4,852 results match your criteria Cellular Signalling [Journal]


Transcriptional activation of SIRT6 via FKHRL1/FOXO3a inhibits the Warburg effect in glioblastoma cells.

Cell Signal 2019 Apr 17. Epub 2019 Apr 17.

State Key Laboratory of Silkworm Genome Biology, Institute of Sericulture and Systems Biology, Southwest University, Beibei, Chongqing 400716, China; Engineering Research Center for Cancer Biomedical and Translational Medicine, Southwest University, Beibei, Chongqing 400716, China; Chongqing Engineering and Technology Research Center for Silk Biomaterials and Regenerative Medicine, Southwest University, Beibei, Chongqing 400716, China; Cancer Center, Medical Research Institute, Southwest University, Beibei, Chongqing, China. Electronic address:

Glioblastoma (GBM) is the most aggressive and malignant form of brain tumors. However, its molecular mechanisms of tumorigenesis and cancer development remained to elucidate. Here, we reported FKHRL1, also called as FOXO3a, was an anti-cancer factor that inhibited the Warburg effect in GBM. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.04.009DOI Listing

Lysophosphatidic acid induces integrin β6 expression in human oral squamous cell carcinomas cells via LPAR1 coupling to Gα and downstream SMAD3 and ETS-1 activation.

Cell Signal 2019 Apr 15. Epub 2019 Apr 15.

Cancer Research Center, School of Medicine, Xiamen University, Xiamen, Fujian, China. Electronic address:

Integrin β6 (ITGB6), an epithelial-specific integrin, is upregulated in oral squamous cell carcinomas (OSCC) and is associated with progression and metastasis of OSCC. Lysophosphatidic acid (LPA), an important bioactive phospholipid present in saliva, has also been related to OSCC cell migration and invasiveness. LPA exerts its biological effects through signal transduction pathways that ultimately regulate gene expression. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.04.008DOI Listing
April 2019
2 Reads

Lipids: Two sites of the same coin in lung fibrosis.

Cell Signal 2019 Apr 15. Epub 2019 Apr 15.

Department of Biochemistry, Universities of Giessen and Marburg Lung Center, Giessen, Germany. Electronic address:

Idiopathic pulmonary fibrosis (IPF) is characterized by progressive extracellular matrix deposition in the lung parenchyma leading to the destruction of lung structure, respiratory failure and premature death. Recent studies revealed that the pathogenesis of IPF is associated with alterations in the synthesis and the activity of lipids, lipid regulating proteins and cell membrane lipid transporters and receptors in different lung cells. Furthermore, deregulated lipid metabolism was found to contribute to the profibrotic phenotypes of lung fibroblasts and alveolar epithelial cells. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S08986568193008
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http://dx.doi.org/10.1016/j.cellsig.2019.04.007DOI Listing
April 2019
1 Read

The relationship between phosphorylation status of focal adhesion kinases, molecular subtypes, tumour microenvironment and survival in patients with primary operable ductal breast cancer.

Cell Signal 2019 Apr 11. Epub 2019 Apr 11.

Unit of Gastrointestinal cancer and Molecular Pathology, Institute of Cancer Sciences, College of Medical, Veterinary and Life Sciences-University of Glasgow, Glasgow, UK.

Background: Despite advances in therapies to treat breast cancer, over 100,000 patients die in the UK of this disease per year, highlighting the need to develop effect predictive and prognostic markers for patients with primary operable ductal breast cancer. Therefore, the aim of the present study was to examine the relationship between membranous, cytoplasmic and nuclear expression of focal adhesion kinase (phosphorylated at Y 397, Y 861 and Y 925), molecular subtypes, tumour microenvironment and survival in patients with primary operable ductal breast cancer.

Methods: Four hundred and seventy-four patients presenting between 1995 and 1998 with primary operable ductal breast cancer were included in this study. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.04.006DOI Listing

MiR-15b regulates cell differentiation and survival by targeting CCNE1 in APL cell lines.

Cell Signal 2019 Apr 6. Epub 2019 Apr 6.

