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Cellular Signalling

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https://www.readbyqxmd.com/read/29331585/cathepsin-l-promotes-ionizing-radiation-induced-u251-glioma-cell-migration-and-invasion-through-regulating-the-gsk-3%C3%AE-cux1-pathway
#1
Yao Fei, Yajie Xiong, Xiao Shen, Yifan Zhao, Ying Zhu, Long Wang, Zhongqin Liang
Cathepsin L (CTSL) is a lysosomal cysteine protease overexpressed and secreted by tumor cells. Our previous study found that CTSL was involved in ionizing radiation (IR)-induced epithelial-mesenchymal transition (EMT) and the increase of glioma invasion and migration. However, the mechanisms by which CTSL promoted this IR-induced glioma migration and invasion remained unclear. In this study, we demonstrated that IR reduced glycogen synthase kinase-3β (GSK-3β) activity, via the CTSL-mediated phosphorylation of its serine-9 residue, in U251 cells...
January 10, 2018: Cellular Signalling
https://www.readbyqxmd.com/read/29331584/protein-neddylation-and-its-alterations-in-human-cancers-for-targeted-therapy
#2
REVIEW
Lisha Zhou, Wenjuan Zhang, Yi Sun, Lijun Jia
Neddylation, a post-translational modification that conjugates an ubiquitin-like protein NEDD8 to substrate proteins, is an important biochemical process that regulates protein function. The best-characterized substrates of neddylation are the cullin subunits of Cullin-RING ligases (CRLs), which, as the largest family of E3 ubiquitin ligases, control many important biological processes, including tumorigenesis, through promoting ubiquitylation and subsequent degradation of a variety of key regulatory proteins...
January 10, 2018: Cellular Signalling
https://www.readbyqxmd.com/read/29331583/importins-%C3%AE-and-%C3%AE-signaling-mediates-endothelial-cell-inflammation-and-barrier-disruption
#3
Antony Leonard, Arshad Rahman, Fabeha Fazal
Nucleocytoplasmic shuttling via importins is central to the function of eukaryotic cells and an integral part of the processes that lead to many human diseases. In this study, we addressed the role of α and β importins in the mechanism of endothelial cell (EC) inflammation and permeability, important pathogenic features of many inflammatory diseases such as acute lung injury and atherosclerosis. RNAi-mediated knockdown of importin α4 or α3 each inhibited NF-κB activation, proinflammatory gene (ICAM-1, VCAM-1, and IL-6) expression, and thereby endothelial adhesivity towards HL-60 cells, upon thrombin challenge...
January 10, 2018: Cellular Signalling
https://www.readbyqxmd.com/read/29331582/inositol-polyphosphates-contribute-to-cellular-circadian-rhythms-implications-for-understanding-lithium-s-molecular-mechanism
#4
Heather Wei, Dominic Landgraf, George Wang, Michael J McCarthy
Most living organisms maintain cell autonomous circadian clocks that synchronize critical biological functions with daily environmental cycles. In mammals, the circadian clock is regulated by inputs from signaling pathways including glycogen synthase kinase 3 (GSK3). The drug lithium has actions on GSK3, and also on inositol metabolism. While it is suspected that lithium's inhibition of GSK3 causes rhythm changes, it is not known if inositol polyphosphates can also affect the circadian clock. We examined whether the signaling molecule inositol hexaphosphate (IP6) has effects on circadian rhythms...
January 10, 2018: Cellular Signalling
https://www.readbyqxmd.com/read/29331508/compartmentalized-crosstalk-of-cftr-and-tmem16a-ano1-through-epac1-and-adcy1
#5
Joana Lérias, Madalena Pinto, Roberta Benedetto, Rainer Schreiber, Margarida Amaral, Massimo Aureli, Karl Kunzelmann
Airway epithelial cells express both Ca2+ activated TMEM16A/ANO1 and cAMP activated CFTR anion channels. Previous work suggested a significant crosstalk of intracellular Ca2+ and cAMP signaling pathways, leading to activation of both chloride channels. We demonstrate that in airway epithelial cells, stimulation of purinergic or muscarinic G-protein coupled receptors (GPCRs) activates TMEM16A and CFTR. Additional expression of Gq/11 and phospholipase C coupled GPCRs strongly enhanced the crosstalk between Ca2+- and cAMP-dependent signaling...
