180 results match your criteria adam17 cytoplasmic

Actin polymerization regulates glycoprotein Ibα shedding.

Platelets 2021 May 12:1-9. Epub 2021 May 12.

Medical College, Jiangsu Institute of Hematology, the First Affiliated Hospital and Collaborative Innovation Center of Hematology, State Key Laboratory of Radiation Medicine and Protection, Soochow University, Key Laboratory of Thrombosis and Hemostasis, Ministry of Health, Suzhou, Jiangsu, China.

Glycoprotein (GP) Ibα shedding mediated by ADAM17 (a disintegrin and metalloproteinase 17) plays an important role in negatively regulating platelet function and thrombus formation. However, the mechanism of GPIbα shedding remains elusive. Here, we show that jasplakinolide (an actin-polymerizing peptide)-induced actin polymerization results in GPIbα shedding and impairs platelet function. Read More

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Targeted truncation of the ADAM17 cytoplasmic domain in mice results in protein destabilization and a hypomorphic phenotype.

J Biol Chem 2021 Jan-Jun;296:100733. Epub 2021 May 4.

Physiology, Biophysics and Systems Biology Program, Weill Cornell Medicine, New York, New York, USA; Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, New York, New York, USA; Institute for Advanced Study, Technical University of Munich, Garching, Germany; Department of Medicine, Weill Cornell Medicine, New York, New York, USA; Department of Biophysics, Physiology and Systems Biology, Weill Cornell Medicine, New York, New York, USA. Electronic address:

A disintegrin and metalloprotease 17 (ADAM17) is a cell-surface metalloprotease that serves as the principle sheddase for tumor necrosis factor α (TNFα), interleukin-6 receptor (IL-6R), and several ligands of the epidermal growth factor receptor (EGFR), regulating these crucial signaling pathways. ADAM17 activation requires its transmembrane domain, but not its cytoplasmic domain, and little is known about the role of this domain in vivo. To investigate, we used CRISPR-Cas9 to mutate the endogenous Adam17 locus in mice to produce a mutant ADAM17 lacking its cytoplasmic domain (Adam17Δcyto). Read More

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Analysis of the Conditions That Affect the Selective Processing of Endogenous Notch1 by ADAM10 and ADAM17.

Int J Mol Sci 2021 Feb 12;22(4). Epub 2021 Feb 12.

Tri-Institutional MD/PhD Program, Memorial Sloan-Kettering Cancer Center, Weill Cornell Medicine, Rockefeller University, New York, NY 10021, USA.

Notch signaling is critical for controlling a variety of cell fate decisions during metazoan development and homeostasis. This unique, highly conserved signaling pathway relies on cell-to-cell contact, which triggers the proteolytic release of the cytoplasmic domain of the membrane-anchored transcription factor Notch from the membrane. A disintegrin and metalloproteinase (ADAM) proteins are crucial for Notch activation by processing its S2 site. Read More

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February 2021

ADAM10 and ADAM17 are degraded by lysosomal pathway via asparagine endopeptidase.

Biochem Biophys Res Commun 2021 01 28;537:15-21. Epub 2020 Dec 28.

Department of Neurology, Renmin Hospital of Wuhan University, Wuhan, 430060, China. Electronic address:

A disintegrin and metalloproteinases 10 (ADAM10) and ADAM17 are transmembrane metalloproteinases that cleave the membrane-anchored proteins. They act as α-secretase that cleaves amyloid precursor protein (APP), precluding the production of amyloid-β, thus protecting against the onset of Alzheimer's disease (AD). However, the degradation pathway of ADAM10 and ADAM17 remains unknown. Read More

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January 2021

[Regulatory Role of Mitochondria in the Shedding of Platelet Membrane Protein GPIbα].

Zhongguo Shi Yan Xue Ye Xue Za Zhi 2020 Oct;28(5):1704-1709

Jiangsu Institute of Hematology, National Clinical Research Center for Hematologic Diseases, NHC Key Laboratory of Thrombosis and Hemostasis, The First Affiliated Hospital of Soochow University, Collaborative Innovation Center of Hematology, State Key Laboratory of Radiation Medicine and Protection, Suzhou 215006, Jiangsu Province, China,E-mail:

Objective: To investigate the role of mitochonaria in the regulation of platelet membrane protein GPIbα shedding and its mechanisms.

Methods: The washed platelets were obtained from peripheral blood in healthy volunteers and co-incubated with mitochondrial inhibitor carbonyl cyanide m-chlorophenyl hydrazone (CCCP), mitochondrial protector cyclosporin A (CsA) or matrix metalloproteinases inhibitor GM6001. After the platelets was stimulated, the effect of mitochondria to the shedding in platelet membrane protein GPIbα was detected by flow cytometry. Read More

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October 2020

ADAM17 cytoplasmic domain modulates Thioredoxin-1 conformation and activity.

Redox Biol 2020 10 24;37:101735. Epub 2020 Sep 24.

Laboratório Nacional de Biociências, LNBio, CNPEM, Campinas, São Paulo, Brazil. Electronic address:

The activity of Thioredoxin-1 (Trx-1) is adjusted by the balance of its monomeric, active and its dimeric, inactive state. The regulation of this balance is not completely understood. We have previously shown that the cytoplasmic domain of the transmembrane protein A Disintegrin And Metalloprotease 17 (ADAM17cyto) binds to Thioredoxin-1 (Trx-1) and the destabilization of this interaction favors the dimeric state of Trx-1. Read More

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October 2020

ADAM17-triggered TNF signalling protects the ageing Drosophila retina from lipid droplet-mediated degeneration.