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:

MicroRNAs have been shown to be involved in various cell processes, including proliferation, apoptosis and differentiation. However, little is known about their function in granulopoiesis. In the present study, overexpression and knockdown experiments revealed that miR-15b was required to block the proliferation of NB4 and HL60 cells and induce them differentiated to granulocyte lineage. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.04.005DOI Listing
April 2019
2 Reads
4.315 Impact Factor

Tumor-secreted GRP78 facilitates the migration of macrophages into tumors by promoting cytoskeleton remodeling.

Cell Signal 2019 Apr 5;60:1-16. Epub 2019 Apr 5.

Institute of Biotechnology, Key Laboratory of Chemical Biology and Molecular Engineering of National Ministry of Education, Shanxi University, Taiyuan 030006, China; Institutes of Biomedical Sciences, Shanxi University, Taiyuan 030006, China; School of Life Science, Shanxi University, Taiyuan 030006, China. Electronic address:

Glucose-regulated protein 78 (GRP78), an important molecular chaperone in the endoplasmic reticulum, is often over-expressed in the central region of advanced tumor and acts as a promoter of tumor progression. As main immune cells in the tumor microenvironment, infiltration of abundant macrophages into advanced tumor further facilitates growth of tumor. Although has potential association between GRP78 and infiltration of macrophages, its underlying mechanisms are poorly understood. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.04.004DOI Listing
April 2019
1 Read

Effects of MCRS1 on proliferation, migration, invasion, and epithelial mesenchymal transition of gastric cancer cells by interacting with Pkmyt1 protein kinase.

Cell Signal 2019 Apr 3;59:171-181. Epub 2019 Apr 3.

Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Jinzhou Medical University, 3 Songpo Road, Jinzhou, Liaoning Province 121000, PR China. Electronic address:

Microspherule protein 1(MCRS1) is known to be an oncogene in several tumors. However, recent studies have shown that MCRS1 inhibits lymphatic metastasis in gastric cancer (GC) patients by inhibiting telomerase activity. Protein kinase, membrane associated tyrosine/threonine 1(Pkmyt1), a member of the WEE1 family, has been found to interact with MCRS1 by yeast two-hybrid assay; however, how these two proteins interact in GC is still unclear. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.04.002DOI Listing
April 2019
3 Reads

Emerging concepts of receptor endocytosis and concurrent intracellular signaling: Mechanisms of guanylyl cyclase/natriuretic peptide receptor-A activation and trafficking.

Cell Signal 2019 Apr 3;60:17-30. Epub 2019 Apr 3.

Department of Physiology, Tulane University Health Sciences Center and School of Medicine, 1430 Tulane Avenue, New Orleans, Louisiana 70112, United States. Electronic address:

Endocytosis is a prominent clathrin-mediated mechanism for concentrated uptake and internalization of ligand-receptor complexes, also known as cargo. Internalization of cargo is the fundamental mechanism for receptor-dependent regulation of cell membrane function, intracellular signal transduction, and neurotransmission, as well as other biological and physiological activities. However, the intrinsic mechanisms of receptor endocytosis and contemporaneous intracellular signaling are not well understood. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S08986568193007
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http://dx.doi.org/10.1016/j.cellsig.2019.03.022DOI Listing
April 2019
9 Reads

PDE10A mutations help to unwrap the neurobiology of hyperkinetic disorders.

Cell Signal 2019 Apr 2;60:31-38. Epub 2019 Apr 2.

IMED Biotech Unit, R&D, AstraZeneca Neuroscience, Boston, MA 024515, USA. Electronic address:

The dual-specific cAMP/cGMP phosphodiesterase PDE10A is exclusively localised to regions of the brain and specific cell types that control crucial brain circuits and behaviours. The downside to this expression pattern is that PDE10A is also positioned to be a key player in pathology when its function is perturbed. The last decade of research has seen a clear role emerge for PDE10A inhibition in modifying behaviours in animal models of psychosis and Huntington's disease. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.04.001DOI Listing

The effects of IFITM1 and IFITM3 gene deletion on IFNγ stimulated protein synthesis.

Cell Signal 2019 Apr 2;60:39-56. Epub 2019 Apr 2.

