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    4659 results match your criteria Cellular Signalling [Journal]

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    Deltex interacts with Eiger and consequently influences the cell death in Drosophila melanogaster.
    Cell Signal 2018 May 15. Epub 2018 May 15.
    Department of Molecular and Human Genetics, Institute of Science, Banaras Hindu University, Varanasi 221005, Uttar Pradesh, India. Electronic address:
    TNF-JNK signaling is one of the highly conserved signaling pathways that regulate a broad spectrum of cellular processes including proliferation and apoptosis. Eiger, the sole homologue of TNF in Drosophila, initiates the TNF-JNK pathway to induce cell death. Previously, Deltex (Dx) has been identified as a Notch signaling component that regulates vesicular trafficking of Notch. Read More

    Role of mitogen-activated protein kinase signaling in the pathogenesis of dengue virus infection.
    Cell Signal 2018 May 15;48:64-68. Epub 2018 May 15.
    Siriraj Center of Research Excellence for Molecular Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand; Department of Anatomy, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand. Electronic address:
    Dengue virus (DENV) infection is a disease that is endemic to many parts of the world, and its increasing prevalence ranks it among the diseases considered to be a significant threat to public health. The clinical manifestations of DENV infection range from mild dengue fever (DF) to more severe dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). Increased proinflammatory cytokines and vascular permeability, both of which cause organ injury, are the hallmarks of severe dengue disease. Read More

    IRAK2 counterbalances oncogenic Smurf1 in colon cancer cells by dictating ER stress.
    Cell Signal 2018 May 9;48:69-80. Epub 2018 May 9.
    Department of General Surgery, Chinese People's Liberation Army General Hospital, Beijing 100853, China. Electronic address:
    The endoplasmic reticulum (ER) is a cellular organelle with central roles in maintaining proteostasis. The accumulation of misfolded proteins in the ER lumen causes ER stress. Cells evoke an evolutionarily conserved adaptive signaling network "unfolded protein response" to restore ER homeostasis, however, how the signaling network is delicately orchestrated remains largely unrevealed. Read More

    Sec6 enhances cell migration and suppresses apoptosis by elevating the phosphorylation of p38 MAPK, MK2, and HSP27.
    Cell Signal 2018 May 2;49:1-16. Epub 2018 May 2.
    Department of Anatomy and Cell Biology, Yamagata University School of Medicine, Yamagata 990-9585, Japan.
    The signaling axis of p38 mitogen-activated protein kinase (p38 MAPK) and MAPK-activated protein kinase 2 (MK2) is the dominant pathway that leads to heat shock protein 27 (HSP27) phosphorylation. After activation of MK2 by p38 MAPK, HSP27 is phosphorylated and depolymerized by MK2, thereby increasing the cell migration and directly interfering with the apoptotic signaling cascades. Sec6 is one of the components of the exocyst complex that is an evolutionarily conserved 8-protein complex. Read More

    Molecular mechanisms of platelet activation and aggregation induced by breast cancer cells.
    Cell Signal 2018 Apr 26;48:45-53. Epub 2018 Apr 26.
    Department of Biology and Biotechnology, University of Pavia, Pavia, Italy.
    Tumor cell-induced platelet aggregation represents a critical process both for successful metastatic spread of the tumor and for the development of thrombotic complications in cancer patients. To get further insights into this process, we investigated and compared the molecular mechanisms of platelet aggregation induced by two different breast cancer cell lines (MDA-MB-231 and MCF7) and a colorectal cancer cell line (Caco-2). All the three types of cancer cells were able to induce comparable platelet aggregation, which, however, was observed exclusively in the presence of CaCl and autologous plasma. Read More

    Modulation of TGFβ/Smad signaling by the small GTPase RhoB.
    Cell Signal 2018 Apr 26;48:54-63. Epub 2018 Apr 26.
    Laboratory of Biochemistry, Department of Medicine, University of Crete, Heraklion 71003, Greece; Institute of Molecular Biology and Biotechnology, Foundation for Research & Technology-Hellas, GR-71110 Heraklion, Greece. Electronic address:
    We have shown previously that the small GTPases RhoA and RhoB play important roles in early TGFβ-induced actin cytoskeleton reorganization and that RhoB is transcriptionally activated by TGFβ and its signaling effectors, the Smad proteins. However, this long-term impact of RhoB gene upregulation by TGFβ on cellular functions is not known. We now show that increased levels of RhoB, but not of RhoA, inhibit the TGFβ/Smad-mediated transcriptional induction of the cell cycle inhibitor p21 gene as well as of a generic Smad-responsive promoter suggesting that RhoB could be part of an auto-inhibitory loop in TGFβ signaling by inhibiting the genomic responses to TGFβ. Read More

