4,814 results match your criteria Cellular Signalling [Journal]


Chemical genetic screen identifies Gapex-5/GAPVD1 and STBD1 as novel AMPK substrates.

Cell Signal 2019 Feb 14. Epub 2019 Feb 14.

Nestlé Institute of Health Sciences SA, Ecole Polytechnique Fédérale de Lausanne (EPFL), Innovation Park, bâtiment G, 1015 Lausanne, Switzerland; School of Life Sciences, EPFL, 1015 Lausanne, Switzerland. Electronic address:

AMP-activated protein kinase (AMPK) is a key regulator of cellular energy homeostasis, acting as a sensor of energy and nutrient status. As such, AMPK is considered a promising drug target for treatment of medical conditions particularly associated with metabolic dysfunctions. To better understand the downstream effectors and physiological consequences of AMPK activation, we have employed a chemical genetic screen in mouse primary hepatocytes in an attempt to identify novel AMPK targets. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.02.001DOI Listing
February 2019

Comparative transcriptomics reveals mechanisms underlying cln3-deficiency phenotypes in Dictyostelium.

Cell Signal 2019 Feb 13. Epub 2019 Feb 13.

Department of Biology, Trent University, Peterborough, Ontario, Canada.

Mutations in CLN3 cause a juvenile form of neuronal ceroid lipofuscinosis (NCL). This devastating neurological disorder, commonly known as Batten disease, is currently untreatable due to a lack of understanding of the physiological role of the protein. Recently, work in the social amoeba Dictyostelium discoideum has provided valuable new insight into the function of CLN3 in the cell. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.02.004DOI Listing
February 2019

Inositol pyrophosphates and Akt: Is the pancreatic β-cell the exception to the rule?

Cell Signal 2019 Feb 8. Epub 2019 Feb 8.

The Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, SE-171 76 Stockholm, Sweden. Electronic address:

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https://linkinghub.elsevier.com/retrieve/pii/S08986568193003
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http://dx.doi.org/10.1016/j.cellsig.2019.02.003DOI Listing
February 2019
1 Read

The biphasic effects of the oxLDL/βGPI/anti-βGPI complex on VSMC proliferation and apoptosis.

Cell Signal 2019 Feb 7. Epub 2019 Feb 7.

Department of Clinical Laboratory and Hematology, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu 212013, China, Zhenjiang, Jiangsu 212013, PR China.

In our previous study, the oxLDL/βGPI/anti-βGPI complex was demonstrated to further enhance the foam cell formation and migration of VSMC, as well as the expression of inflammatory cytokines, via the TLR4/NF-κB pathway. However, sparse information is available on other pro-atherogenic pathogenic effects of the oxLDL/βGPI/anti-βGPI complex, such as effects on proliferation and apoptosis. In the present study, we focused on the biphasic effects and underlying mechanisms of the oxLDL/βGPI/anti-βGPI complex on VSMC survival. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.02.002DOI Listing
February 2019

Inhibition of MALAT1 reduces tumor growth and metastasis and promotes drug sensitivity in colorectal cancer.

Cell Signal 2019 Feb 1;57:21-28. Epub 2019 Feb 1.

School of Pharmacy, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, PR China. Electronic address:

Human metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA known to be highly expressed in several tumors. In colorectal cancer (CRC), MALAT1 promotes cell proliferation, metastasis, and invasion in vitro and in vivo. This study aimed to investigate the effect of MALAT1 on the proliferation, migration, and drug sensitivity of CRC cells in vitro and in vivo and the mechanisms involved therein. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.01.013DOI Listing
February 2019

Minocycline inhibits PDGF-BB-induced human aortic smooth muscle cell proliferation and migration by reversing miR-221- and -222-mediated RECK suppression.

Cell Signal 2019 Feb 1;57:10-20. Epub 2019 Feb 1.

Medicine/Cardiovascular Medicine, University of Missouri School of Medicine, Columbia, MO, USA; Department of Medical Pharmacology and Physiology, University of Missouri School of Medicine, Columbia, MO, USA; Research Service, Harry S. Truman Memorial Veterans' Hospital, Columbia, MO, USA; Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA. Electronic address:

Minocycline, a tetracycline antibiotic, is known to exert vasculoprotective effects independent of its anti-bacterial properties; however the underlying molecular mechanisms are not completely understood. Reversion Inducing Cysteine Rich Protein with Kazal Motifs (RECK) is a cell surface expressed, membrane anchored protein, and its overexpression inhibits cancer cell migration. We hypothesized that minocycline inhibits platelet-derived growth factor (PDGF)-induced human aortic smooth muscle cell (SMC) proliferation and migration via RECK upregulation. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.01.014DOI Listing
February 2019
1 Read

MiR-146a attenuates liver fibrosis by inhibiting transforming growth factor-β1 mediated epithelial-mesenchymal transition in hepatocytes.

Cell Signal 2019 Jan 31. Epub 2019 Jan 31.