University of Edinburgh, Institute of Genetics and Molecular Medicine, Edinburgh EH4 2XR, United Kingdom; Regional Centre for Applied Molecular Oncology, Masaryk Memorial Cancer Institute, 656 53 Brno, Czech Republic; University of Gdansk, International Centre for Cancer Vaccine Science, Department of Chemistry, Gdansk, Poland. Electronic address:

Interferon-induced transmembrane proteins IFITM1 and IFITM3 (IFITM1/3) play a role in both RNA viral restriction and in human cancer progression. Using immunohistochemical staining of FFPE tissue, we identified subgroups of cervical cancer patients where IFITM1/3 protein expression is inversely related to metastasis. Guide RNA-CAS9 methods were used to develop an isogenic IFITM1/IFITM3 double null cervical cancer model in order to define dominant pathways triggered by presence or absence of IFITM1/3 signalling. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.024DOI Listing

Electrical stimulation activates calpain 2 and subsequently upregulates collagens via the integrin β1/TGF-β1 signaling pathway.

Cell Signal 2019 Mar 30;59:141-151. Epub 2019 Mar 30.

Department of Gynecology and Obstetrics, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, PR China. Electronic address:

Stress urinary incontinence (SUI) is a public health issue attributed to weakened pelvic supporting tissues. Electrical stimulation (ES) is one of the first-line conservative treatments for SUI. However, the underlying mechanism of ES in the treatment of SUI is not clear. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.023DOI Listing

Exome sequencing and bioinformatic approaches reveals rare sequence variants involved in cell signalling and elastic fibre homeostasis: new evidence in the development of ectopic calcification.

Cell Signal 2019 Mar 26;59:131-140. Epub 2019 Mar 26.

Department of Life Sciences, University of Modena and Reggio Emilia, Modena, Italy. Electronic address:

Elastic fibres undergo aberrant mineralization in genetic as well as in acquired pathologic conditions causing severe impairment of tissue mechanical properties. Despite the number of investigations performed so far, the pathogenesis of these alterations is still elusive, due to both the complexity of the elastin network and the involvement of many genes and/or pro-osteogenic signalling pathways. Whole Exome Sequencing (WES) was performed on DNA from three patients affected by beta-thalassemia exhibiting soft connective tissue calcification. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.020DOI Listing
March 2019
1 Read

TRIB1 induces macrophages to M2 phenotype by inhibiting IKB-zeta in prostate cancer.

Cell Signal 2019 Mar 26;59:152-162. Epub 2019 Mar 26.

Department of Urology, Huadu District People's Hospital, Southern Medical University, Guangzhou 510800, China; Department of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine and Diagnostics, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou 510180, China; Guangdong Provincial Institute of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China. Electronic address:

Immunotherapy has made great breakthroughs in the field of cancer. However, the immunotherapeutic effect of prostate cancer is unsatisfactory. We found that the expression of TRIB1 was significantly correlated with the infiltration of CD163+ macrophages in prostate cancer. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.017DOI Listing

The signaling effects of ATP on melanoma-like skin cancer.

Cell Signal 2019 Mar 26;59:122-130. Epub 2019 Mar 26.

Academic Coordination, Campus Chapecó, Universidade Federal da Fronteira Sul, Chapecó, Brazil. Electronic address:

Melanoma is a type of skin cancer originated by the malignant transformation of melanocytes. Increasing incidence and mortality require efforts focused on studies and research about this cancer. Its microenvironment is rich in extracellular ATP, but there are no studies evaluating the ectonucleotidases and ATP effects on tumor-derived melanoma cells with known amounts of ATP. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.021DOI Listing
March 2019
2 Reads

Adrenoceptor α signalling countervails the taming effects of synchronous cyclic nucleotide-elevation on thrombin-induced human platelet activation and aggregation.

Cell Signal 2019 Mar 26;59:96-109. Epub 2019 Mar 26.

Cardiovascular Research Centre (CVRC), School of Medical Sciences, Örebro University, 70182 Örebro, Sweden.