    RASAL2 inhibits tumor angiogenesis via p-AKT/ETS1 signaling in bladder cancer.
    Cell Signal 2018 Apr 24;48:38-44. Epub 2018 Apr 24.
    Department of Urology, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, PR China. Electronic address:
    Muscle-invasive or metastatic bladder cancer (BCa) is a life-threatening disease for patients, and tumor angiogenesis is believed to play a critical role in the progression of BCa. However, its underlying mechanism of tumor angiogenesis is still poorly understood. In this study, we discovered that RASAL2, a RAS GTPase activating protein, could inhibit BCa angiogenesis based on our shRNA/siRNA knockdown or ectopic cDNA expression experiments. Read More

    The cAMP-induced G protein subunits dissociation monitored in live Dictyostelium cells by BRET reveals two activation rates, a positive effect of caffeine and potential role of microtubules.
    Cell Signal 2018 Apr 24;48:25-37. Epub 2018 Apr 24.
    Department of Chemistry and Biochemistry, University of Arizona, Tucson, AZ 85721-0088, USA. Electronic address:
    To study the dynamics and mechanisms controlling activation of the heterotrimeric G protein Gα2βγ in Dictyostelium in response to stimulation by the chemoattractant cyclic AMP (cAMP), we monitored the G protein subunit interaction in live cells using bioluminescence resonance energy transfer (BRET). We found that cAMP induces the cAR1-mediated dissociation of the G protein subunits to a similar extent in both undifferentiated and differentiated cells, suggesting that only a small number of cAR1 (as expressed in undifferentiated cells) is necessary to induce the full activation of Gα2βγ. In addition, we found that treating cells with caffeine increases the potency of cAMP-induced Gα2βγ activation; and that disrupting the microtubule network but not F-actin inhibits the cAMP-induced dissociation of Gα2βγ. Read More

    TRIM8 regulated autophagy modulates the level of cleaved Caspase-3 subunit to inhibit genotoxic stress induced cell death.
    Cell Signal 2018 Apr 17;48:1-12. Epub 2018 Apr 17.
    Department of Biochemistry, Faculty of Science, The Maharaja Sayajirao University of Baroda, Vadodara, Gujarat 390002, India. Electronic address:
    In cancer patients, treatment modalities like chemotherapy and radiation exert their anticancer effects by inducing DNA damage. The cancer cells can survive under genotoxic stress by inducing DNA damage response (DDR) or can undergo cell death. The process of autophagy is emerging as crucial regulator of cell survival during different stress conditions. Read More

    Activation of the non-canonical NF-κB/p52 pathway in vascular endothelial cells by RANKL elicits pro-calcific signalling in co-cultured smooth muscle cells.
    Cell Signal 2018 Jul 17;47:142-150. Epub 2018 Apr 17.
    School of Biotechnology, Dublin City University, Glasnevin, Dublin 9, Ireland; National Institute for Cellular Biotechnology, Dublin City University, Glasnevin, Dublin 9, Ireland. Electronic address:
    Background: The intimal endothelium is known to condition the underlying medial smooth muscle cell (SMC) layer of the vessel wall, and is highly responsive to receptor-activator of nuclear factor-κB ligand (RANKL) and tumour necrosis factor-related apoptosis-inducing ligand (TRAIL), pro-calcific and anti-calcific agents, respectively. In this paper, we tested the hypothesis that RANKL-induced activation of endothelial NF-κB signalling is essential for pro-calcific activation of the underlying SMCs.

    Methods: For these studies, human aortic endothelial and smooth muscle cell mono-cultures (HAECs, HASMCs) were treated with RANKL (0-25 ng/ml ± 5 ng/ml TRAIL) for 72 h. Read More

    S6 kinase 1 plays a key role in mitochondrial morphology and cellular energy flow.
    Cell Signal 2018 Apr 17;48:13-24. Epub 2018 Apr 17.
    Department of Pharmacology and Medical Science, Metabolic Syndrome and Cell Signaling Laboratory, Institute for Cancer Research, College of Medicine, Chungnam National University, Daejeon 35015, South Korea. Electronic address:
    Mitochondrial morphology, which is associated with changes in metabolism, cell cycle, cell development and cell death, is tightly regulated by the balance between fusion and fission. In this study, we found that S6 kinase 1 (S6K1) contributes to mitochondrial dynamics, homeostasis and function. Mouse embryo fibroblasts lacking S6K1 (S6K1-KO MEFs) exhibited more fragmented mitochondria and a higher level of Dynamin related protein 1 (Drp1) and active Drp1 (pS616) in both whole cell extracts and mitochondrial fraction. Read More

    EphA3 maintains radioresistance in head and neck cancers through epithelial mesenchymal transition.
    Cell Signal 2018 Jul 10;47:122-130. Epub 2018 Apr 10.
    Department of Otolaryngology, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Republic of Korea. Electronic address:
    Radiotherapy is a well-established therapeutic modality used in the treatment of many cancers. However, radioresistance remains a serious obstacle to successful treatment. Radioresistance can cause local recurrence and distant metastases in some patients after radiation treatment. Read More

