Regulatory Mechanisms for Proteolytic Systems in Oxidative Stress

2013 ◽  
Vol 65 ◽  
pp. S5
Author(s):  
Kelvin J.A. Davies
Keyword(s):  
Oxidative Stress ◽  
Regulatory Mechanisms

Melatonin: a novel strategy for prevention of obesity and fat accumulation in peripheral organs through the improvements of circadian rhythms and antioxidative capacity

2020 ◽  
Vol 3 (1) ◽  
pp. 58-76 ◽  
Author(s):  
Bohan Rong ◽  
Qiong Wu ◽  
Chao Sun
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Circadian Rhythms ◽  
Regulatory Mechanisms ◽  
Antioxidative Capacity ◽  
Unicellular Alga ◽  
Peripheral Tissues ◽  
Peripheral Organs ◽  
Regulatory Effects ◽  
Novel Strategy

Melatonin is a well-known molecule for its involvement in circadian rhythm regulation and its contribution to protection against oxidative stress in organisms including unicellular alga, animals and plants. Currently, the bio-regulatory effects of melatonin on the physiology of various peripheral tissues have drawn a great attention of scientists. Although melatonin was previously defined as a neurohormone secreted from pineal gland, recently it has been identified that virtually, every cell has the capacity to synthesize melatonin and the locally generated melatonin has multiple pathophysiological functions, including regulations of obesity and metabolic syndromes. Herein, we focus on the effects of melatonin on fat deposition in various peripheral organs/tissues. The two important regulatory mechanisms related to the topic, i.e., the improvements of circadian rhythms and antioxidative capacity will be thoroughly discussed since they are linked to several biomarkers involved in obesity and energy imbalance, including metabolism and immunity. Furthermore, several other functions of melatonin which may serve to prevent or promote obesity and energy dysmetabolism-induced pathological states are also addressed. The organs of special interest include liver, pancreas, skeletal muscle, adipose tissue and the gut microbiota.

Regulatory mechanisms of cellular response to oxidative stress

1999 ◽  
Vol 31 (4) ◽  
pp. 319-324 ◽  
Author(s):  
Ken Itoh ◽  
Tetsuro Ishii ◽  
Nobunao Wakabayashi ◽  
Masayuki Yamamoto
Keyword(s):  
Oxidative Stress ◽  
Cellular Response ◽  
Regulatory Mechanisms

scholarly journals Transcriptome Analysis Reveals IsiA-Regulatory Mechanisms Underlying Iron Depletion and Oxidative-Stress Acclimation in Synechocystis sp. Strain PCC 6803

2020 ◽  
Vol 86 (13) ◽  
Author(s):  
Yarui Cheng ◽  
Tianyuan Zhang ◽  
Li Wang ◽  
Wenli Chen
Keyword(s):  
Oxidative Stress ◽  
Network Analysis ◽  
Iron Deficiency ◽  
Regulatory Mechanisms ◽  
Functional Modules ◽  
Iron Stress ◽  
Iron Starvation ◽  
Stress Acclimation ◽  
And Oxidative Stress ◽  
Coexpression Network Analysis

ABSTRACT Microorganisms in nature are commonly exposed to various stresses in parallel. The isiA gene encodes an iron stress-induced chlorophyll-binding protein which is significantly induced under iron starvation and oxidative stress. Acclimation of oxidative stress and iron deficiency was investigated using a regulatory mutant of the Synechocystis sp. strain PCC 6803. In this study, the ΔisiA mutant grew more slowly in oxidative-stress and iron depletion conditions compared to the wild-type (WT) counterpart under the same conditions. Thus, we performed transcriptome sequencing (RNA-seq) analysis of the WT strain and the ΔisiA mutant under double-stress conditions to obtain a comprehensive view of isiA-regulated genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses showed significant differences between the WT strain and ΔisiA mutant, mainly related to photosynthesis and the iron-sulfur cluster. The deletion of isiA affects the expression of various genes that are involved in cellular processes and structures, such as photosynthesis, phycobilisome, and the proton-transporting ATPase complex. Weighted gene coexpression network analysis (WGCNA) demonstrated three functional modules in which the turquoise module was negatively correlated with superoxide dismutase (SOD) activity. Coexpression network analysis identified several hub genes of each module. Cotranscriptional PCR and reads coverage using the Integrative Genomics Viewer demonstrated that isiA, isiB, isiC, ssl0461, and dfp belonged to the isi operon. Three sRNAs related to oxidative stress were identified. This study enriches our knowledge of IsiA-regulatory mechanisms under iron deficiency and oxidative stress. IMPORTANCE This study analyzed the impact of isiA deletion on the transcriptomic profile of Synechocystis. The isiA gene encodes an iron stress-induced chlorophyll-binding protein, which is significantly induced under iron starvation. The deletion of isiA affects the expression of various genes that are involved in photosynthesis and ABC transporters. WGCNA revealed three functional modules in which the blue module was correlated with oxidative stress. We further demonstrated that the isi operon contained the following five genes: isiA, isiB, isiC, ssl0461, and dfp by cotranscriptional PCR. Three sRNAs were identified that were related to oxidative stress. This study enhances our knowledge of IsiA-regulatory mechanisms under iron deficiency and oxidative stress.