The healthy vascular endothelium constantly releases autacoids which cause an increase of intracellular cyclic nucleotides to tame platelets from inappropriate activation. Elevating cGMP and cAMP, in line with previous reports, cooperated in the inhibition of isolated human platelet intracellular calcium-mobilization, dense granules secretion, and aggregation provoked by thrombin. Further, platelet alpha granules secretion and, most relevant, integrin αβ activation in response to thrombin are shown to be prominently affected by the combined elevation of cGMP and cAMP. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.019DOI Listing
March 2019
1 Read

Ovarian tumor domain-containing ubiquitin aldehyde binding protein 1 inhibits inflammation by regulating Nur77 stability.

Cell Signal 2019 Mar 21;59:85-95. Epub 2019 Mar 21.

Department of Biochemistry and Molecular Biology, College of Medicine, Yeungnam University, Daegu, South Korea. Electronic address:

Nur77 (NR4A1) plays an important role in various inflammatory responses. Nur77 is rapidly degraded in cells and its protein level is critically controlled. Although few E3 ligases regulating the Nur77 protein have been defined, the deubiquitinase (DUB) responsible for Nur77 stability has not been reported to date. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.018DOI Listing

TMEPAI/PMEPA1 inhibits Wnt signaling by regulating β-catenin stability and nuclear accumulation in triple negative breast cancer cells.

Cell Signal 2019 Mar 16;59:24-33. Epub 2019 Mar 16.

Department of Experimental Pathology, Graduate School of Comprehensive Human Sciences and Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan; Transborder Medical Research Center, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan.

Transmembrane prostate androgen-induced protein (TMEPAI) is a type I transmembrane protein induced by several intracellular signaling pathways such as androgen, TGF-β, EGF, and Wnt signaling. It has been reported that TMEPAI functions to suppress TGF-β and androgen signaling but here, we report a novel function of TMEPAI in Wnt signaling suppression. First, we show that TMEPAI significantly inhibits TCF/LEF transcriptional activity stimulated by Wnt3A, LiCl, and β-catenin. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.016DOI Listing

Identification of novel PCTAIRE-1/CDK16 substrates using a chemical genetic screen.

Cell Signal 2019 Mar 14;59:53-61. Epub 2019 Mar 14.

Nestlé Research, École Polytechnique Fédérale de Lausanne (EPFL) Innovation Park, bâtiment H, 1015 Lausanne, Switzerland; School of Life Sciences, EPFL, 1015 Lausanne, Switzerland. Electronic address:

PCTAIRE-1 (also known as cyclin-dependent protein kinase (CDK) 16), is a Ser/Thr kinase that has been implicated in many cellular processes, including cell cycle, spermatogenesis, neurite outgrowth, and vesicle trafficking. Most recently, it has been proposed as a novel X-linked intellectual disability (XLID) gene, where loss-of-function mutations have been identified in human patients. The precise molecular mechanisms that regulate PCTAIRE-1 remained largely obscure, and only a few cellular targets/substrates have been proposed with no clear functional significance. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.012DOI Listing
March 2019
1 Read

Characterisation of the Ral GTPase inhibitor RBC8 in human and mouse platelets.

Cell Signal 2019 Mar 14;59:34-40. Epub 2019 Mar 14.

From the School of Physiology, Pharmacology & Neuroscience, University of Bristol, Bristol BS8 1TD, United Kingdom.

The Ral GTPases, RalA and RalB, have been implicated in numerous cellular processes, but are most widely known for having regulatory roles in exocytosis. Recently, we demonstrated that deletion of both Ral genes in a platelet-specific mouse gene knockout caused a substantial defect in surface exposure of P-selectin, with only a relatively weak defect in platelet dense granule secretion that did not alter platelet functional responses such as aggregation or thrombus formation. We sought to investigate the function of Rals in human platelets using the recently described Ral inhibitor, RBC8. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.015DOI Listing

Panobinostat (LBH589) inhibits Wnt/β-catenin signaling pathway via upregulating APCL expression in breast cancer.

Cell Signal 2019 Mar 14;59:62-75. Epub 2019 Mar 14.

State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China. Electronic address:

Breast cancer is the most common malignant disease among women worldwide and the novel therapeutic agents are urgently needed. Panobinostat (LBH589), a pan-HDACs inhibitor, has shown promising anti-tumor effect in recent years. However, the targets of this compound are largely unclear because of its low selectivity. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.014DOI Listing
March 2019
3 Reads
4.315 Impact Factor

The γ-secretase inhibitor GSI-I interacts synergistically with the proteasome inhibitor bortezomib to induce ALK+ anaplastic large cell lymphoma cell apoptosis.

