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Journal of Cellular Signaling
ISSN: 2692-0638
Resveratrol and Astaxanthin Protect Primary Human Nasal Epithelial Cells Cultured at an Air-liquid Interface from an Acute Oxidant Exposure
Oxidative stress (OS) in the airway epithelium is associated with cell damage, inflammation, and mitochondrial dysfunction that may initiate or worsen respiratory disease. However, it is unclear whether exogenous antioxidants can provide protection to the airway epithelium from OS. Resveratrol and astaxanthin are nutritional compounds that have shown diverse benefits including protection against OS and inflammation in various situations.
J Cell Signal, 2022, Volume 3, Issue 4, p207-217 | DOI: 10.33696/Signaling.3.084Redox Homeostasis in Well-differentiated Primary Human Nasal Epithelial Cells
Oxidative stress (OS) in the airway epithelium is associated with inflammation, cell damage, and mitochondrial dysfunction that may initiate or worsen respiratory disease. Redox regulation maintains the equilibrium of pro-oxidant/antioxidant reactions but can be disturbed by environmental exposures. The mechanism(s) underlying the induction and impact of OS on airway epithelium and how these influences on respiratory disease is poorly understood.
J Cell Signal, 2022, Volume 3, Issue 4, p193-206 | DOI: 10.33696/Signaling.3.083MAGIs: Junctional Scaffolds Linking Inter-Cellular Junction Architecture, Actin Cytoskeleton Dynamics, and Signaling Pathways
MAGIs (membrane-associated guanylate-kinases (MAGUK) inverted) are apical scaffolds conserved across evolution, which regulate cellular junctions. Low expression of MAGIs has been associated with tumorigenesis in a wide variety of cancers. This “tumor-suppressive” function of MAGIs has stimulated many studies to better understand the processes they control, and how their misregulation could contribute to cancer progression.
J Cell Signal, 2022, Volume 3, Issue 3, p141-147 | DOI: 10.33696/Signaling.3.076Expression and Localization of Phosphoinositide-Specific Phospholipases C in Cultured, Differentiating and Stimulated Human Osteoblasts
The osteoblasts contribute to bone homeostasis maintaining the bone mass, and intervene in bone injuries repair. Insights in the events leading to the proliferation and differentiation of osteoblasts might allow uncover potential molecular targets to control the complex mechanisms underlying bone remodeling. Signal transduction pathways contribute to the differentiation and metabolic activities of osteoblasts, with special regard to calcium-related signaling, including the Phosphoinositide (PI) pathway.
J Cell Signal, 2022, Volume 3, Issue 1, p44-61 | DOI: 10.33696/Signaling.3.067Differentiation and Subtype Specification of Enteric Neurons: Current Knowledge of Transcription Factors, Signaling Molecules and Signaling Pathways Involved
The enteric nervous system is the largest component of the autonomic nervous system. It contains a broad network of interconnected plexuses and enteric neuronal subtypes which are in charge of the normal functioning of the gastrointestinal tract. Vagal and sacral neural crest cells are at the basis of the enteric nervous system development. These cells undergo multiple processes such as migration, proliferation and differentiation to finally form a functional enteric nervous system.
J Cell Signal, 2022, Volume 3, Issue 1, p14-27 | DOI: 10.33696/Signaling.3.064Improving Obesity and Insulin Resistance by Targeting Skeletal Muscle MKP-1
Obesity has reached a global epidemic and it predisposes to the development of insulin resistance, type 2 diabetes and related metabolic diseases. Current interventions against obesity and/or type 2 diabetes such as calorie restriction, exercise, genetic manipulations or established pharmacological treatments have not been successful for many patients with obesity and/or type 2 diabetes.
J Cell Signal, 2020, Volume 1, Issue 4, p160-168 | DOI: 10.33696/Signaling.1.025Dendorbium Nobile Lindl. Alkaloids Suppress NF-κB and NLRP3 Signaling Pathways to Attenuate Lipopolysaccharide-induced Neuroinflammation
The important immune cells in the brain are called microglia acting as the central junction between neuroinflammation and neurodegenerative diseases. In patients of cognitive disorders and Alzheimer’s disease (AD) animal models, amoebic morphology and inflammatory pathways are activated to release numerous cells in the inflammatory factors by active microglia.
J Cell Signal, 2020, Volume 1, Issue 4, p102-114 | DOI: 10.33696/Signaling.1.019Is Citrate A Critical Signal in Immunity and Inflammation?
When immune cells are activated, they undergo metabolic change in order to have sufficient energy to function effectively. The Krebs cycle is one of the most important pathways involved in this response and citrate, a critical component of this pathway, regulates carbohydrate and lipid metabolism.
J Cell Signal, 2020, Volume 1, Issue 3 | DOI: 10.33696/Signaling.1.017Emerging Role of TRPML1 Mucolipin Endolysosomal Channel in Cancer
The transient receptor potential mucolipin 1 (TRPML1) is an endolysosomal channel belonging to the TRP family. Clinically, mutations of TRPML1 have been responsible for a severe lysosomal storage disorder called mucolipidosis type IV.
J Cell Signal, 2020, Volume 1, Issue 1, p4-7 | DOI: 10.33696/Signaling.1.002Flow Cytometric Characterization of Accidental Cell Death Highlights Connections to Regulated Cell Death
Damage-Associated Molecular Patterns (DAMPs) are known by their nature to cause inflammatory responses in numerous disease states from cancer, trauma to age related diseases (e.g. atherosclerosis, Alzheimer’s and Parkinson’s diseases), these molecules are released by cells undergoing cell death.
J Cell Signal, 2020, Volume 1, Issue 1, p1-3 | DOI: 10.33696/Signaling.1.001Scientific Archives is a global publisher initiated with the mission of ensuring equal opportunity for accessing science to research community all over the world. Spreading research findings with great relevance to all channels without any barrier is our goal. We want to overcome the challenges of Open Access with ensured quality and transparency.