Department of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai, PR China; Shanghai Institute of Liver disease, Shanghai, PR China. Electronic address:

Epithelial-mesenchymal transition (EMT) has emerged as a vital process in embryogenesis, carcinogenesis, and tissue fibrosis. Transforming growth factor-beta 1 (TGF-β1)-mediated signaling pathways play important roles in the EMT process. MicroRNA-146a (miR-146a) has been suggested as a significant regulatory molecule in fibrogenesis. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.01.012DOI Listing
January 2019

Understanding and exploiting cell signalling convergence nodes and pathway cross-talk in malignant brain cancer.

Cell Signal 2019 Jan 30;57:2-9. Epub 2019 Jan 30.

Department of Microbiology and Immunology, The University of Melbourne, Melbourne, VIC 3000, Australia; Department of Surgery, The University of Melbourne, The Royal Melbourne Hospital, Parkville, VIC 3050, Australia. Electronic address:

In cancer, complex intracellular and intercellular signals constantly evolve for the advantage of the tumour cells but to the disadvantage of the whole organism. Decades of intensive research have revealed the critical roles of cellular signalling pathways in regulating complex cell behaviours which influence tumour development, growth and therapeutic response, and ultimately patient outcome. Most studies have focussed on specific pathways and the resulting tumour cell function in a rather linear fashion, partly due to the available methodologies and partly due to the traditionally reductionist approach to research. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.01.011DOI Listing
January 2019

Fine particulate matter (PM) enhances FcεRI-mediated signaling and mast cell function.

Cell Signal 2019 Jan 29. Epub 2019 Jan 29.

Department of Epidemiology, College of Public Health, Zhengzhou University, Zhengzhou 450001, People's Republic of China; Department of Immunology, Duke University Medical Center, Durham, NC 27710, USA. Electronic address:

Persistent exposure to ambient fine particulate matter (PM) can exacerbate allergic diseases in humans. Mast cells play an important role in allergic inflammation in peripheral tissues, such as skin, mucosa, and lung. Engagement of the high-affinity Fc receptor leads to mast cell degranulation, releasing a variety of highly active mediators including histamine, leukotrienes, and inflammatory cytokines. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.01.010DOI Listing
January 2019

ER stress activation impairs the expression of circadian clock and clock-controlled genes in NIH3T3 cells via an ATF4-dependent mechanism.

Cell Signal 2019 Jan 28. Epub 2019 Jan 28.

Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Northwest A&F University, Yangling 712100, Shaanxi, China; Key Laboratory of Animal Biotechnology of the Ministry of Agriculture, Northwest A&F University, Yangling 712100, Shaanxi, China. Electronic address:

Endoplasmic reticulum (ER) stress and circadian clockwork signaling pathways mutually regulate various cellular functions, but the details regarding the cross-talk between these pathways in mammalian cells are unclear. In this study, whether perturbation of ER stress signaling affects the cellular circadian clockwork and transcription of clock-controlled genes was investigated in NIH3T3 mouse fibroblasts. An NIH3T3 cell model stably expressing luciferase (Luc) under the control of the Bmal1 clock gene promoter was established using a lentiviral system. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.01.008DOI Listing
January 2019
4.315 Impact Factor

Src family kinases, HCK and FGR, associate with local inflammation and tumour progression in colorectal cancer.

Cell Signal 2019 Apr 23;56:15-22. Epub 2019 Jan 23.

Unit of Experimental Therapeutics, Institute of Cancer Sciences, University of Glasgow, Garscube Estate, Glasgow, United Kingdom.

Background: In colorectal cancer (CRC), inflammatory responses have been reported to associate with patient survival. However, the specific signalling pathways responsible for regulating inflammatory responses are not clear. Src family kinases (SFKs) impact tumourigenic processes, including inflammation. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.01.007DOI Listing

Evolving complexity of MIF signaling.

Cell Signal 2019 Jan 23. Epub 2019 Jan 23.

Institute of Pathology, RWTH Aachen University Hospital, Aachen, Germany; Department of Nephrology and Immunology, RWTH Aachen University Hospital, Aachen, Germany. Electronic address:

Macrophage migration inhibitory factor (MIF) is a cytokine expressed in various cell types, including hematopoietic, epithelial, endothelial, mesenchymal and neuronal cells. Altered MIF expression has been associated with a multitude of diseases ranging from inflammatory disorders like sepsis, lupus and rheumatoid arthritis to organ pathologies such as heart failure, myocardial infarction, acute kidney injury, organ fibrosis and a number of malignancies. The implication of MIF in these diseases was supported by numerous animal studies. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S08986568193001
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http://dx.doi.org/10.1016/j.cellsig.2019.01.006DOI Listing
January 2019
6 Reads

A steroid alkaloid derivative 02F04 upregulates thymic stromal lymphopoietin expression slowly and continuously through a novel Gq/11-ROCK-ERK1/2 signaling pathway in mouse keratinocytes.

Cell Signal 2019 Jan 18. Epub 2019 Jan 18.