Cell Signal 2019 Mar 14;59:76-84. Epub 2019 Mar 14.

Department of Hematology, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu, China. Electronic address:

Single agent treatment of the γ-secretase inhibitor (GSI-I) or proteasome inhibitor in anaplastic lymphoma kinase positive anaplastic large cell lymphoma (ALK+ ALCL) shows limited response and considerable toxicity. Here, we examined the effects of the combination of low dose GSI-I and the proteasome inhibitor bortezomib (BTZ) in ALK+ ALCL cells in vivo and in vitro. We found that ALK+ ALCL cells treated with the BTZ and GSI-I combination treatment showed elevated apoptosis, consistent with increased caspase activation, compared with BTZ or GSI-I alone. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.013DOI Listing

Activation of PERK-eIF2α-ATF4 pathway contributes to diabetic hepatotoxicity: Attenuation of ER stress by Morin.

Cell Signal 2019 Mar 12;59:41-52. Epub 2019 Mar 12.

Herbal Research Laboratory, Food, Drug & Chemical Toxicology Group, CSIR-Indian Institute of Toxicology Research, Vishvigyan Bhavan 31, M.G Marg, Lucknow 226001, Uttar Pradesh, India; Academy of Scientific and Innovative Research (AcSIR), CSIR-Indian Institute of Toxicology Research, Lucknow, India. Electronic address:

Hyperglycemia associated ER stress has been found as a critical contributor in the pathogenesis of type 2 diabetes mellitus. However, reports regarding molecular mechanisms involved are limited. This study was aimed to identify the role of ER stress in regulating hepatic glucose metabolism and its link with oxidative stress. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.008DOI Listing
March 2019
2 Reads

AKT2 phosphorylation of hexokinase 2 at T473 promotes tumorigenesis and metastasis in colon cancer cells via NF-κB, HIF1α, MMP2, and MMP9 upregulation.

Cell Signal 2019 Mar 12;58:99-110. Epub 2019 Mar 12.

Zhejiang Academy of Medical Sciences, Hangzhou 310013, Zhejiang, PR China. Electronic address:

It has been well-established that AKT2 plays an important role in the development and progression of colon cancer; however, its precise function remains unclear. In the present study, we found that AKT2 can interact with and phosphorylate hexokinase 2 (HK2), the rate-limiting enzyme in glycolysis. Moreover, threonine phosphorylation dramatically increases its catalytic activity and enhances glycolysis. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.011DOI Listing

The role and therapeutic potential of connexins, pannexins and their channels in Parkinson's disease.

Cell Signal 2019 Mar 12;58:111-118. Epub 2019 Mar 12.

Department of In Vitro Toxicology and Dermato-Cosmetology, Vrije Universiteit Brussel, Laarbeeklaan 103, B-1090 Brussels, Belgium. Electronic address:

Lack of effective medication for slowing down progression of Parkinson's disease (PD) as a highly prevalent neurodegenerative disorder requires novel avenues of scientific investigation to elucidate the underlying molecular and cellular mechanisms. Studying connexins, pannexins and their channels has uncovered their potential role in mediating communication and signaling pathways that drive neurodegenerative diseases, including PD. Indeed, given their critical role in tissue homeostasis, it is not surprising that connexins, pannexins and their channels are frequently involved in pathological processes. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.010DOI Listing
March 2019
1 Read
4.315 Impact Factor

The tumor suppressor Sef is a scaffold for the classical NF-κB/RELA:P50 signaling module.

Cell Signal 2019 Mar 9;59:110-121. Epub 2019 Mar 9.