    MAGI proteins can differentially regulate the signaling pathways of 5-HTR by enhancing receptor trafficking and PLC recruitment.
    Cell Signal 2018 Jul 3;47:109-121. Epub 2018 Apr 3.
    Department of Cellular and Molecular Medicine, University of Ottawa, 451 Smyth Dr., Ottawa, Ontario K1H 8M5, Canada. Electronic address:
    MAGI proteins are Membrane-Associated Guanylate Kinase Inverted proteins that belong to the MAGUK family. They are scaffolding proteins that were shown to mediate the trafficking and signaling of various G protein-coupled receptors (GPCRs). They contain PDZ domains in their structure and many GPCRs interact with these proteins via the PDZ motifs on the carboxyl terminal end of a receptor. Read More

    α-cyano-4-hydroxycinnamate impairs pancreatic cancer cells by stimulating the p38 signaling pathway.
    Cell Signal 2018 Jul 30;47:101-108. Epub 2018 Mar 30.
    Institute for Experimental Surgery, Rostock University Medical Center, Schillingallee 69a, 18057 Rostock, Germany. Electronic address:
    Multiple studies are currently targeting dysregulated cancer cell metabolism with distinct combinations of inhibitors. In this study, we evaluated in pancreatic cancer cells metformin, which blocks oxidative phosphorylation, in combination with α-cyano-4-hydroxycinnamate, which has been reported to inhibit the export of lactate from the cytosol. The combination of metformin with α-cyano-4-hydroxycinnamate had a major inhibitory effect on the migration of 6606PDA cells. Read More

    Inhibition of DNMT suppresses the stemness of colorectal cancer cells through down-regulating Wnt signaling pathway.
    Cell Signal 2018 Jul 27;47:79-87. Epub 2018 Mar 27.
    Department of Pharmacy, Changhai Hospital, The Second Military Medical University, Shanghai, China. Electronic address:
    Cancer stem cell (CSC) theory reveals a new insight into the understanding of tumorigenesis and metastasis. Recently, DNA methylation is suggested to be a potential epigenetic mechanism for maintenance of CSCs. What's more, studies have shown that DNA methyltransferase (DNMT) is essential for CSCs and deletion of DNMT can reduce tumorigenesis by limiting CSC pool. Read More

    Melatonin therapy for diabetic cardiomyopathy: A mechanism involving Syk-mitochondrial complex I-SERCA pathway.
    Cell Signal 2018 Jul 28;47:88-100. Epub 2018 Mar 28.
    Department of Cardiology, Chinese PLA General Hospital, Beijing, China. Electronic address:
    Melatonin and its metabolites have been demonstrated to modulate the glucose, dyslipidemia and other metabolic disorders. This study aimed to explore a novel mechanism responsible for diabetic cardiomyopathy development, and also validated whether melatonin played a protective role in repairing damaged heart in the diabetes setting. Our data demonstrated that spleen tyrosine kinase (Syk) was activated by chronic high-glucose stimulus and contributed to the development of diabetic cardiomyopathy. Read More

    Caveolin-1 deficiency protects pancreatic β cells against palmitate-induced dysfunction and apoptosis.
    Cell Signal 2018 Jul 26;47:65-78. Epub 2018 Mar 26.
    Department of Endocrinology and Metabolism, The Third Affiliated Hospital of Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Diabetology, Guangzhou 510630, China. Electronic address:
    Lipotoxicity leads to insulin secretion deficiency, which is among the important causes for the onset of type 2 diabetes mellitus. Thus, the restoration of β-cell mass and preservation of its endocrine function are long-sought goals in diabetes research. Previous studies have suggested that the membrane protein caveolin-1 (Cav-1) is implicated in β-cell apoptosis and insulin secretion, however, the underlying mechanisms still remains unclear. Read More

    Heat shock protein 60 involvement in vascular smooth muscle cell proliferation.
    Cell Signal 2018 Jul 26;47:44-51. Epub 2018 Mar 26.
    Institute of Cardiovascular Sciences, Albrechtsen Research Centre, St Boniface Hospital, Canada; Departments of Physiology and Pathophysiology, Canada. Electronic address:
    Aim: Heat shock protein 60 (Hsp60) is a mediator of stress-induced vascular smooth muscle cell (VSMC) proliferation. This study will determine, first, if the mitochondrial or cytoplasmic localization of Hsp60 is critical to VSMC proliferation and, second, the mechanism of Hsp60 induction of VSMC proliferation with a focus on modification of nucleocytoplasmic trafficking.