Laboratory of Pharmacotherapy of Life-Style Related Diseases, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai 980-8578, Miyagi, Japan. Electronic address:

Thymic stromal lymphopoietin (TSLP), a master switch of allergic inflammation, plays an important role in the pathogenesis of allergic diseases. Although many compounds upregulate TSLP expression in vivo or in vitro, most of them are pollutants or toxicants. In the previous study, for the first time, we found that a steroid alkaloid derivative 02F04, which has a unique skeletal structure compared with other TSLP-inducing chemicals, significantly induced TSLP production in mouse keratinocytes. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S08986568193000
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http://dx.doi.org/10.1016/j.cellsig.2019.01.005DOI Listing
January 2019
5 Reads

SGTb regulates a surface localization of a guidance receptor BOC to promote neurite outgrowth.

Cell Signal 2019 Mar 9;55:100-108. Epub 2019 Jan 9.

Department of Molecular Cell Biology, Single Cell Network Research Center, Sungkyunkwan University School of Medicine, Suwon 16419, Republic of Korea; Samsung Biomedical Research Institute, Samsung Medical Center, Seoul, Republic of Korea. Electronic address:

Neuritogenesis is a critical event for neuronal differentiation and neuronal circuitry formation during neuronal development and regeneration. Our previous study revealed a critical role of a guidance receptor BOC in a neuronal differentiation and neurite outgrowth. However, regulatory mechanisms for BOC signaling pathway remain largely unexplored. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.01.003DOI Listing
March 2019
3 Reads

BMP6 increases TGF-β1 production by up-regulating furin expression in human granulosa-lutein cells.

Cell Signal 2019 Mar 8;55:109-118. Epub 2019 Jan 8.

Department of Obstetrics and Gynaecology, BC Children's Hospital Research Institute, University of British Columbia, Vancouver, British Columbia V5Z 4H4, Canada. Electronic address:

Bone morphogenetic protein 6 (BMP6) and transforming growth factor-β1 (TGF-β1) are key intraovarian regulators that play essential roles in regulating mammalian follicular function and promoting oocyte maturation. Furin, a member of the subtilisin-like proprotein convertase family, promotes the activation of diverse functional proteins by cleaving protein precursors in the secretory pathway. The aim of this study was to investigate the effect and underlying molecular mechanisms by which BMP6 regulates the expression of furin to increase TGF-β1 production. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.01.002DOI Listing
March 2019
2 Reads

Liver parenchymal cells lacking Lipocalin 2 (LCN2) are prone to endoplasmic reticulum stress and unfolded protein response.

Cell Signal 2019 Mar 4;55:90-99. Epub 2019 Jan 4.

Institute of Molecular Pathobiochemistry, Experimental Gene Therapy and Clinical Chemistry (IFMPEGKC), RWTH Aachen University Hospital, Germany. Electronic address:

Unfolded protein response (UPR) is an adaptive mechanism allowing the endoplasmic reticulum (ER) to react to an accumulation of unfolded proteins in its lumen, also known as ER stress. The UPR is interconnected with inflammation through several pathways such as reactive oxygen species (ROS) production resulting from the protein folding or alternatively, activation of nuclear factor-κB (NF-κB) and c-Jun N-terminal kinase (JNK) via IRE1, or induction of acute phase response (APR). Lipocalin 2 (LCN2) is one of the APR proteins induced under inflammatory conditions and up-regulated during ER stress. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S08986568193000
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http://dx.doi.org/10.1016/j.cellsig.2019.01.001DOI Listing
March 2019
6 Reads

Cellular signaling in pseudoxanthoma elasticum: an update.

Cell Signal 2019 Mar 4;55:119-129. Epub 2019 Jan 4.

Center for Medical Genetics, Ghent University Hospital, Ghent, Belgium; Department of Biomolecular Medicine, Ghent University, Belgium. Electronic address:

Pseudoxanthoma elasticum is an autosomal recessive genodermatosis with variable expression, due to mutations in the ABCC6 or ENPP1 gene. It is characterized by elastic fiber mineralization and fragmentation, resulting in skin, eye and cardiovascular symptoms. Significant advances have been made in the last 20 years with respect to the phenotypic characterization and pathophysiological mechanisms leading to elastic fiber mineralization. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S08986568183031
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http://dx.doi.org/10.1016/j.cellsig.2018.12.009DOI Listing
March 2019
2 Reads

Tmub1 negatively regulates liver regeneration via inhibiting STAT3 phosphorylation.

Cell Signal 2019 Mar 2;55:65-72. Epub 2019 Jan 2.

Department of Hepatobiliary Surgery, Daping Hospital (Army Medical Center), Third Military Medical University (Army Medical University), Chongqing 400042, China. Electronic address:

Tmub1 (transmembrane and ubiquitin-like domain-containing 1) plays negative roles in rat hepatocyte proliferation, but its underlying molecular mechanisms in liver regeneration regulation have yet to be revealed. Here, we show that in vivo transfection of Tmub1 overexpression vectors impaired mouse liver regeneration after partial hepatectomy (PHx). Loss- and gain-of-function analyses in human hepatocyte Lo2 cells indicated that Tmub1 inhibits the phosphorylation of STAT3 and the activation of STAT3 signaling. Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.12.013DOI Listing
March 2019
1 Read
4.315 Impact Factor

IER family proteins are regulators of protein phosphatase PP2A and modulate the phosphorylation status of CDC25A.

Cell Signal 2019 Mar 30;55:81-89. Epub 2018 Dec 30.