scholarly journals Systematic Review of Calcium Channels and Intracellular Calcium Signaling: Relevance to Pesticide Neurotoxicity

2021 ◽  
Vol 22 (24) ◽  
pp. 13376
Author(s):  
Carmen Costas-Ferreira ◽  
Lilian R. F. Faro
Keyword(s):  
Oxidative Stress ◽  
Systematic Review ◽  
Nervous System ◽  
Neuronal Death ◽  
Regulatory Mechanisms ◽  
Extracellular Medium ◽  
Intracellular Calcium Signaling ◽  
Different Types ◽  
Ca2 Channels ◽  
Over Time

Pesticides of different chemical classes exert their toxic effects on the nervous system by acting on the different regulatory mechanisms of calcium (Ca2+) homeostasis. Pesticides have been shown to alter Ca2+ homeostasis, mainly by increasing its intracellular concentration above physiological levels. The pesticide-induced Ca2+ overload occurs through two main mechanisms: the entry of Ca2+ from the extracellular medium through the different types of Ca2+ channels present in the plasma membrane or its release into the cytoplasm from intracellular stocks, mainly from the endoplasmic reticulum. It has also been observed that intracellular increases in the Ca2+ concentrations are maintained over time, because pesticides inhibit the enzymes involved in reducing its levels. Thus, the alteration of Ca2+ levels can lead to the activation of various signaling pathways that generate oxidative stress, neuroinflammation and, finally, neuronal death. In this review, we also discuss some proposed strategies to counteract the detrimental effects of pesticides on Ca2+ homeostasis.

Redox-regulatory mechanisms induced by oxidative stress in Brassica juncea roots monitored by 2-DE proteomics

PROTEOMICS ◽  
2011 ◽  
Vol 11 (7) ◽  
pp. 1346-1350 ◽  
Author(s):  
Sophie Alvarez ◽  
Ashley Galant ◽  
Joseph M. Jez ◽  
Leslie M. Hicks
Keyword(s):  
Oxidative Stress ◽  
Brassica Juncea ◽  
Regulatory Mechanisms

scholarly journals Oxidative Stress-Induced Diseases via the ASK1 Signaling Pathway

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Mayumi Soga ◽  
Atsushi Matsuzawa ◽  
Hidenori Ichijo
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Protein Kinase ◽  
Endoplasmic Reticulum Stress ◽  
Signaling Pathway ◽  
Mitogen Activated Protein Kinase ◽  
Regulatory Mechanisms ◽  
Cellular Functions ◽  
Mapk Kinase ◽  
Mitogen Activated Protein

Apoptosis signal-regulating kinase 1 (ASK1) is a mitogen-activated protein kinase (MAPK) kinase kinase that activates the downstream MAPKs, c-Jun N-terminal kinase (JNK) and p38. ASK1 is activated by various types of stress, such as oxidative stress, endoplasmic reticulum stress, and infection, and regulates various cellular functions. Recently, it has been reported that ASK1 is associated with various diseases induced by oxidative stress. In this review, we introduce recent findings of the regulatory mechanisms of ASK1 and the oxidative stress-induced diseases mediated by the ASK1 signaling pathway.