Department of Biology, Technion-Israel Institute of Technology, Haifa 3200003, Israel. Electronic address:

The classical NF-κB transcription factor (RelA:p50) and the tumor suppressor Sef axis constitute a negative regulatory loop in which Sef, a target of NF-κB/RelA:p50, fine-tunes NF-κB/RelA:p50 transcriptional-activation in response to inflammatory stimuli trough binding to p50. Similar to the inhibitor IκBα, Sef sequesters NF-κB/RelA:p50 in the cytoplasm of unstimulated cells. Despite its key roles in regulating multiple cellular processes and its potential role as mediator between inflammation and cancer, Sef structural domains required to fulfill its tasks are poorly characterized, and how Sef specificity towards RelA:p50 is achieved is unknown. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.01.009DOI Listing

IQGAP1 mediates podocyte injury in diabetic kidney disease by regulating nephrin endocytosis.

Cell Signal 2019 Mar 9;59:13-23. Epub 2019 Mar 9.

Department of Nephrology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan 250014, China. Electronic address:

Diabetic kidney disease (DKD) is a complication associated with diabetes and is a major public health problem in modern society. Podocyte injury is the central target of the development of DKD, and the loss or dysregulation of nephrin, a key structural and signalling molecule located in the podocyte slit diaphragm (SD), initiates potentially catastrophic downstream events within podocytes. IQGAP1, a scaffold protein containing multiple protein-binding domains that regulates endocytosis, can interact with nephrin in podocytes. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.009DOI Listing
March 2019
3 Reads
4.315 Impact Factor

N-acetylcytidine is required for sustained NLRP3 inflammasome activation via HMGB1 pathway in microglia.

Cell Signal 2019 Mar 7;58:44-52. Epub 2019 Mar 7.

Department of Neurology, the Third Affiliated Hospital of Guizhou Medical University, Duyun 558000, China; Medical Laboratory Center, Third Affiliated Hospital of Guizhou Medical University, Duyun 558000, China; Department of Neurology, the Affiliated Hospital of Guizhou Medical University, Guiyang 550004, China. Electronic address:

Persistent inflammasome activation contributes to chronic, low grade inflammation. However, it is unclear how the inflammasome activation is sustained after initiation. Here we reported that N-acetylcytidine (N4A), a nucleoside metabolite, activated microglia and sustained NLRP3 inflammasome activation by inducing HMGB1 signaling. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.007DOI Listing

Lactate accelerates calcification in VSMCs through suppression of BNIP3-mediated mitophagy.

Cell Signal 2019 Mar 6;58:53-64. Epub 2019 Mar 6.

Department of Cardiology, Zhongda Hospital, School of Medicine, Southeast University, Nanjing 210009, PR China. Electronic address:

Arterial media calcification is one of the major complications of diabetes mellitus, which is related to oxidative stress and apoptosis. Mitophagy is a special regulation of mitochondrial homeostasis and takes control of intracellular ROS generation and apoptotic pathways. High circulating levels of lactate usually accompanies diabetes. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.006DOI Listing
March 2019
1 Read

Activated CRH receptors inhibit autophagy by repressing conversion of LC3BI to LC3BII.

Cell Signal 2019 Mar 5;58:119-130. Epub 2019 Mar 5.

Department of Pharmacology, Nanjing Medical University, Nanjing 211116, PR China. Electronic address:

Clinical studies have elucidated the negative correlation between microtubules-associated protein 1 light chain 3-B (LC3B) protein expression and overall survival of breast cancer patients. Our previous data demonstrated corticortropin-releasing hormone family (CRHs) suppressed migration of breast cancer cells via CRH receptors (CRHRs). Here, we showed that the activation of CRHRs (CRHR1 and CRHR2) remarkably reduced the conversion of LC3BI to LC3BII and hence repressed macroautophagy/autophagy, resulting in migration inhibition. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S08986568193003
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http://dx.doi.org/10.1016/j.cellsig.2019.03.001DOI Listing
March 2019
4 Reads

The E3 ubiquitin ligase HECW1 targets thyroid transcription factor 1 (TTF1/NKX2.1) for its degradation in the ubiquitin-proteasome system.

Cell Signal 2019 Mar 5;58:91-98. Epub 2019 Mar 5.

Department of Physiology and Cell Biology, The Ohio State University, Columbus, OH, USA. Electronic address:

Thyroid transcription factor 1 (TTF1/NKX2.1), is a nuclear protein member of the NKX2 family of homeodomain transcription factors. It plays a critical role in regulation of multiple organ functions by promoting gene expression, such as thyroid hormone in thyroid and surfactant proteins in the lung. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.005DOI Listing
March 2019
1 Read

G protein αq exerts expression level-dependent distinct signaling paradigms.