January 10, 2018: Cellular Signalling
https://www.readbyqxmd.com/read/29329782/lpa-induced-migration-of-ovarian-cancer-cells-requires-activation-of-erm-proteins-via-lpa1-and-lpa2
#6
Jeongrak Park, Jin-Hyuck Jang, Seojin Oh, Minhye Kim, Changhoon Shin, Minseok Jeong, Kyun Heo, Jong Bae Park, Sang Ryong Kim, Yong-Seok Oh
Lysophosphatidic acid (LPA) has been implicated in the pathology of human ovarian cancer. This phospholipid elicits a wide range of cancer cell responses, such as proliferation, trans-differentiation, migration, and invasion, via various G-protein-coupled LPA receptors (LPARs). Here, we explored the cellular signaling pathway via which LPA induces migration of ovarian cancer cells. LPA induced robust phosphorylation of ezrin/radixin/moesin (ERM) proteins, which are membrane-cytoskeleton linkers, in the ovarian cancer cell line OVCAR-3...
January 9, 2018: Cellular Signalling
https://www.readbyqxmd.com/read/29329781/dopamine-transporter-trafficking-is-regulated-by-neutral-sphingomyelinase-2-ceramide-kinase
#7
Jong Hoon Won, Seok Kyun Kim, In Chul Shin, Hae Chan Ha, Ji Min Jang, Moon Jung Back, Dae Kyong Kim
Dopamine (DA) reuptake is the primary mechanism to terminate dopaminergic transmission in the synaptic cleft. The dopamine transporter (DAT) has an important role in the regulation of DA reuptake. This study provides anatomical and physiological evidence that DAT recycling is regulated by ceramide kinase via the sphingomyelin pathway. First, the results show that DAT and neutral sphingomyelinase 2 (nSMase2) were successfully co-precipitated from striatal samples and were colocalized in the mouse striatum or PC12 cells...
January 9, 2018: Cellular Signalling
https://www.readbyqxmd.com/read/29329780/oncogenic-rac1-and-nras-drive-resistance-to-endoplasmic-reticulum-stress-through-mek-erk-signalling
#8
Michael D Bright, Paul A Clarke, Paul Workman, Faith E Davies
Cancer cells are able to survive under conditions that cause endoplasmic reticulum stress (ER-stress), and can adapt to this stress by upregulating cell-survival signalling pathways and down-regulating apoptotic pathways. The cellular response to ER-stress is controlled by the unfolded protein response (UPR). Small Rho family GTPases are linked to many cell responses including cell growth and apoptosis. In this study, we investigate the function of small GTPases in cell survival under ER-stress. Using siRNA screening we identify that RAC1 promotes cell survival under ER-stress in cells with an oncogenic N92I RAC1 mutation...
January 9, 2018: Cellular Signalling
https://www.readbyqxmd.com/read/29329779/receptor-and-cellular-compartment-specific-activation-of-the-camp-pka-pathway-by-%C3%AE-1-adrenergic-and-eta-endothelin-receptors
#9
Ryan D Martin, Yalin Sun, Kyla Bourque, Nicolas Audet, Asuka Inoue, Jason C Tanny, Terence E Hébert
The signaling functions of many G protein-coupled receptors (GPCRs) expressed in the myocardium are incompletely understood. Among these are the endothelin receptor (ETR) family and α1-adrenergic receptor (α1-AR), which are thought to couple to the G protein Gαq. In this study, we used transcriptome analysis to compare the signaling networks downstream of these receptors in primary neonatal rat cardiomyocytes. This analysis indicated increased expression of target genes of cAMP responsive element modulator (CREM) after 24 h treatment with the α1-AR agonist phenylephrine, but not the ETR agonist endothelin-1, suggesting a specific role for the α1-AR in promoting cAMP production in cardiomyocytes...
January 9, 2018: Cellular Signalling
https://www.readbyqxmd.com/read/29325876/nogo-a-interacts-with-trka-to-alter-nerve-growth-factor-signaling-in-nogo-a-overexpressing-pc12-cells
#10
Robert G Farrer, Gwendolyn L Kartje
The Nogo-A protein, originally discovered as a potent myelin-associated inhibitor of neurite outgrowth, is also expressed by certain neurons, especially during development and after injury, but its role in neuronal function is not completely known. In this report, we overexpressed Nogo-A in PC12 cells to use as a model to identify potential neuronal signaling pathways affected by endogenously expressed Nogo-A. Unexpectedly, our results show that viability of Nogo-A-overexpressing cells was reduced progressively due to apoptotic cell death following NGF treatment, but only after 24 h...