Division of Health Sciences, Kanazawa University Graduate School of Medical Science, 5-11-80 Kodatsuno, Kanazawa, Ishikawa 920-0942, Japan. Electronic address:

Proteins encoded by immediate-early response (IER) family genes, IER2, IER5, and IER5L, share homology at their N-terminal regions. IER5 binds to protein phosphatase 2A (PP2A) and enhances dephosphorylation of PP2A target proteins such as heat shock factor HSF1. Here, we show the expression of IER family genes and the target protein-specific function of IER proteins. Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.12.012DOI Listing
March 2019
1 Read

MicroRNA-26b-5p enhances T cell responses by targeting PIM-2 in hepatocellular carcinoma.

Cell Signal 2018 Dec 26. Epub 2018 Dec 26.

Department Three of Oncology, The First People's Hospital of Shangqiu, 476100, Henan, China.

Background: Hepatocellular carcinoma (HCC) is a common tumor malignancy threatening a significant number of people worldwide. Although microRNAs (miRNAs) have been shown to play essential role in tumorigenesis, little is known about their role in T cells functions during HCC progression.

Methods: The abundances of miR-26b-5p were detected in HCC tissues or cells, T cells and H22 cells by quantitative real-time polymerase chain reaction (qRT-PCR). Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.11.011DOI Listing
December 2018
1 Read
4.315 Impact Factor

Insulin induces Thr484 phosphorylation and stabilization of SIK2 in adipocytes.

Cell Signal 2019 Mar 23;55:73-80. Epub 2018 Dec 23.

Department of Experimental Medical Science, Lund University, Diabetes, Metabolism and Endocrinology, 22184 Lund, Sweden. Electronic address:

Aims/hypothesis: Salt-inducible kinase 2 (SIK2) is downregulated in adipose tissue from obese or insulin-resistant individuals and inhibition of SIK isoforms results in reduced glucose uptake and insulin signalling in adipocytes. However, the regulation of SIK2 itself in response to insulin in adipocytes has not been studied in detail. The aim of our work was to investigate effects of insulin on various aspects of SIK2 function in adipocytes. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S08986568183032
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http://dx.doi.org/10.1016/j.cellsig.2018.12.011DOI Listing
March 2019
7 Reads

Mechanical exposure and diacerein treatment modulates integrin-FAK-MAPKs mechanotransduction in human osteoarthritis chondrocytes.

Cell Signal 2019 Apr 21;56:23-30. Epub 2018 Dec 21.

Ludwig Boltzmann Department for Rehabilitation, Ludwig Boltzmann Cluster for Arthritis and Rehabilitation, Saalfelden, Austria; Department of Biophysics, Medical University Graz, Graz, Austria.

Background: Progression of osteoarthritis (OA) is characterized by an excessive production of matrix degrading enzymes and insufficient matrix repair. Despite of active research in this area, it is still unclear how the combination of mechanical exposure and drug therapy works. This study was done to explore the impact of the disease modifying OA drug (DMOAD) diacerein and moderate tensile strain on the anabolic metabolism and the integrin-FAK-MAPKs signal transduction cascade of OA and non-OA chondrocytes. Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.12.010DOI Listing
April 2019
1 Read

Cadmium results in accumulation of autophagosomes-dependent apoptosis through activating Akt-impaired autophagic flux in neuronal cells.

Cell Signal 2019 Mar 19;55:26-39. Epub 2018 Dec 19.

Jiangsu Key Laboratory for Molecular and Medical Biotechnology, Jiangsu Key Laboratory for Microbes and Functional Genomics, College of Life Sciences, Nanjing Normal University, Nanjing 210023, PR China. Electronic address:

Environmental exposure to cadmium (Cd) links to neurodegenerative disorders. Autophagy plays an important role in controlling cell survival/death. However, how autophagy contributes to Cd's neurotoxicity remains enigmatic. Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.12.008DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6378698PMC
March 2019
1 Read
4.315 Impact Factor

Differential effects of protein kinase C-eta on apoptosis versus senescence.

Cell Signal 2019 Mar 15;55:1-7. Epub 2018 Dec 15.

Department of Microbiology, Immunology & Genetics, University of North Texas Health Science Center, Fort Worth, TX, USA.

Protein kinase C-eta (PKCη) is considered an anti-apoptotic kinase, which promotes cell survival and chemoresistance in several cancers, including breast cancer. We have recently shown that PKCη positively regulates the anti-apoptotic protein Mcl-1 in breast cancer cells, and depletion of PKCη induced proteasomal degradation of Mcl-1. We therefore examined if depletion of PKCη would enhance cellular sensitivity to chemotherapeutic agents. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S08986568183030
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http://dx.doi.org/10.1016/j.cellsig.2018.12.003DOI Listing
March 2019
8 Reads

TCF7L2 and EGR1 synergistic activation of transcription of LCN2 via an ERK1/2-dependent pathway in esophageal squamous cell carcinoma cells.

Cell Signal 2019 Mar 14;55:8-16. Epub 2018 Dec 14.