Cell Signal 2019 Mar 5;58:34-43. Epub 2019 Mar 5.

Department of Chemistry and Biochemistry, The University of Toledo, Toledo, OH 43606, USA. Electronic address:

G protein αq-coupled receptors (Gq-GPCRs) primarily signal through GαqGTP mediated phospholipase Cβ (PLCβ) stimulation and the subsequent hydrolysis of phosphatidylinositol 4, 5 bisphosphate (PIP2). Though Gq-heterotrimer activation results in both GαqGTP and Gβγ, unlike Gi/o-receptors, it is unclear if Gq-coupled receptors employ Gβγ as a major signal transducer. Compared to Gi/o- and Gs-coupled receptors, we observed that most cell types exhibit a limited free Gβγ generation upon Gq-pathway and Gαq/11 heterotrimer activation. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.02.006DOI Listing

SLFN5 suppresses cancer cell migration and invasion by inhibiting MT1-MMP expression via AKT/GSK-3β/β-catenin pathway.

Cell Signal 2019 Mar 4;59:1-12. Epub 2019 Mar 4.

Collaborative Research Center, Shanghai University of Medicine and Health Sciences, Shanghai, China; Shanghai Key Laboratory of Molecular Imaging, Shanghai University of Medicine and Health Sciences, Shanghai, China. Electronic address:

Human SLFN5 inhibits invasions of IFNα-sensitive renal clear-cell carcinoma and melanoma cells. However, whether this inhibition is confined to these IFNα-sensitive cancers is unclear. Here we show that SLFN5 expressions on both mRNA and protein levels are significantly higher in non/low-invasive cancer cell lines (breast cancer cell line MCF7, colorectal cancer cell line HCT116 and lung cancer cell line A549) than in highly-invasive cancer cell lines (fibrosarcoma cell line HT1080 and renal clear cell cancer cell line 786-0). Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.004DOI Listing

Fibulin-4 deficiency differentially affects cytoskeleton structure and dynamics as well as TGFβ signaling.

Cell Signal 2019 Mar 4;58:65-78. Epub 2019 Mar 4.

Department of Molecular Genetics, Erasmus University Medical Center, Rotterdam, the Netherlands; Department of Vascular Surgery, Erasmus University Medical Center, Rotterdam, the Netherlands; Department of Radiation Oncology, Erasmus University Medical Center, Rotterdam, the Netherlands. Electronic address:

Fibulin-4 is an extracellular matrix (ECM) protein essential for elastogenesis and mutations in this protein lead to aneurysm formation. In this study, we isolated vascular smooth muscle cells (VSMCs) from mice with reduced fibulin-4 protein expression (Fibulin-4) and from mice with a smooth muscle cell specific deletion of the Fibulin-4 gene (Fibulin-4/SM22Cre). We subsequently analyzed and compared the molecular consequences of reduced Fibulin-4 expression versus total ablation of Fibulin-4 expression with regard to effects on the SMC specific contractile machinery, cellular migration and TGFβ signaling. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.02.008DOI Listing
March 2019
1 Read

Altered recruitment of Lyn, Syk and ZAP-70 into lipid rafts of activated B cells in Systemic Lupus Erythematosus.

Cell Signal 2019 Mar 3;58:9-19. Epub 2019 Mar 3.

Grupo de Inmunología Celular e Inmunogenética (GICIG), Sede de investigación Universitaria (SIU), Facultad de Medicina, Universidad de Antioquia, Carrera 53, # 61-30, Medellín, Colombia; Grupo de Reumatología, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia. Electronic address:

There is evidence that B cells from patients with Systemic Lupus Erythematosus (SLE) could be hyperactivated due to changes in their lipid rafts (LR) composition, leading to altered BCR-dependent signals. This study aimed to characterize possible alterations in the recruitment of protein tyrosine kinases (PTK) into B cells LR from SLE patients. Fifteen patients with SLE and ten healthy controls were included. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.003DOI Listing

Regulation of endothelial cell survival and death by the MAP kinase/ERK kinase kinase 3 - glyceraldehyde-3-phosphate dehydrogenase signaling axis.