scholarly journals A subcellular map of the human kinome

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Haitao Zhang ◽  
Xiaolei Cao ◽  
Mei Tang ◽  
Guoxuan Zhong ◽  
Yuan Si ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Phosphorylation ◽  
Oxidative Stress Response ◽  
Regulatory Mechanisms ◽  
Disease Mechanisms ◽  
Human Kinome ◽  
Cellular Compartments ◽  
And Oxidative Stress ◽  
Liquid Liquid Phase Separation

The human kinome comprises 538 kinases playing essential functions by catalyzing protein phosphorylation. Annotation of subcellular distribution of the kinome greatly facilitates investigation of normal and disease mechanisms. Here, we present Kinome Atlas (KA), an image-based map of the kinome annotated to 10 cellular compartments. 456 epitope-tagged kinases, representing 85% of the human kinome, were expressed in HeLa cells and imaged by immunofluorescent microscopy under a similar condition. KA revealed kinase family-enriched subcellular localizations, and discovered a collection of new kinase localizations at mitochondria, plasma membrane, extracellular space, and other structures. Furthermore, KA demonstrated the role of liquid-liquid phase separation in formation of kinase condensates. Identification of MOK as a mitochondrial kinase revealed its function in cristae dynamics, respiration, and oxidative stress response. Although limited by possible mislocalization due to overexpression or epitope tagging, this subcellular map of the kinome can be used to refine regulatory mechanisms involving protein phosphorylation.

scholarly journals ATAC-seq identifies chromatin landscapes linked to the regulation of oxidative stress in the human fungal pathogen Candida albicans

2020 ◽  
Author(s):  
Sabrina Jenull ◽  
Michael Tscherner ◽  
Theresia Mair ◽  
Karl Kuchler
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Candida Albicans ◽  
Fungal Pathogen ◽  
Transcriptional Control ◽  
Chromatin Accessibility ◽  
Environmental Adaptation ◽  
Regulatory Mechanisms ◽  
Chromatin Regulation ◽  
Genomic Regions

AbstractHuman fungal pathogens often encounter fungicidal stress conditions upon host invasion, but they can swiftly adapt by transcriptional reprogramming that enables pathogen survival. Fungal immune evasion is tightly connected to chromatin regulation. Hence, fungal chromatin modifiers pose alternative treatment options to combat fungal infections. Here, we present an ATAC-seq protocol adapted for the opportunistic pathogen Candida albicans to gain further insight into the interplay of chromatin accessibility and gene expression mounted during fungal adaptation to oxidative stress. The ATAC-seq workflow facilitates the robust detection of genomic regions with accessible chromatin, but also allows for the precise modeling of nucleosome positions in C. albcians. Importantly, the data reveal genes with altered chromatin accessibility in upstream regulatory regions, which correlate with transcriptional regulation during the oxidative stress response. Interestingly, many genes show increased chromatin accessibility yet no change in gene expression upon stress exposure. Such chromatin signatures could predict yet unknown regulatory factors under highly dynamic transcriptional control. In addition, de novo motif analysis in genomic regions with increased chromatin accessibility upon hydrogen peroxide treatment shows significant enrichment for Cap1 binding sites, a major factor of oxidative stress responses in C. albicans. Taken together, the ATAC-seq workflow enables the identification of chromatin signatures and uncovers the dynamics of regulatory mechanisms mediating environmental adaptation of C. albicans to host immune surveillance.ImportanceThe opportunistic fungal pathogen Candida albicans colonizes and infects various tissues and organs of the human host. This is due to its rapid environmental adaptation facilitated by changes in gene expression coupled to chromatin alterations. Recent advances in chromatin profiling approaches, such as the development of ATAC-seq, shed light on the dynamic interplay of chromatin accessibility and transcriptional control. The here presented expansion of the ATAC-seq method to C. albicans demonstrates the robustness of ATAC-seq to detect dynamic modulations of chromatin accessibility in response to oxidative stress. This work serves as a basis to further exploit this application to characterize regulatory mechanisms that drive fungal environmental adaptation, such as during host invasion, and thus, will open novel antifungal treatment strategies targeting fungal chromatin regulation.

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