    Methods And Results: Hsp60 was overexpressed in primary rabbit VSMCs with or without a mitochondrial targeting sequence (AdHsp60). Read More

    A novel regulatory function of CDKN1A/p21 in TNFα-induced matrix metalloproteinase 9-dependent migration and invasion of triple-negative breast cancer cells.
    Cell Signal 2018 Jul 26;47:27-36. Epub 2018 Mar 26.
    Department of Gastrointestinal and General Surgery, Medical University of Wroclaw, Poland. Electronic address:
    Metastasis is the leading cause of mortality in patients with highly invasive cancers and, as such, is a major problem for medicine. It has been increasingly recognized that cancer-related inflammation plays an important role in promoting invasion and the metastatic process in which cell motility and upregulation of proteolytic enzymes are crucial events. TNFα is a proinflammatory cytokine known to stimulate synthesis of MMP9, a zinc- and calcium-dependent endopeptidase contributing to the regulation of ECM remodeling and cell signaling. Read More

    IL-7-induced phosphorylation of the adaptor Crk-like and other targets.
    Cell Signal 2018 Jul 24;47:131-141. Epub 2018 Mar 24.
    Cancer and Inflammation Program, CCR, NCI, NIH, Bldg 560, Frederick, MD 21702, USA. Electronic address:
    IL-7 is required for T cell differentiation and mature T cell homeostasis and promotes pro-B cell proliferation and survival. Tyrosine phosphorylation plays a central role in IL-7 signaling. We identified by two-dimensional electrophoresis followed by anti-phosphotyrosine immunoblotting and mass spectrometry sixteen tyrosine phosphorylated proteins from the IL-7-dependent cell line D1. Read More

    Thrombin promotes PAI-1 expression and migration in keratinocytes via ERK dependent Smad linker region phosphorylation.
    Cell Signal 2018 Jul 22;47:37-43. Epub 2018 Mar 22.
    School of Health and Biomedical Sciences, RMIT University, Bundoora, VIC 3083, Australia; School of Pharmacy, The University of Queensland, Wooloongabba, QLD 4102, Australia; Department of Immunology, Monash University, Melbourne, VIC 3004, Australia. Electronic address:
    Keratinocyte proliferation and migration is essential during re-epithelialisation for the restoration of the epithelial barrier during skin wound healing. Numerous growth factors are involved in the stimulation of keratinocyte proliferation and migration. The signalling pathways that drive these processes during wound healing are not well defined. Read More

    Wuho/WDR4 deficiency inhibits cell proliferation and induces apoptosis via DNA damage in mouse embryonic fibroblasts.
    Cell Signal 2018 Jul 21;47:16-26. Epub 2018 Mar 21.
    Institute of Cellular and Organismic Biology, Academia Sinica, No. 128, Academia Road, Sec. 2, Nangang, Taipei 11529, Taiwan; Department of Biochemistry, Duke University, Durham, NC, United States.
    Wuho known as WDR4 encodes a highly conserved WD40-repeat protein, which has known homologues of WDR4 in human and mouse. Wuho-FEN1 interaction may have a critical role in the growth and development, and in the maintenance of genome stability. However, how Wuho gene deletion contributes to cell growth inhibition and apoptosis is still unknown. Read More

    Adenylate cyclases: Receivers, transducers, and generators of signals.
    Cell Signal 2018 Jun 18;46:135-144. Epub 2018 Mar 18.
    Max-Planck-Institut für Entwicklungsbiologie, Abt. Proteinevolution, Max-Planck-Ring 5, 72076 Tübingen, Germany. Electronic address:
    Class III adenylate cyclases (ACs) are widespread signaling proteins, which translate diverse intracellular and extracellular stimuli into a uniform intracellular signal. They are typically composed of an N-terminal array of input domains and transducers, followed C-terminally by a catalytic domain, which, as a dimer, generates the second messenger cAMP. The input domains, which receive stimuli, and the transducers, which propagate the signals, are often found in other signaling proteins. Read More

    Dishevelled: A masterful conductor of complex Wnt signals.
    Cell Signal 2018 Jul 17;47:52-64. Epub 2018 Mar 17.
    Immunology and Molecular Microbiology, Texas Tech University Health Sciences Center, Lubbock, TX, USA. Electronic address:
    The Dishevelled gene was first identified in Drosophila mutants with disoriented hair and bristle polarity [1-3]. The Dsh gene (Dsh/Dvl, in Drosophila and vertebrates respectively) gained popularity when it was discovered that it plays a key role in segment polarity during early embryonic development in Drosophila [4]. Subsequently, the vertebrate homolog of Dishevelled genes were identified in Xenopus (Xdsh), mice (Dvl1, Dvl2, Dvl3), and in humans (DVL1, DVL2, DVL3) [5-10]. Read More

    MiR-34a/miR-93 target c-Ski to modulate the proliferaton of rat cardiac fibroblasts and extracellular matrix deposition in vivo and in vitro.
    Cell Signal 2018 Jun 15;46:145-153. Epub 2018 Mar 15.
    The Department of Cardiovascular Surgery, Xiangya Hospital, Central South University, Changsha 410008, China. Electronic address:
    Cardiac fibrosis is associated with diverse heart diseases. In response to different pathological irritants, cardiac fibroblasts may be induced to proliferate and differentiate into cardiac myofibroblasts, thus contributing to cardiac fibrosis. TGF-β signaling is implicated in the development of heart failure through the induction of cardiac fibrosis. Read More