January 8, 2018: Cellular Signalling
https://www.readbyqxmd.com/read/29288710/hbp-induces-the-expression-of-monocyte-chemoattractant-protein-1-via-the-fak-pi3k-akt-and-p38-mapk-nf-%C3%AE%C2%BAb-pathways-in-vascular-endothelial-cells
#11
Mengling Chang, Feng Guo, Zengding Zhou, Xiaoqin Huang, Lei Yi, Yi Dou, Jingning Huan
Inflammation is characterized by early influx of polymorphonuclear neutrophils (PMNs), followed by a second wave of monocyte recruitment. PMNs mediate monocyte recruitment via their release of heparin binding protein (HBP), which activates CCR2 (CC-chemokine receptor 2) on monocytes. However, the pathways for such signal transmission remain unknown. Accumulating evidences have highlighted the importance of leukocyte-endothelial cell interactions in the initiation of inflammation. In this study, an interesting finding is that HBP enhances the secretion of monocyte chemotactic protein 1(MCP-1), ligand of CCR2, from a third party, the endothelial cells (ECs)...
December 27, 2017: Cellular Signalling
https://www.readbyqxmd.com/read/29284139/coordinated-d-cyclin-foxd1-activation-drives-mitogenic-activity-of-sonic-hedgehog-signaling-pathway
#12
Dustin M Fink, Miranda R Sun, Galen W Heyne, Joshua L Everson, Hannah M Chung, Sookhee Park, Michael D Sheets, Robert J Lipinski
Sonic Hedgehog (Shh) signaling plays key regulatory roles in embryonic development and postnatal homeostasis and repair. Modulation of the Shh pathway is known to cause malformations and malignancies associated with dysregulated tissue growth. However, our understanding of the molecular mechanisms by which Shh regulates cellular proliferation is incomplete. Here, using mouse embryonic fibroblasts, we demonstrate that the Forkhead box gene Foxd1 is transcriptionally regulated by canonical Shh signaling and required for downstream proliferative activity...
December 25, 2017: Cellular Signalling
https://www.readbyqxmd.com/read/29277445/biased-g-protein-coupled-receptor-agonism-mediates-neu1-sialidase-and-matrix-metalloproteinase-9-crosstalk-to-induce-transactivation-of-insulin-receptor-signaling
#13
Fiona Haxho, Sabah Haq, Myron R Szewczuk
G protein-coupled receptors (GPCR) can participate in a number of signaling pathways, and this property led to the concept of biased GPCR agonism. Agonists, antagonists and allosteric modulators can bind to GPCRs in different ways, creating unique conformations that differentially modulate signaling through one or more G proteins. A unique neuromedin B (NMBR) GPCR-signaling platform controlling mammalian neuraminidase-1 (Neu1) and matrix metalloproteinase-9 (MMP9) crosstalk has been reported in the activation of the insulin receptor (IR) through the modification of the IR glycosylation...
December 24, 2017: Cellular Signalling
https://www.readbyqxmd.com/read/29269047/coordinated-regulation-of-hepatic-foxo1-pgc-1%C3%AE-and-srebp-1c-facilitates-insulin-action-and-resistance
#14
Mini P Sajan, Mackenzie C Lee, Fabienne Foufelle, Joshua Sajan, Courtney Cleland, Robert V Farese
Type 2 diabetes is characterized by insulin resistance, hyperinsulinemia and hepatic overproduction of glucose and lipids. Insulin increases lipogenic enzyme expression by activating Akt and aPKC which activate SREBP-1c; this pathway is hyperactivated in insulin-resistant states. Insulin suppresses gluconeogenic enzyme expression by Akt-dependent phosphorylation/inactivation of FoxO1 and PGC-1α; this pathway is impaired in insulin-resistant states by aPKC excess, which displaces Akt from scaffolding-protein WD40/ProF, where Akt phosphorylates/inhibits FoxO1...
December 18, 2017: Cellular Signalling
https://www.readbyqxmd.com/read/29269046/tgf-%C3%AE-1-up-regulates-cadherin-11-expression-through-snail-a-potential-mechanism-for-human-trophoblast-cell-differentiation
#15
Jung-Chien Cheng, Yuyin Yi, Hsun-Ming Chang, Peter C K Leung
Cadherins are transmembrane proteins that mediate cell-cell adhesion by promoting the formation of adherens junctions. The regulated expression of cadherins is thought to play important roles in both normal and diseased placental development. Cadherin-11, also known as OB-cadherin, is expressed in human placenta and has been shown to be involved in regulation of trophoblast cell differentiation. We have demonstrated that transforming growth factor-beta1 (TGF-β1) promotes human trophoblast cell differentiation...
