scholarly journals Claudin-2: Roles beyond Permeability Functions

2019 ◽  
Vol 20 (22) ◽  
pp. 5655 ◽  
Author(s):  
Shruthi Venugopal ◽  
Shaista Anwer ◽  
Katalin Szászi
Keyword(s):  
Signaling Pathways ◽  
Cell Fate ◽  
Energy Efficient ◽  
Disease Stage ◽  
Cell Fate Determination ◽  
Leaky Epithelia ◽  
Cellular Processes ◽  
Cellular Events ◽  
Fine Control ◽  
Complex Signaling

Claudin-2 is expressed in the tight junctions of leaky epithelia, where it forms cation-selective and water permeable paracellular channels. Its abundance is under fine control by a complex signaling network that affects both its synthesis and turnover in response to various environmental inputs. Claudin-2 expression is dysregulated in many pathologies including cancer, inflammation, and fibrosis. Claudin-2 has a key role in energy-efficient ion and water transport in the proximal tubules of the kidneys and in the gut. Importantly, strong evidence now also supports a role for this protein as a modulator of vital cellular events relevant to diseases. Signaling pathways that are overactivated in diseases can alter claudin-2 expression, and a good correlation exists between disease stage and claudin-2 abundance. Further, loss- and gain-of-function studies showed that primary changes in claudin-2 expression impact vital cellular processes such as proliferation, migration, and cell fate determination. These effects appear to be mediated by alterations in key signaling pathways. The specific mechanisms linking claudin-2 to these changes remain poorly understood, but adapters binding to the intracellular portion of claudin-2 may play a key role. Thus, dysregulation of claudin-2 may contribute to the generation, maintenance, and/or progression of diseases through both permeability-dependent and -independent mechanisms. The aim of this review is to provide an overview of the properties, regulation, and functions of claudin-2, with a special emphasis on its signal-modulating effects and possible role in diseases.

scholarly journals LncRNAs Regulatory Networks in Cellular Senescence

2019 ◽  
Vol 20 (11) ◽  
pp. 2615 ◽  
Author(s):  
Pavan Kumar Puvvula
Keyword(s):  
Signaling Pathways ◽  
Cell Fate ◽  
Regulatory Networks ◽  
Translation Regulation ◽  
Reading Frame ◽  
Downstream Signaling ◽  
Cellular Processes ◽  
Fate Decision ◽  
Functional Mechanisms

Long noncoding RNAs (lncRNAs) are a class of transcripts longer than 200 nucleotides with no open reading frame. They play a key role in the regulation of cellular processes such as genome integrity, chromatin organization, gene expression, translation regulation, and signal transduction. Recent studies indicated that lncRNAs are not only dysregulated in different types of diseases but also function as direct effectors or mediators for many pathological symptoms. This review focuses on the current findings of the lncRNAs and their dysregulated signaling pathways in senescence. Different functional mechanisms of lncRNAs and their downstream signaling pathways are integrated to provide a bird’s-eye view of lncRNA networks in senescence. This review not only highlights the role of lncRNAs in cell fate decision but also discusses how several feedback loops are interconnected to execute persistent senescence response. Finally, the significance of lncRNAs in senescence-associated diseases and their therapeutic and diagnostic potentials are highlighted.

scholarly journals Glycogen Synthase Kinase-3 Is Required for EfficientDictyosteliumChemotaxis

2010 ◽  
Vol 21 (15) ◽  
pp. 2788-2796 ◽  
Author(s):  
Regina Teo ◽  
Kimberley J. Lewis ◽  
Josephine E. Forde ◽  
W. Jonathan Ryves ◽  
Jonathan V. Reddy ◽  
...  
Keyword(s):  
Cell Signaling ◽  
Signaling Pathways ◽  
Cell Fate ◽  
Glycogen Synthase ◽  
Cell Aggregation ◽  
Glycogen Synthase Kinase ◽  
Glycogen Synthase Kinase 3 ◽  
Cell Fate Determination ◽  
Cell Signaling Pathways