Cell Signal 2019 Mar 2;58:20-33. Epub 2019 Mar 2.

Department of Immunopathology, SA Pathology, Women's and Children's Hospital, North Adelaide, South Australia 5006, Australia; Discipline of Paediatrics and the Robinson Research Institute, University of Adelaide, South Australia 5001, Australia. Electronic address:

Endothelial cell injury and death precede atherosclerosis development. Thus, it is important to understand the mechanisms that lead to these early changes in endothelial cells. Although members of the MAP kinase/ERK kinase (MEK) kinase 3 (MEKK3)-MEK5-ERK5 module play an essential role in underpinning endothelial cell survival, how they execute these actions remain poorly understood. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.03.002DOI Listing
March 2019
4.315 Impact Factor

RGS2 promotes the translation of stress-associated proteins ATF4 and CHOP via its eIF2B-inhibitory domain.

Cell Signal 2019 Mar 1;59:163-170. Epub 2019 Mar 1.

Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario N6A 5C1, Canada; Department of Biology, Faculty of Science, University of Western Ontario, London, Ontario N6A 5B7, Canada. Electronic address:

Regulator of G protein signaling 2 (RGS2) is upregulated by multiple forms of stress and can augment translational attenuation associated with the phosphorylation of the initiation factor eIF2, a hallmark of several stress-induced coping mechanisms. Under stress-induced translational inhibition, key factors, such as ATF4, are selectively expressed via alternative translation mechanisms. These factors are known to regulate molecular switches that control cell fate by regulating pro-survival and pro-apoptotic signals. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.02.007DOI Listing

Multiple phosphorylation sites on the RegA phosphodiesterase regulate Dictyostelium development.

Cell Signal 2019 May 19;57:65-75. Epub 2019 Feb 19.

Department of Microbiology and Molecular Genetics, Oklahoma State University, Stillwater, OK 74078-3020, United States. Electronic address:

In Dictyostelium, the intracellular cAMP-specific phosphodiesterase RegA is a negative regulator of cAMP-dependent protein kinase (PKA), a key determinant in the timing of developmental morphogenesis and spore formation. To assess the role of protein kinases in the regulation of RegA function, this study identified phosphorylation sites on RegA and characterized the role of these modifications through the analysis of phospho-mimetic and phospho-ablative mutations. Mutations affecting residue T676 of RegA, a presumed target of the atypical MAP kinase Erk2, altered the rate of development and impacted cell distribution in chimeric organisms suggesting that phosphorylation of this residue reduces RegA function and regulates cell localization during multicellular development. Read More

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http://dx.doi.org/10.1016/j.cellsig.2019.02.005DOI Listing

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

Cell Signal 2019 May 14;57:45-57. Epub 2019 Feb 14.

Nestlé Research, École 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

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

Cell Signal 2019 Feb 14;58:79-90. Epub 2019 Feb 14.

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
1 Read

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

Cell Signal 2019 Feb 8;58:131-136. Epub 2019 Feb 8.

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

The inositol pyrophosphate, diphosphoinositol pentakisphosphate (IP), is thought to negatively regulate the critical insulin signaling protein Akt/PKB. Knockdown of the IP-generating inositol hexakisphosphate kinase 1 (IP6K1) results in a concomitant increase in signaling through Akt/PKB in most cell types so far examined. Total in vivo knockout of IP6K1 is associated with a phenotype resistant to high-fat diet, due to enhanced Akt/PKB signaling in classic insulin regulated tissues, counteracting insulin resistance. Read More

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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
5 Reads

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

Cell Signal 2019 May 7;57:29-44. 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
May 2019
1 Read

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

Cell Signal 2019 May 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
May 2019
1 Read

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 May 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
May 2019
2 Reads
4.315 Impact Factor

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

Cell Signal 2019 Jan 31;58:1-8. 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
4.315 Impact Factor

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

Cell Signal 2019 May 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
May 2019
1 Read

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

Cell Signal 2019 May 29;57:102-109. 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
May 2019
4.315 Impact Factor

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

Cell Signal 2019 May 28;57:89-101. 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
May 2019
1 Read
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