Department of Pathology, Shantou Central Hospital, Affiliated Shantou Hospital of Sun Yat-sen University, Shantou 515041, China; Guangdong Province Key Laboratory of Malignant Tumor Epigenetics and Genes Regulation, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, China. Electronic address:

High level expression of lipocalin 2 (LCN2) usually indicates poor prognosis in esophageal squamous cell carcinoma (ESCC) and many other cancers. Our previous study showed LCN2 promotes migration and invasion of ESCC cells through a novel positive feedback loop. However, the key transcription activation protein (KTAP) in the loop had not yet been identified. Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.12.007DOI Listing
March 2019
3 Reads

Effects of long non-coding RNA LINC00667 on renal tubular epithelial cell proliferation, apoptosis and renal fibrosis via the miR-19b-3p/LINC00667/CTGF signaling pathway in chronic renal failure.

Cell Signal 2019 Feb 26;54:102-114. Epub 2018 Oct 26.

Department of Nephrology, Linyi People's Hospital, No. 27, Jiefang Road, Linyi 276003, China. Electronic address:

The global prevalence of chronic renal failure (CRF) has significantly elevated with various reports indicating there to be a 10% worldwide rate. The functions of long non-coding RNAs (lncRNAs) and their deeper association with CRF at present remain poorly understood. Hence, the aim of the present study was to investigate the altered expressions of lncRNA LINC00667 in CRF and its associated effects on renal tubular epithelial cell proliferation, apoptosis and renal fibrosis through the microRNA-19b-3p (miR-19b-3p)/LINC00667/connective tissue growth factor (CTGF) signaling pathway. Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.10.016DOI Listing
February 2019
2 Reads
4.315 Impact Factor

The RNA helicase DHX33 is required for cancer cell proliferation in human glioblastoma and confers resistance to PI3K/mTOR inhibition.

Cell Signal 2019 Feb 12;54:170-178. Epub 2018 Dec 12.

Department of Biology, Southern University of Science and Technology, Shenzhen, Guangdong, China. Electronic address:

Human Glioblastoma is one deadly disease; the median survival time is reported to be 13.9 months after treatment. In the present study, we discovered that DHX33 is highly expressed in 84% of all Glioblastoma multiforme (GBM). Read More

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https://linkinghub.elsevier.com/retrieve/pii/S08986568183030
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http://dx.doi.org/10.1016/j.cellsig.2018.12.005DOI Listing
February 2019
4 Reads

A potential regulatory network among WDR86-AS1, miR-10b-3p, and LITAF is possibly involved in preeclampsia pathogenesis.

Cell Signal 2019 Mar 12;55:40-52. Epub 2018 Dec 12.

Department of Obstetrics and Gynecology, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, PR China.

Preeclampsia (PE), a pregnancy-specific disorder, is a leading cause of perinatal maternal and fetal mortality and morbidity. Impaired migration and invasion of trophoblastic cells and an imbalanced systemic maternal inflammatory response have been proposed as possible causes of pathogenesis of PE. Comparative analysis of PE-affected placentas and healthy placentas has uncovered differentially expressed long noncoding RNAs, microRNAs, and mRNAs. Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.12.006DOI Listing
March 2019
3 Reads

Novel aspects of PCSK9 and lipoprotein receptors in renal disease-related dyslipidemia.

Cell Signal 2019 Mar 12;55:53-64. Epub 2018 Dec 12.

Dept. of Nephrology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.

Chronic kidney disease (CKD) is a global health problem with a profound impact on quality of life. Cardiovascular disease is established as a major cause of morbidity and mortality in patients with CKD. Dyslipidemia is frequently observed in CKD patients, suggesting a causal relation between dyslipidemia and cardiovascular disease in CKD patients. Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.12.001DOI Listing
March 2019
3 Reads

miRNA networks modulate human endothelial cell adaptation to cyclic hypoxia.

Cell Signal 2019 Feb 12;54:150-160. Epub 2018 Dec 12.

Department of Biology and Pharmaceutical Botany, Medical University of Gdansk, Gdansk, Poland. Electronic address:

Solid tumor microenvironments are often subjected to various levels of hypoxia. Although regulation of gene expression has been examined extensively, most studies have focused on prolonged hypoxia. The tumor microenvironment, however, experiences waves of hypoxia and reoxygenation that stimulate the expression of pro-angiogenic factors that promote blood vessel formation. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S08986568183029
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http://dx.doi.org/10.1016/j.cellsig.2018.11.020DOI Listing
February 2019
13 Reads

The effects of IKK-beta inhibition on early NF-kappa-B activation and transcription of downstream genes.

Cell Signal 2019 Mar 10;55:17-25. Epub 2018 Dec 10.

Biomedical Engineering, The University of Texas, Austin, TX, USA; Diagnostic Medicine, The University of Texas, Austin, TX, USA; Livestrong Cancer Institutes, The University of Texas, Austin, TX, USA; Oncology, The University of Texas, Austin, TX, USA. Electronic address:

Small molecule approaches targeting the nuclear factor kappa B (NF-kB) pathway, a regulator of inflammation, have thus far proven unsuccessful in the clinic in part due to the complex pleiotropic nature of this network. Downstream effects depend on multiple factors including stimulus-specific temporal patterns of NF-kB activity. Despite considerable advances, genome-level impact of changes in temporal NF-kB activity caused by inhibitors and their stimulus dependency remains unexplored. Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.12.004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6348059PMC
March 2019
2 Reads

A non-canonical JAGGED1 signal to JAK2 mediates osteoblast commitment in cranial neural crest cells.

