanisms in ischemic-reperfused rat hearts." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 3 (September 2005): H1242—H1250. http://dx.doi.org/10.1152/ajpheart.00859.2004.

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Mechanisms regulating ischemia and reperfusion (I/R)-induced changes in mRNA translation in the heart are poorly defined, as are the factors that initiate these changes. Because cellular energy status affects mRNA translation under physiological conditions, it is plausible that I/R-induced changes in translation may in part be a result of altered cellular energy status. Therefore, the purpose of the studies described herein was to compare the effects of I/R with those of altered energy substrate availability on biomarkers of mRNA translation in the heart. Isolated adult rat hearts were perfused with glucose or a combination of glucose plus palmitate, and effects of I/R on various biomarkers of translation were subsequently analyzed. When compared with hearts perfused with glucose plus palmitate, hearts perfused with glucose alone exhibited increased phosphorylation of eukaryotic elongation factor (eEF)2, the α-subunit of eukaryotic initiation factor (eIF)2, and AMP-activated protein kinase (AMPK), and these hearts also exhibited enhanced association of eIF4E with eIF4E binding protein (4E-BP)1. Regardless of the energy substrate composition of the buffer, phosphorylation of eEF2 and AMPK was greater than control values after ischemia. Phosphorylation of eIF2α and eIF4E and the association of eIF4E with 4E-BP1 were also greater than control values after ischemia but only in hearts perfused with glucose plus palmitate. Reperfusion reversed the ischemia-induced increase in eEF2 phosphorylation in hearts perfused with glucose and reversed ischemia-induced changes in eIF4E, eEF2, and AMPK phosphorylation in hearts perfused with glucose plus palmitate. Because many ischemia-induced changes in mRNA translation are mimicked by the removal of a metabolic substrate under normal perfusion conditions, the results suggest that cellular energy status represents an important modulator of I/R-induced changes in mRNA translation.

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Pitaru, S., C. A. G. McCulloch, and S. A. Narayanan. "Cellular origins and differentiation control mechanisms during periodontal development and wound healing." Journal of Periodontal Research 29, no. 2 (March 1994): 81–94. http://dx.doi.org/10.1111/j.1600-0765.1994.tb01095.x.

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Fraga de Andrade, Isabela, Charu Mehta, and Emery H. Bresnick. "Post-transcriptional control of cellular differentiation by the RNA exosome complex." Nucleic Acids Research 48, no. 21 (October 29, 2020): 11913–28. http://dx.doi.org/10.1093/nar/gkaa883.

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Abstract Given the complexity of intracellular RNA ensembles and vast phenotypic remodeling intrinsic to cellular differentiation, it is instructive to consider the role of RNA regulatory machinery in controlling differentiation. Dynamic post-transcriptional regulation of protein-coding and non-coding transcripts is vital for establishing and maintaining proteomes that enable or oppose differentiation. By contrast to extensively studied transcriptional mechanisms governing differentiation, many questions remain unanswered regarding the involvement of post-transcriptional mechanisms. Through its catalytic activity to selectively process or degrade RNAs, the RNA exosome complex dictates the levels of RNAs comprising multiple RNA classes, thereby regulating chromatin structure, gene expression and differentiation. Although the RNA exosome would be expected to control diverse biological processes, studies to elucidate its biological functions and how it integrates into, or functions in parallel with, cell type-specific transcriptional mechanisms are in their infancy. Mechanistic analyses have demonstrated that the RNA exosome confers expression of a differentiation regulatory receptor tyrosine kinase, downregulates the telomerase RNA component TERC, confers genomic stability and promotes DNA repair, which have considerable physiological and pathological implications. In this review, we address how a broadly operational RNA regulatory complex interfaces with cell type-specific machinery to control cellular differentiation.

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Das, Maitreyi, and Fulvia Verde. "Role of Cdc42 dynamics in the control of fission yeast cell polarization." Biochemical Society Transactions 41, no. 6 (November 20, 2013): 1745–49. http://dx.doi.org/10.1042/bst20130241.

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Cell polarization is fundamental to many cellular processes, including cell differentiation, cell motility and cell fate determination. A key regulatory enzyme in the control of cell morphogenesis is the conserved Rho GTPase Cdc42, which breaks symmetry via self-amplifying positive-feedback mechanisms. Additional mechanisms of control, including competition between different sites of polarized cell growth and time-delayed negative feedback, define a cellular-level system that promotes Cdc42 oscillatory dynamics and modulates activated Cdc42 intracellular distribution.

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Varma, Tushar K., Tracy E. Toliver-Kinsky, Cheng Y. Lin, Aristides P. Koutrouvelis, Joan E. Nichols, and Edward R. Sherwood. "Cellular Mechanisms That Cause Suppressed Gamma Interferon Secretion in Endotoxin-Tolerant Mice." Infection and Immunity 69, no. 9 (September 1, 2001): 5249–63. http://dx.doi.org/10.1128/iai.69.9.5249-5263.2001.

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ABSTRACT Endotoxin (lipopolysaccharide [LPS]) tolerance is a state of altered immunity characterized, in part, by suppression of LPS-induced gamma interferon (IFN-γ) expression. However, the cellular mediators regulating LPS-induced production of IFN-γ in normal mice and the effect of LPS tolerance on these mediators has not been well characterized. Our studies show that macrophage dysfunction is the primary factor causing suppressed IFN-γ expression in LPS-tolerant mice. Specifically, LPS-tolerant macrophages have a markedly impaired ability to induce IFN-γ secretion by T cells and NK cells obtained from either control or LPS-tolerant mice. However, T cells and NK cells isolated from LPS-tolerant mice produce normal levels of IFN-γ when cocultured with control macrophages or exogenous IFN-γ-inducing factors. Assessment of important IFN-γ-regulating factors showed that interleukin-12 (IL-12) and costimulatory signals provided by IL-15, IL-18, and CD86 are largely responsible for LPS-induced IFN-γ expression in control mice. IL-10 is an inhibitor of IFN-γ production in both the control and LPS-tolerant groups. Expression of IL-12 and the IL-12 receptor β1 (IL-12Rβ1) and IL-12Rβ2 subunits are suppressed in the spleens of LPS-tolerant mice. LPS-tolerant splenocytes also exhibit decreased production of IL-15 and IL-15Rα. However, expression of IL-18 and the B7 proteins CD80 and CD86 are unchanged or increased compared to controls after induction of LPS tolerance. CD28, a major receptor for B7 proteins, is also increased in the spleens of LPS-tolerant mice. Expression of the inhibitory cytokine IL-10 and the IL-10R are sustained after induction of LPS tolerance. These data show that suppression of IFN-γ production in LPS-tolerant mice is largely due to macrophage dysfunction and provide insight into the cellular alterations that occur in LPS tolerance. This study also better defines the factors that mediate LPS-induced IFN-γ production in normal mice.

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