    Dictyostelium Erk2 is an atypical MAPK required for chemotaxis.
    Cell Signal 2018 Jun 15;46:154-165. Epub 2018 Mar 15.
    Department of Microbiology and Molecular Genetics, Oklahoma State University, Stillwater, OK 74078-3020, USA. Electronic address:
    The Dictyostelium genome encodes only two MAPKs, Erk1 and Erk2, and both are expressed during growth and development. Reduced levels of Erk2 expression have been shown previously to restrict cAMP production during development but still allow for chemotactic movement. In this study the erk2 gene was disrupted to eliminate Erk2 function. Read More

    Distinct signalling properties of insulin receptor substrate (IRS)-1 and IRS-2 in mediating insulin/IGF-1 action.
    Cell Signal 2018 Jul 14;47:1-15. Epub 2018 Mar 14.
    Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Faculty of Health and Medical Sciences, Copenhagen, Denmark. Electronic address:
    Insulin/IGF-1 action is driven by a complex and highly integrated signalling network. Loss-of-function studies indicate that the major insulin/IGF-1 receptor substrate (IRS) proteins, IRS-1 and IRS-2, mediate different biological functions in vitro and in vivo, suggesting specific signalling properties despite their high degree of homology. To identify mechanisms contributing to the differential signalling properties of IRS-1 and IRS-2 in the mediation of insulin/IGF-1 action, we performed comprehensive mass spectrometry (MS)-based phosphoproteomic profiling of brown preadipocytes from wild type, IRS-1 and IRS-2 mice in the basal and IGF-1-stimulated states. Read More

    Inositol hexakisphosphate kinase 1 is a metabolic sensor in pancreatic β-cells.
    Cell Signal 2018 Jun 6;46:120-128. Epub 2018 Mar 6.
    The Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, SE-171 76 Stockholm, Sweden; School of Interdisciplinary Bioscience and Bioengineering, Pohang University of Science and Technology, Pohang, Gyeongbuk 37673, Republic of Korea. Electronic address:
    Diphosphoinositol pentakisphosphate (IP) is critical for the exocytotic capacity of the pancreatic β-cell, but its regulation by the primary instigator of β-cell exocytosis, glucose, is unknown. The high K for ATP of the IP-generating enzymes, the inositol hexakisphosphate kinases (IP6K1 and 2) suggests that these enzymes might serve as metabolic sensors in insulin secreting β-cells and act as translators of disrupted metabolism in diabetes. We investigated this hypothesis and now show that glucose stimulation, which increases the ATP/ADP ratio, leads to an early rise in IP concentration in β-cells. Read More

    STAT6 is a cargo of exportin 1: Biological relevance in primary mediastinal B-cell lymphoma.
    Cell Signal 2018 Jun 1;46:76-82. Epub 2018 Mar 1.
    Normandie Univ, INSERM UMR1245, UNICAEN, Caen, France. Electronic address:
    Primary mediastinal B-cell lymphoma (PMBL) is a distinct B-cell lymphoma subtype with unique clinicopathological and molecular features. PMBL cells are characterised by several genetic abnormalities that conduct to the constitutive activation of the Janus kinase 2/signal transducer and activator of transcription 6 (JAK2/STAT6) signalling pathway. Among recurrent genetic changes in PMBL, we previously reported that the XPO1 gene encoding exportin 1 that controls the nuclear export of cargo proteins and RNAs, is mutated (p. Read More

    Targeting of cathepsin C induces autophagic dysregulation that directs ER stress mediated cellular cytotoxicity in colorectal cancer cells.
    Cell Signal 2018 Jun 1;46:92-102. Epub 2018 Mar 1.
    Department of Biotechnology, Daegu University, Gyeongsan, Gyeongbuk 38453, Republic of Korea. Electronic address:
    As Autophagy is a pivotal mechanism of cancer cell survival and the development of chemotherapeutic resistance; therefore, new approaches are warranted for its targeting which may be fulfilled by cathepsins regulation. Amongst cathepsins, cathepsin C (CTSC) is highly expressed in various cancers and possesses significant therapeutic potential in autoimmune disorders; however, its role in colorectal cancer has not been explored. Herein, we aimed to investigate the role of CTSC in autophagy regulation mediated colorectal carcinoma cell proliferation. Read More

    Sonic hedgehog signaling pathway promotes INSM1 transcription factor in neuroendocrine lung cancer.
    Cell Signal 2018 Jun 1;46:83-91. Epub 2018 Mar 1.
    Department of Genetics, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA; Department of Pediatrics, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA. Electronic address:
    Neuroendocrine (NE) lung tumors account for 20% of total lung cancer cases and represent a subset of aggressive tumors with metastatic potential. High-risk NE lung cancer patients display disseminated disease, N-myc expression/amplification, and poorly differentiated tumors. In this study, we investigate the molecular mechanisms underlying a zinc-finger transcription factor, INSM1 in NE lung cancer. Read More