Cell Signal 2019 Feb 8;54:130-138. Epub 2018 Dec 8.

Department of Otolaryngology, Emory University, Atlanta, GA, USA. Electronic address:

During craniofacial development, cranial neural crest (CNC) cells migrate into the developing face and form bone through intramembranous ossification. Loss of JAGGED1 (JAG1) signaling in the CNC cells is associated with maxillary hypoplasia or maxillary bone deficiency (MBD) in mice and recapitulates the MBD seen in humans with Alagille syndrome. JAGGED1, a membrane-bound NOTCH ligand, is required for normal craniofacial development, and Jagged1 mutations in humans are known to cause Alagille Syndrome, which is associated with cardiac, biliary, and bone phenotypes and these children experience increased bony fractures. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S08986568183030
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http://dx.doi.org/10.1016/j.cellsig.2018.12.002DOI Listing
February 2019
8 Reads

Cleavage of arrestin-3 by caspases attenuates cell death by precluding arrestin-dependent JNK activation.

Cell Signal 2019 Feb 4;54:161-169. Epub 2018 Dec 4.

Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN, United States. Electronic address:

The two non-visual subtypes, arrestin-2 and arrestin-3, are ubiquitously expressed and bind hundreds of G protein-coupled receptors. In addition, these arrestins also interact with dozens of non-receptor signaling proteins, including c-Src, ERK and JNK, that regulate cell death and survival. Arrestin-3 facilitates the activation of JNK family kinases, which are important players in the regulation of apoptosis. Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.11.023DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6321783PMC
February 2019
2 Reads

Selective proteolysis by matrix metalloproteinases of photo-oxidised dermal extracellular matrix proteins.

Cell Signal 2019 Feb 3;54:191-199. Epub 2018 Dec 3.

Division of Cell Matrix Biology & Regenerative Medicine, The University of Manchester, Manchester, UK. Electronic address:

Photodamage in chronically sun-exposed skin manifests clinically as deep wrinkles and histologically as extensive remodelling of the dermal extracellular matrix (ECM) and in particular, the elastic fibre system. We have shown previously that loss of fibrillin microfibrils, a key elastic fibre component, is a hallmark of early photodamage and that these ECM assemblies are susceptible in vitro to physiologically attainable doses of ultraviolet radiation (UVR). Here, we test the hypotheses that UVR-mediated photo-oxidation is the primary driver of fibrillin microfibril and fibronectin degradation and that prior UVR exposure will enhance the subsequent proteolytic activity of UVR-upregulated matrix metalloproteinases (MMPs). Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.11.024DOI Listing
February 2019
13 Reads

Interplay between interferon-stimulated gene 15/ISGylation and interferon gamma signaling in breast cancer cells.

Cell Signal 2019 Feb 27;54:91-101. Epub 2018 Nov 27.

Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico.

Interferon-stimulated gene 15 (ISG15) is a ubiquitin-like protein that conjugates to its target proteins to modify them through ISGylation, but the relevance of ISG15 expression and its effects have been not completely defined. Herein, we examined the interplay between ISG15/ISGylation and the interferon-gamma (IFN-γ) signaling pathway in mammary tumors and compared it with that in normal mammary tissues. Our results indicated that mammary tumors had higher levels of ISG15 mRNA and ISG15 protein than the adjacent normal mammary tissue. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S08986568183029
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http://dx.doi.org/10.1016/j.cellsig.2018.11.021DOI Listing
February 2019
5 Reads

Heparan sulfate proteoglycan - A common receptor for diverse cytokines.

Cell Signal 2019 Feb 27;54:115-121. Epub 2018 Nov 27.

Department of Medical Biochemistry and Microbiology, SciLifeLab Uppsala, The Biomedical Center, University of Uppsala, Uppsala, Sweden. Electronic address:

Heparan sulfate proteoglycans (HSPG) are macromolecular glyco-conjugates expressed ubiquitously on the cell surface and in the extracellular matrix where they interact with a wide range of ligands to regulate many aspects of cellular function. The capacity of the side glycosaminoglycan chain heparan sulfate (HS) being able to interact with diverse protein ligands relies on its complex structure that is generated by a controlled biosynthesis process, involving the actions of glycosyl-transferases, sulfotransferases and the glucuronyl C5-epimerase. It is believed that activities of the modification enzymes control the HS structures that are designed to serve the biological functions in a given cell or biological status. Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.11.022DOI Listing
February 2019
1 Read

Signaling transduction regulated by 5-hydroxytryptamine 1A receptor and orexin receptor 2 heterodimers.

Cell Signal 2019 Feb 24;54:46-58. Epub 2018 Nov 24.