Glycogen synthase kinase-3 (GSK3) is a highly conserved protein kinase that is involved in several important cell signaling pathways and is associated with a range of medical conditions. Previous studies indicated a major role of the Dictyostelium homologue of GSK3 (gskA) in cell fate determination during morphogenesis of the fruiting body; however, transcriptomic and proteomic studies have suggested that GSK3 regulates gene expression much earlier during Dictyostelium development. To investigate a potential earlier role of GskA, we examined the effects of loss of gskA on cell aggregation. We find that cells lacking gskA exhibit poor chemotaxis toward cAMP and folate. Mutants fail to activate two important regulatory signaling pathways, mediated by phosphatidylinositol 3,4,5-trisphosphate (PIP3) and target of rapamycin complex 2 (TORC2), which in combination are required for chemotaxis and cAMP signaling. These results indicate that GskA is required during early stages of Dictyostelium development, in which it is necessary for both chemotaxis and cell signaling.

Role of Cdc42 dynamics in the control of fission yeast cell polarization

2013 ◽  
Vol 41 (6) ◽  
pp. 1745-1749 ◽  
Author(s):  
Maitreyi Das ◽  
Fulvia Verde
Keyword(s):  
Cell Fate ◽  
Rho Gtpase ◽  
Cellular Level ◽  
Cell Polarization ◽  
Cell Fate Determination ◽  
Cell Morphogenesis ◽  
Oscillatory Dynamics ◽  
Cellular Processes ◽  
Polarized Cell Growth

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.

scholarly journals Validation of commercial ERK antibodies against the ERK orthologue of the scleractinian coral Stylophora pistillata

F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 577
Author(s):  
Lucile Courtial ◽  
Vincent Picco ◽  
Gilles Pagès ◽  
Christine Ferrier-Pagès
Keyword(s):  
Cell Fate ◽  
Cell Cycle Regulation ◽  
Signalling Pathway ◽  
Immune Reactivity ◽  
Cell Fate Determination ◽  
Stylophora Pistillata ◽  
Cellular Processes ◽  
Extracellular Signal ◽  
Living Organisms ◽  
Cycle Regulation

The extracellular signal-regulated protein kinase (ERK) signalling pathway controls key cellular processes, such as cell cycle regulation, cell fate determination and the response to external stressors. Although ERK functions are well studied in a variety of living organisms ranging from yeast to mammals, its functions in corals are still poorly known. The present work aims to give practical tools to study the expression level of ERK protein and the activity of the ERK signalling pathway in corals. The antibody characterisation experiment was performed five times and identical results were obtained. The present study validated the immune-reactivity of commercially available antibodies directed against ERK and its phosphorylated/activated forms on protein extracts of the reef-building coral Stylophora pistillata.

scholarly journals Drosophila as a Model System to Study Cell Signaling in Organ Regeneration

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Sara Ahmed-de-Prado ◽  
Antonio Baonza
Keyword(s):  
Drosophila Melanogaster ◽  
Signaling Pathways ◽  
Cell Fate ◽  
Cellular Responses ◽  
Model System ◽  
Signaling Networks ◽  
Cellular Processes ◽  
Organ Regeneration ◽  
Ability To Regenerate ◽  
Genetic Mechanisms

Regeneration is a fascinating phenomenon that allows organisms to replace or repair damaged organs or tissues. This ability occurs to varying extents among metazoans. The rebuilding of the damaged structure depends on regenerative proliferation that must be accompanied by proper cell fate respecification and patterning. These cellular processes are regulated by the action of different signaling pathways that are activated in response to the damage. The imaginal discs of Drosophila melanogaster have the ability to regenerate and have been extensively used as a model system to study regeneration. Drosophila provides an opportunity to use powerful genetic tools to address fundamental problems about the genetic mechanisms involved in organ regeneration. Different studies in Drosophila have helped to elucidate the genes and signaling pathways that initiate regeneration, promote regenerative growth, and induce cell fate respecification. Here we review the signaling networks involved in regulating the variety of cellular responses that are required for discs regeneration.

rugose (rg), a Drosophila A kinase Anchor Protein, Is Required for Retinal Pattern Formation and Interacts Genetically With Multiple Signaling Pathways