    Extracellular nucleotides enhance agonist potency at the parathyroid hormone 1 receptor.
    Cell Signal 2018 Jun 1;46:103-112. Epub 2018 Mar 1.
    Department of Physiology and Pharmacology, Schulich School of Medicine & Dentistry, The University of Western Ontario, London, Canada; Bone and Joint Institute, The University of Western Ontario, London, Canada; Department of Biology, Faculty of Science, The University of Western Ontario, London, Canada. Electronic address:
    Parathyroid hormone (PTH) activates the PTH/PTH-related peptide receptor (PTH1R) on osteoblasts and other target cells. Mechanical stimulation of cells, including osteoblasts, causes release of nucleotides such as ATP into the extracellular fluid. In addition to its role as an energy source, ATP serves as an agonist at P2 receptors and an allosteric regulator of many proteins. Read More

    ARF GTPases control phenotypic switching of vascular smooth muscle cells through the regulation of actin function and actin dependent gene expression.
    Cell Signal 2018 Jun 27;46:64-75. Epub 2018 Feb 27.
    Department of Pharmacology and Physiology, Faculty of Medicine, Université de Montréal, Montreal, QC H3C 3J7, Canada. Electronic address:
    Vascular smooth muscle cells (VSMC) can exhibit a contractile or a synthetic phenotype depending on the extracellular stimuli present and the composition of the extracellular matrix. Uncontrolled activation of the synthetic VSMC phenotype is however associated with the development of cardiovascular diseases. Here, we aimed to elucidate the role of the ARF GTPases in the regulation of VSMC dedifferentiation. Read More

    Understanding the mechanism of bias signaling of the insulin-like growth factor 1 receptor: Effects of LL37 and HASF.
    Cell Signal 2018 Jun 28;46:113-119. Epub 2018 Feb 28.
    Duke Cardiovascular Research Center, and Mandel Center for Hypertension and Atherosclerosis Research, Duke University Medical Center, NC 27710, USA. Electronic address:
    The development of biased agonist drugs is widely recognized to be important for the treatment of many diseases, including cardiovascular disease. While GPCR biased agonism has been heavily characterized there is a distinct lack of information with respect to RTK biased agonism both in the identification of biased agonists as well as their attendant mechanisms. One such RTK, the Insulin-like Growth Factor 1 Receptor (IGF1R) plays an important role in a range of biological and disease processes. Read More

    NOX4-driven ROS formation regulates proliferation and apoptosis of gastric cancer cells through the GLI1 pathway.
    Cell Signal 2018 Jun 26;46:52-63. Epub 2018 Feb 26.
    Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Institute of Digestive Disease, Shanghai 200001, China. Electronic address:
    NADPH Oxidase 4 (NOX4), a member of the NOX family, has emerged as a significant source of reactive oxygen species, playing an important role in tumor cell proliferation, apoptosis, and other physiological processes. However, the potential function of NOX4 in gastric cancer (GC) cell proliferation is yet unknown. The aim of this study was to illustrate whether NOX4 plays a role in regulating gastric cancer cell growth. Read More

    Pro-inflammatory cytokine and high doses of ionizing radiation have similar effects on the expression of NF-kappaB-dependent genes.
    Cell Signal 2018 Jun 21;46:23-31. Epub 2018 Feb 21.
    Maria Skłodowska-Curie Institute, Oncology Center, Gliwice Branch, Gliwice, Poland. Electronic address:
    The NF-κB transcription factors are activated via diverse molecular mechanisms in response to various types of stimuli. A plethora of functions associated with specific sets of target genes could be regulated differentially by this factor, affecting cellular response to stress including an anticancer treatment. Here we aimed to compare subsets of NF-κB-dependent genes induced in cells stimulated with a pro-inflammatory cytokine and in cells damaged by a high dose of ionizing radiation (4 and 10 Gy). Read More

    LPS-mediated cell surface expression of CD74 promotes the proliferation of B cells in response to MIF.
    Cell Signal 2018 Jun 21;46:32-42. Epub 2018 Feb 21.
    Department of Vascular Biology, Institute for Stroke and Dementia Research (ISD), Klinikum der Universität München, Ludwig-Maximilians-University of Munich (LMU), Feodor-Lynen-Straße 17, D-81377 Munich, Germany. Electronic address:
    Macrophage migration inhibitory factor (MIF) is a chemokine-like inflammatory cytokine, which plays a pivotal role in the pathogenesis of inflammatory and cardiovascular diseases as well as cancer. We previously identified MIF as a novel B cell chemokine that promotes B cell migration through non-cognate interaction with the CXC chemokine receptor CXCR4 and CD74, the surface form of MHC class II invariant chain. In this study, we have analyzed the regulation of the MIF receptors under inflammatory conditions by investigating the impact of lipopolysaccharide (LPS), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) on CD74 and CXCR4 expression in B lymphocytes. Read More