Neurobiology Key Laboratory, Jining Medical University, Colleges of Shandong, Jining 272067, PR China; Division of Biomedical Sciences, Warwick Medical School, University of Warwick, Coventry CV4 7AL, UK. Electronic address:

As G-protein-coupled receptors (GPCRs), 5-hydroxytryptamine 1A receptor (5-HT1AR) and orexin receptor 2 (OX2R) regulate the levels of the cellular downstream molecules. The heterodimers of different GPCRs play important roles in various of neurological diseases. Moreover, 5-HT1AR and OX2R are involved in the pathogenesis of neurological diseases such as depression with deficiency of hippocampus plasticity. Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.11.014DOI Listing
February 2019
2 Reads

NanoBRET ligand binding at a GPCR under endogenous promotion facilitated by CRISPR/Cas9 genome editing.

Cell Signal 2019 Feb 22;54:27-34. Epub 2018 Nov 22.

Molecular Endocrinology and Pharmacology, Harry Perkins Institute of Medical Research, QEII Medical Centre, Nedlands, Western Australia 6009, Australia; Centre for Medical Research, The University of Western Australia, Crawley, Western Australia 6009, Australia; Australian Research Council Centre for Personalised Therapeutics Technologies, Australia; Dimerix Limited, Nedlands, Western Australia 6009, Australia. Electronic address:

Bioluminescence resonance energy transfer (BRET) is a versatile tool used to investigate membrane receptor signalling and function. We have recently developed a homogenous NanoBRET ligand binding assay to monitor interactions between G protein-coupled receptors and fluorescent ligands. However, this assay requires the exogenous expression of a receptor fused to the nanoluciferase (Nluc) and is thus not applicable to natively-expressed receptors. Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.11.018DOI Listing
February 2019
8 Reads

The status of MAPK cascades contributes to the induction and activation of Gata4 and Nkx2.5 during the stepwise process of cardiac differentiation.

Cell Signal 2019 Feb 22;54:17-26. Epub 2018 Nov 22.

Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China. Electronic address:

Cardiac differentiation in vitro is a complex, stepwise process that is rigidly governed by a subset of transcription factors and signaling cascades. In this study, we investigated the cooperation of cardiac-specific transcription factors Gata4 and Nkx2.5, as well as mitogen-activated protein kinase (MAPK) cascades. Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.11.019DOI Listing
February 2019
7 Reads

Regulation of the stability and activity of CDC25A and CDC25B by protein phosphatase PP2A and 14-3-3 binding.

Cell Signal 2019 Feb 20;54:10-16. Epub 2018 Nov 20.

Division of Health Sciences, Graduate School of Medical Science, Kanazawa University, 5-11-80 Kodatsuno, Kanazawa, Ishikawa 920-0942, Japan. Electronic address:

Cyclin-dependent kinase (CDK)-activating phosphatases, CDC25A and CDC25B, are labile proteins, and their levels vary in a cell cycle-dependent manner. Immediate-early response IER5 protein negatively regulates the cellular CDC25B levels, and stress-induced IER5 expression potentiates G2/M arrest. IER5 binds to protein phosphatase PP2A and regulates the PP2A substrate specificity. Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.11.017DOI Listing
February 2019
1 Read

How do chemokines navigate neutrophils to the target site: Dissecting the structural mechanisms and signaling pathways.

Cell Signal 2019 Feb 19;54:69-80. Epub 2018 Nov 19.

Department of Medicine (Cardiology), Duke University, Durham, NC, USA.

Chemokines play crucial roles in combating microbial infection and initiating tissue repair by recruiting neutrophils in a timely and coordinated manner. In humans, no less than seven chemokines (CXCL1, CXCL2, CXCL3, CXCL5, CXCL6, CXCL7, and CXCL8) and two receptors (CXCR1 and CXCR2) mediate neutrophil functions but in a context dependent manner. Neutrophil-activating chemokines reversibly exist as monomers and dimers, and their receptor binding triggers conformational changes that are coupled to G-protein and β-arrestin signaling pathways. Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.11.004DOI Listing
February 2019
10 Reads

Low expression of PDK1 inhibits renal cell carcinoma cell proliferation, migration, invasion and epithelial mesenchymal transition through inhibition of the PI3K-PDK1-Akt pathway.

Cell Signal 2019 Apr 20;56:1-14. Epub 2018 Nov 20.

Department of Urology, Jiangxi Cancer Hospital, Nanchang 330029, PR China. Electronic address:

As the most commonly occurring form of primary renal tumor, renal cell carcinoma (RCC) is a malignancy accompanied by a high mortality rate. 3-phosphoinositide-dependent protein kinase 1 (PDK1) has been established as a protein target and generated considerable interest in both the pharmaceutical and academia industry. The aim of the current study was to investigate the effect of si-PDK1 on the RCC cell apoptosis, proliferation, migration, invasion and epithelial mesenchymal transition (EMT) in connection with the PI3K-PDK1-Akt pathway. Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.11.016DOI Listing
April 2019
8 Reads

A novel Rhein derivative: Activation of Rac1/NADPH pathway enhances sensitivity of nasopharyngeal carcinoma cells to radiotherapy.

Cell Signal 2019 Feb 18;54:35-45. Epub 2018 Nov 18.