Genetics ◽  
2002 ◽  
Vol 161 (2) ◽  
pp. 693-710
Author(s):  
Hoda K Shamloula ◽  
Mkajuma P Mbogho ◽  
Angel C Pimentel ◽  
Zosia M A Chrzanowska-Lightowlers ◽  
Vanneta Hyatt ◽  
...  
Keyword(s):  
Pattern Formation ◽  
Signaling Pathways ◽  
Cell Fate ◽  
Genetic Interaction ◽  
Cell Phenotype ◽  
Cell Fate Determination ◽  
Cone Cell ◽  
Anchor Protein ◽  
Fate Determination ◽  
Cone Cells

Abstract In the developing Drosophila eye, cell fate determination and pattern formation are directed by cell-cell interactions mediated by signal transduction cascades. Mutations at the rugose locus (rg) result in a rough eye phenotype due to a disorganized retina and aberrant cone cell differentiation, which leads to reduction or complete loss of cone cells. The cone cell phenotype is sensitive to the level of rugose gene function. Molecular analyses show that rugose encodes a Drosophila A kinase anchor protein (DAKAP 550). Genetic interaction studies show that rugose interacts with the components of the EGFR- and Notch-mediated signaling pathways. Our results suggest that rg is required for correct retinal pattern formation and may function in cell fate determination through its interactions with the EGFR and Notch signaling pathways.

scholarly journals Validation of commercial ERK antibodies against the ERK orthologue of the scleractinian coral Stylophora pistillata

F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 577
Author(s):  
Lucile Courtial ◽  
Vincent Picco ◽  
Gilles Pagès ◽  
Christine Ferrier-Pagès
Keyword(s):  
Cell Fate ◽  
Cell Cycle Regulation ◽  
Signalling Pathway ◽  
Immune Reactivity ◽  
Cell Fate Determination ◽  
Stylophora Pistillata ◽  
Cellular Processes ◽  
Extracellular Signal ◽  
Living Organisms ◽  
Cycle Regulation

The extracellular signal-regulated protein kinase (ERK) signalling pathway controls key cellular processes, such as cell cycle regulation, cell fate determination and the response to external stressors. Although ERK functions are well studied in a variety of living organisms ranging from yeast to mammals, its functions in corals are still poorly known. The present work aims to give practical tools to study the expression level of ERK protein and the activity of the ERK signalling pathway in corals. The antibody characterisation experiment was performed five times and identical results were obtained. The present study validated the immune-reactivity of commercially available antibodies directed against ERK and its phosphorylated/activated forms on protein extracts of the reef-building coral Stylophora pistillata.

scholarly journals Insulin Receptor Trafficking: Consequences for Insulin Sensitivity and Diabetes

2019 ◽  
Vol 20 (20) ◽  
pp. 5007 ◽  
Author(s):  
Yang Chen ◽  
Lili Huang ◽  
Xinzhou Qi ◽  
Chen Chen
Keyword(s):  
Insulin Resistance ◽  
Insulin Receptor ◽  
Signaling Pathways ◽  
Severe Insulin Resistance ◽  
Cellular Events ◽  
Wide Range ◽  
Key Factor ◽  
Complex Signaling

Insulin receptor (INSR) has been extensively studied in the area of cell proliferation and energy metabolism. Impaired INSR activities lead to insulin resistance, the key factor in the pathology of metabolic disorders including type 2 diabetes mellitus (T2DM). The mainstream opinion is that insulin resistance begins at a post-receptor level. The role of INSR activities and trafficking in insulin resistance pathogenesis has been largely ignored. Ligand-activated INSR is internalized and trafficked to early endosome (EE), where INSR is dephosphorylated and sorted. INSR can be subsequently conducted to lysosome for degradation or recycled back to the plasma membrane. The metabolic fate of INSR in cellular events implies the profound influence of INSR on insulin signaling pathways. Disruption of INSR-coupled activities has been identified in a wide range of insulin resistance-related diseases such as T2DM. Accumulating evidence suggests that alterations in INSR trafficking may lead to severe insulin resistance. However, there is very little understanding of how altered INSR activities undermine complex signaling pathways to the development of insulin resistance and T2DM. Here, we focus this review on summarizing previous findings on the molecular pathways of INSR trafficking in normal and diseased states. Through this review, we provide insights into the mechanistic role of INSR intracellular processes and activities in the development of insulin resistance and diabetes.

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