    Physiological functions of FBW7 in cancer and metabolism.
    Cell Signal 2018 Jun 21;46:15-22. Epub 2018 Feb 21.
    Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, United States. Electronic address:
    FBW7 is one of the most well characterized F-box proteins that serve as substrate recognition subunits of SCF (Skp1-Cullin 1-F-box proteins) E3 ubiquitin ligase complexes. SCF plays key roles in regulating cell cycle progression, differentiation, and stem cell maintenance largely through targeting a broad range of oncogenic substrates for proteasome-dependent degradation. The identification of an increasing number of FBW7 substrates for ubiquitination, and intensive in vitro and in vivo studies have revealed a network of signaling components controlled by FBW7 that contributes to metabolic regulation as well as its tumor suppressor role. Read More

    p66Shc regulates migration of castration-resistant prostate cancer cells.
    Cell Signal 2018 Jun 17;46:1-14. Epub 2018 Feb 17.
    Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, United States; Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE, United States; Section of Urology, Department of Surgery, University of Nebraska Medical Center, Omaha, NE, United States; College of Pharmacy, Kaohsiung Medical University, Kaohsiung 807, Taiwan. Electronic address:
    Metastatic castration-resistant (CR) prostate cancer (PCa) is a lethal disease for which no effective treatment is currently available. p66Shc is an oxidase previously shown to promote androgen-independent cell growth through generation of reactive oxygen species (ROS) and is elevated in clinical PCa and multiple CR PCa cell lines. We hypothesize p66Shc also increases the migratory activity of PCa cells through ROS and investigate the associated mechanism. Read More

    Identification of macrophage-related candidate genes in lupus nephritis using bioinformatics analysis.
    Cell Signal 2018 Jun 17;46:43-51. Epub 2018 Feb 17.
    Center for Kidney Disease, 2nd Affiliated Hospital of Nanjing Medical University, 262 North Zhongshan Road, Nanjing, Jiangsu, China. Electronic address:
    Lupus nephritis (LN) is a chronic autoimmune disorder. Here we try to identify the candidate genes in macrophages related to LN. We performed a systematic search in the Gene Expression Omnibus (GEO) database for microarray in human mononuclear cells and mouse macrophages of LN. Read More

    CEACAM1 resists hypoxia-induced inhibition of tube formation of human dermal lymphatic endothelial cells.
    Cell Signal 2018 May 7;45:145-152. Epub 2018 Feb 7.
    Laboratory of Microvascular Medicine, Medical Research Center, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan 250014, PR China. Electronic address:
    Tube formation is one of the fundamental events required by angiogenesis and lymphangiogenesis. To date, there is little knowledge on the effects of hypoxia on tube formation of human dermal lymphatic endothelial cells (HDLECs). In this study, we found that tube formation of HDLECs was inhibited under hypoxic condition with decreased expressions of VEGF-D, CEACAM1 and Prox1 genes. Read More

    Intracellular zinc increase affects phosphorylation state and subcellular localization of protein kinase C delta (δ).
    Cell Signal 2018 Apr 16;44:148-157. Epub 2018 Feb 16.
    Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, OH 45701, USA. Electronic address:
    Protein kinase C delta (PKCδ) is a Ser/Thr-specific kinase involved in many fundamental cellular processes including growth, differentiation and apoptosis. PKCδ is expressed ubiquitously in all known cell types, and can be activated by diacylglycerol, phorbol esters and other kinases. Multiple lines of evidence have indicated that the mode of activation greatly influences the role PKCδ plays in cellular function. Read More

    TNIP1 reduction sensitizes keratinocytes to post-receptor signalling following exposure to TLR agonists.
    Cell Signal 2018 May 5;45:81-92. Epub 2018 Feb 5.
    Department of Pharmaceutical Sciences, University of Connecticut, Storrs, CT 06269-3092, USA; Stem Cell Institute, University of Connecticut, Storrs, CT 06269-3092, USA. Electronic address:
    Cell level inflammatory signalling is a combination of initiation at cell membrane receptors and modulation by cytoplasmic regulatory proteins. For keratinocytes, the predominant cell type in the epidermis, this would include toll-like receptors (TLR) and cytoplasmic proteins that propagate or dampen post-receptor signalling. We previously reported that increased levels of tumor necrosis factor α induced protein 3-interacting protein 1 (TNIP1) in HaCaT keratinocytes leads to decreased expression of stress response and inflammation-associated genes. Read More

    Cadherins in vascular smooth muscle cell (patho)biology: Quid nos scimus?
    Cell Signal 2018 May 3;45:23-42. Epub 2018 Feb 3.
    Department of Biomedicine, Laboratory for Signal Transduction, University Hospital Basel and University of Basel, Basel, Switzerland. Electronic address:
    Vascular smooth muscle cells (SMCs) phenotypes span a reversible continuum from quiescent/contractile (differentiated) to proliferative/synthetic (dedifferentiated) enabling them to perform a diversity of functions that are context-dependent and important for vascular tone-diameter homeostasis, vasculogenesis, angiogenesis or vessel reparation after injury. Dysregulated phenotype modulation and failure to maintain/regain the mature differentiated and contractile phenotypic state is pivotal in the development of vascular diseases such as atherosclerosis and restenosis after angioplasty and coronary bypass grafting. Many functions of SMCs such as adhesion, migration, proliferation, contraction, differentiation and apoptosis are regulated by a broad spectrum of cell-cell and cell-matrix adhesion molecules. Read More