College of Pharmacy, Guangxi Medical University, Nanning, Guangxi 530021, China. Electronic address:

Radiation resistance and recurrent have become the major factors resulting in poor prognosis in the clinical treatment of patients with nasopharyngeal carcinoma (NPC). New strategies to enhance the efficacy of radiotherapy have been focused on the development of radiosensitizers and searching for directly targets that modulated tumor radiosensitivity. A novel potential radiosensitizer 1,8-Dihydroxy -3-(2'-(4″-methylpiperazin-1″-yl) ethyl-9,10-anthraquinone -3-carboxylate (RP-4) was designed and synthesized based on molecular docking technology, which was expected to regulate the radiosensitivity of tumor cells through targeting Rac1. Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.11.015DOI Listing
February 2019
7 Reads

Upregulated BMP-Smad signaling activity in the glucuronyl C5-epimerase knock out MEF cells.

Cell Signal 2019 Feb 17;54:122-129. Epub 2018 Nov 17.

Department of Medical Biochemistry and Microbiology, The Biomedical Center, University of Uppsala, Uppsala, Sweden; Science for Life Laboratory Uppsala, The Biomedical Center, University of Uppsala, Uppsala, Sweden. Electronic address:

Glucuronyl C5-epimerase (Hsepi) catalyzes the conversion of glucuronic acid to iduronic acid in the process of heparan sulfate biosynthesis. Targeted interruption of the gene, Glce, in mice resulted in neonatal lethality with varied defects in organ development. To understand the underlying molecular mechanisms of the phenotypes, we used mouse embryonic fibroblasts (MEF) as a model to examine selected signaling pathways. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S08986568183028
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http://dx.doi.org/10.1016/j.cellsig.2018.11.010DOI Listing
February 2019
12 Reads

miR-382-5p modulates the ATRA-induced differentiation of acute promyelocytic leukemia by targeting tumor suppressor PTEN.

Cell Signal 2019 Feb 17;54:1-9. Epub 2018 Nov 17.

Central Laboratory of Yong-Chuan Hospital, Chongqing Medical University, Chongqing 402160, China; Key Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Department of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, China. Electronic address:

In acute promyelocytic leukemia (APL), all-trans retinoic acid (ATRA) treatment induces granulocytic differentiation and maturation. MicroRNAs play pivotal roles in formation of the leukemic phenotype. Previously, microRNA-382-5p (miR-382-5p) was upregulated in acute myeloid leukemia (AML) with t(15;17). Read More

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https://linkinghub.elsevier.com/retrieve/pii/S08986568183028
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http://dx.doi.org/10.1016/j.cellsig.2018.11.012DOI Listing
February 2019
14 Reads
4.315 Impact Factor

Signal interaction between the tumour and inflammatory cells in patients with gastrointestinal cancer: Implications for treatment.

Cell Signal 2019 Feb 17;54:81-90. Epub 2018 Nov 17.

Wolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, College of MVLS, University of Glasgow, United Kingdom.

Over the last 15 years there has been a change in how we understand the impact of the interaction between the tumour and the host on cancer outcomes. From the simplistic view that the make-up of tumours cells largely determines their aggressiveness to a more complex view that the interaction between the products of tumour and host cell signal transduction pathways is crucial in determining whether the tumour cell is eliminated or survives in the host. Of the host cells, those with an immune/inflammatory function are most well documented to inhibit or promote tumour cell proliferation and dissemination. Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.11.013DOI Listing
February 2019
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ACTL6A interacts with p53 in acute promyelocytic leukemia cell lines to affect differentiation via the Sox2/Notch1 signaling pathway.

Cell Signal 2019 Jan 15;53:390-399. Epub 2018 Nov 15.

Central Laboratory of Yong-Chuan Hospital, Chongqing Medical University, Chongqing 402160, China; Key Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Department of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, China.

Actin-like 6A (ACTL6A), a component of BAF chromatin remodeling complexes, is important for cell differentiation. Nevertheless, its role and mechanism in acute promyelocytic leukemia (APL) has not been reported. To identify the genes that may participate in the development of APL, we analyzed data from an APL cDNA microarray (GSE12662) in the NCBI database, and found that ACTL6A was up-regulated in APL patients. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S08986568183027
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http://dx.doi.org/10.1016/j.cellsig.2018.11.009DOI Listing
January 2019
14 Reads
4.315 Impact Factor

Phosphorylation and inhibition of ceramide kinase by protein kinase C-β: Their changes by serine residue mutations.

Cell Signal 2019 Feb 15;54:59-68. Epub 2018 Nov 15.

Laboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, Chiba University, Inohana 1-8-1, Chuo-ku, Chiba 260-8675, Japan.

Ceramide kinase (CerK) phosphorylates ceramide to ceramide-1-phosphate (C1P), and various roles for the CerK/C1P pathway in the regulation of cellular/biological functions have been demonstrated. CerK is constitutively phosphorylated at several serine (Ser, S) residues, however, the roles of Ser residues, including their phosphorylation, in CerK activity, have not yet been elucidated in detail. Therefore, we conducted the present study to investigate this issue. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S08986568183027
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http://dx.doi.org/10.1016/j.cellsig.2018.11.008DOI Listing
February 2019
7 Reads