December 18, 2017: Cellular Signalling
https://www.readbyqxmd.com/read/29242170/a-shift-in-the-il-6-stat3-signalling-pathway-imbalance-towards-the-shp2-pathway-in-severe-asthma-results-in-reduced-proliferation-process
#16
Ikhlass Haj Salem, Sophie Plante, Abdelilah S Gounni, Mahmoud Rouabhia, Jamila Chakir
BACKGROUND: Bronchial fibroblasts are the main structural cells responsible for extracellular matrix production and turnover in lung tissue. They play a key role in airway remodelling in asthma through different cytokines including interleukin (IL-6). OBJECTIVE: To decipher IL-6 signalling in bronchial fibroblasts obtained from severe eosinophilic asthmatics compared to mild asthmatics and healthy controls. METHODS: Human bronchial fibroblasts were isolated from bronchial biopsies of mild and severe eosinophilic asthmatics and non-atopic healthy controls...
December 11, 2017: Cellular Signalling
https://www.readbyqxmd.com/read/29242169/c60-fullerenes-disrupt-cellular-signalling-leading-to-trpc4-and-trpc6-channels-opening-by-the-activation-of-muscarinic-receptors-and-g-proteins-in-small-intestinal-smooth-muscles
#17
Dariia O Dryn, Mariia I Melnyk, Lina T Al Kury, Yuriy I Prylutskyy, Uwe Ritter, Alexander V Zholos
The effect of water-soluble pristine C60 fullerene nanoparticles (C60NPs) on receptor-operated cation channels formed by TRPC4/C6 proteins in ileal smooth muscle cells was investigated for the first time. Activation of these channels subsequent to acetylcholine binding to the expressed in these cells M2 and M3 muscarinic receptors represents the key event in the parasympathetic control of gastrointestinal smooth muscle motility and cholinergic excitation-contraction coupling. Experiments were performed on single collagenase-dispersed mouse ileal myocytes using patch-clamp techniques with symmetrical 125mM Cs+ solutions and [Ca2+]i 'clamped' at 100nM in order to isolate the muscarinic cation current (mICAT)...
December 11, 2017: Cellular Signalling
https://www.readbyqxmd.com/read/29242168/akt1-distinctively-suppresses-myd88-depenedent-and-trif-dependent-toll-like-receptor-signaling-in-a-kinase-activity-independent-manner
#18
Kosuke Zenke, Masashi Muroi, Ken-Ichi Tanamoto
We found that AKT1, a primary effector molecule of PI3K-AKT signaling, distinctively suppressed Toll-like receptor (TLR)-mediated MyD88-dependent and Toll/IL-1R domain-containing adaptor inducing IFN-β (TRIF)-dependent signaling by inhibiting NF-κB activation and IRF3 activity independently of its kinase activity. In AKT1 knockout RAW264.7 cells, lipopolysaccharide (LPS)-induced transcription and protein production of cytokines including IL-1β and TNF-α (regulated by the MyD88-dependent pathway), as well as IFN-β and RANTES (C-C motif chemokine ligand 5: CCL-5; regulated by the TRIF-dependent pathways) was enhanced compared to wild type cells...
December 11, 2017: Cellular Signalling
https://www.readbyqxmd.com/read/29199045/the-mechanism-of-myocardial-hypertrophy-regulated-by-the-interaction-between-mhrt-and-myocardin
#19
Ying Luo, Yao Xu, Chen Liang, Weibing Xing, Tongcun Zhang
As a strong transactivator of promoters containing CarG boxes, myocardin was critical for the cardiac muscle program and necessary for normal cardiogenesis. So it probably represents a viable therapeutic biomarker in the setting of cardiac hypertrophy and failure. In recent years, the studies of regulation of cardiac hypertrophy via myocardin are so common, and the molecular mechanism is becoming more and more clear. Here, we have revealed a kind of interaction between mhrt and myocardin shown as a feedback regulatory mechanism in the regulation of cardiac hypertrophy...
December 1, 2017: Cellular Signalling
https://www.readbyqxmd.com/read/29196224/phosphorylation-of-mig6-negatively-regulates-the-ubiquitination-and-degradation-of-egfr-mutants-in-lung-adenocarcinoma-cell-lines
#20
Gandhi T K Boopathy, Julia Lim Sze Lynn, Sheena Wee, Jayantha Gunaratne, Wanjin Hong
Activating mutations in the kinase domain of epidermal growth factor receptor (EGFR) leads to constitutively active kinase, improves the EGFR stability and promotes malignant transformation in lung adenocarcinoma. Despite the clinical significance, the mechanism by which the increased kinase activity stabilizes the receptor is not completely understood. Using SILAC phosphoproteomic approach, we identify that Mig6 is highly phosphorylated at S256 in EGFR mutants (19del and L858R). Loss of Mig6 contributes to efficient degradation of EGFR wildtype and mutants in lung cancer cells...
November 28, 2017: Cellular Signalling
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