    Ripk3 regulates cardiac microvascular reperfusion injury: The role of IP3R-dependent calcium overload, XO-mediated oxidative stress and F-action/filopodia-based cellular migration.
    Cell Signal 2018 May 3;45:12-22. Epub 2018 Feb 3.
    Center for Cardiovascular Research and Alternative Medicine, Wyoming University, Laramie, WY 82071, USA.
    Ripk3-mediated cellular apoptosis is a major contributor to the pathogenesis of myocardial ischemia reperfusion (IR) injury. However, the mechanisms by which Ripk3 influences microvascular homeostasis and endothelial apoptosis are not completely understood. In this study, loss of Ripk3 inhibited endothelial apoptosis, alleviated luminal swelling, maintained microvasculature patency, reduced the expression of adhesion molecules and limited the myocardial inflammatory response. Read More

    Cysteinyl leukotriene receptor 1 regulates glucose-stimulated insulin secretion (GSIS).
    Cell Signal 2018 Jun 2;46:129-134. Epub 2018 Feb 2.
    Department of cardiovascular surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 510120, PR China. Electronic address:
    Insulin resistance is an important pathological hallmark of type 2 diabetes mellitus. Glucose-stimulated insulin secretion (GSIS) plays a key role in maintaining blood glucose levels within normal range. Impaired GSIS has been associated with type 2 diabetes, however, the underlying molecular mechanisms remain largely unknown. Read More

    New insights into the Vav1 activation cycle in lymphocytes.
    Cell Signal 2018 May 2;45:132-144. Epub 2018 Feb 2.
    Centro de Investigación del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC), University of Salamanca, 37007 Salamanca, Spain; Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC), University of Salamanca, 37007 Salamanca, Spain; Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), Consejo Superior de Investigaciones Científicas (CSIC), University of Salamanca, 37007 Salamanca, Spain. Electronic address:
    Vav1 is a hematopoietic-specific Rho GDP/GTP exchange factor and signaling adaptor. Although these activities are known to be stimulated by direct Vav1 phosphorylation, little information still exists regarding the regulatory layers that influence the overall Vav1 activation cycle. Using a collection of cell models and activation-mimetic Vav1 mutants, we show here that the dephosphorylated state of Vav1 in nonstimulated T cells requires the presence of a noncatalytic, phospholipase Cγ1-Slp76-mediated inhibitory pathway. Read More

    Osmotic stress induced toxicity exacerbates Parkinson's associated effects via dysregulation of autophagy in transgenic C. elegans model.
    Cell Signal 2018 May 2;45:71-80. Epub 2018 Feb 2.
    Laboratory of Functional Genomics and Molecular Toxicology, Division of Toxicology and Experimental Medicine, CSIR-Central Drug Research Institute, Lucknow, 226 031, UP, India. Electronic address:
    The accumulation of aggregate-prone proteins is a major representative of many neurological disorders, including Parkinson's disease (PD) wherein the cellular clearance mechanisms, such as the ubiquitin-proteasome and autophagy pathways are impaired. PD, known to be associated with multiple genetic and environmental factors, is characterized by the aggregation of α-synuclein protein and loss of dopaminergic neurons in midbrain. This disease is also associated with other cardiovascular ailments. Read More

    Bradykinin mediates myogenic differentiation in murine myoblasts through the involvement of SK1/Spns2/S1P axis.
    Cell Signal 2018 May 3;45:110-121. Epub 2018 Feb 3.
    Dipartimento di Scienze Biomediche Sperimentali e Cliniche "Mario Serio", Università di Firenze, Viale GB Morgagni 50, 50134 Firenze, Italy; Istituto interuniversitario di Miologia, IIM, Padova, Italy.
    Skeletal muscle tissue retains a remarkable regenerative capacity due to the activation of resident stem cells that in pathological conditions or after tissue damage proliferate and commit themselves into myoblasts. These immature myogenic cells undergo differentiation to generate new myofibers or repair the injured ones, giving a strong contribution to muscle regeneration. Cytokines and growth factors, potently released after tissue injury by leukocytes and macrophages, are not only responsible of the induction of the initial inflammatory response, but can also affect skeletal muscle regeneration. Read More

    Egr-1 is required for neu/HER2-induced mammary tumors.
    Cell Signal 2018 May 2;45:102-109. Epub 2018 Feb 2.
    Department of Life Science, Hanyang University, Seoul 04763, Republic of Korea; Natural Science Institute, Hanyang University, Seoul 04763, Republic of Korea. Electronic address:
    Egr-1 is known to function mainly as a tumor suppressor through direct regulation of multiple tumor suppressor genes. To determine the role of Egr-1 in breast tumors in vivo, we used mouse models of breast cancer induced by HER2/neu. We compared neu-overexpressing Egr-1 knockout mice (neu/Egr-1 KO) to neu-overexpressing Egr-1 wild type or heterozygote mice (neu/Egr-1 WT or neu/Egr-1 het) with regard to onset of tumor appearance and number of tumors per mouse. Read More

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