EMBO J 2020 09 26;39(17):e104415. Epub 2020 Jul 26.

Sir William Dunn School of Pathology, University of Oxford, Oxford, UK.

Animals have evolved multiple mechanisms to protect themselves from the cumulative effects of age-related cellular damage. Here, we reveal an unexpected link between the TNF (tumour necrosis factor) inflammatory pathway, triggered by the metalloprotease ADAM17/TACE, and a lipid droplet (LD)-mediated mechanism of protecting retinal cells from age-related degeneration. Loss of ADAM17, TNF and the TNF receptor Grindelwald in pigmented glial cells of the Drosophila retina leads to age-related degeneration of both glia and neurons, preceded by an abnormal accumulation of glial LDs. Read More

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September 2020

Canine oviductal exosomes improve oocyte development via EGFR/MAPK signaling pathway.

Reproduction 2020 10;160(4):613-625

Department of Theriogenology and Biotechnology, College of Veterinary Medicine, Seoul National University, Seoul, Republic of Korea.

Oviduct cells produce a favorable environment for the development of gametes by generating multiple growth factors. Particularly, in canine species, immature oocytes undergo serial maturation processes in the oviduct, while the other mammals already possess matured oocytes in ovulatory follicles. However, little is known about the potential effect exhibited by the components released from canine oviduct cells (OCs) for modulating the biological function of oocytes. Read More

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October 2020

A disintegrin and metalloproteinase domain 17-epidermal growth factor receptor signaling contributes to oral cancer pain.

Pain 2020 10;161(10):2330-2343

Bluestone Center for Clinical Research, New York University College of Dentistry, New York, NY, United States.

Cancer cells secrete pronociceptive mediators that sensitize adjacent sensory neurons and cause pain. Identification and characterization of these mediators could pinpoint novel targets for cancer pain treatment. In this study, we identified candidate genes in cancer cell lines that encode for secreted or cell surface proteins that may drive nociception. Read More

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October 2020

The role of activated leukocyte cell adhesion molecule (ALCAM) in cancer progression, invasion, metastasis and recurrence: A novel cancer stem cell marker and tumor-specific prognostic marker.

Exp Mol Pathol 2020 08 5;115:104443. Epub 2020 May 5.

Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Iran. Electronic address:

Activated leukocyte cell adhesion molecule (ALCAM) or CD166 is a 100 to 105 KDa transmembrane immunoglobulin which is involved in activation of T-cells, hematopoiesis, neutrophils trans-endothelial migration, angiogenesis, inflammation and tumor propagation and invasiveness through formation of homophilic and heterophilic interactions. Recently, many studies have proposed that the expression pattern of ALCAM is highly associated with the grade, stage and invasiveness of tumors. Although ALCAM is a valuable prognostic marker in different carcinomas, similar expression patterns in different tumor types may be associated with completely different prognostic states, making it to be a tumor-type-dependent prognostic marker. Read More

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The lysosome: A potential juncture between SARS-CoV-2 infectivity and Niemann-Pick disease type C, with therapeutic implications.

FASEB J 2020 06 5;34(6):7253-7264. Epub 2020 May 5.

Lipoprotein Metabolism Section, Translational Vascular Medicine Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA.

Drug repurposing is potentially the fastest available option in the race to identify safe and efficacious drugs that can be used to prevent and/or treat COVID-19. By describing the life cycle of the newly emergent coronavirus, SARS-CoV-2, in light of emerging data on the therapeutic efficacy of various repurposed antimicrobials undergoing testing against the virus, we highlight in this review a possible mechanistic convergence between some of these tested compounds. Specifically, we propose that the lysosomotropic effects of hydroxychloroquine and several other drugs undergoing testing may be responsible for their demonstrated in vitro antiviral activities against COVID-19. Read More

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Hypoxia-induced release, nuclear translocation, and signaling activity of a DLK1 intracellular fragment in glioma.

Oncogene 2020 05 24;39(20):4028-4044. Epub 2020 Mar 24.

Department of Laboratory Medicine, Division of Translational Cancer Research, Lund University, Lund, Sweden.

Glioblastoma multiforme is characterized in part by severe hypoxia associated with tumor necrosis. The cellular response to hypoxia can influence several properties of tumor cells associated with aggressive tumor growth, including metabolic adaptations and tumor cell migration and invasion. Here, we found that Delta Like Non-Canonical Notch Ligand 1 (DLK1) expression was elevated as compared with normal brain in a genetically engineered mouse model of glioma, and that DLK1 expression increased with tumor grade in human glioma samples. Read More

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Proteolytic processing of PD-L1 by ADAM proteases in breast cancer cells.

Cancer Immunol Immunother 2020 Jan 3;69(1):43-55. Epub 2019 Dec 3.

Department of Biochemistry and Molecular Biophysics, Kansas State University, 141 Chalmers Hall, Manhattan, KS, 66506, USA.

Expression of programmed death ligand 1 (PD-L1) on the surface of tumor cells and its interaction with programmed cell death protein 1 (PD-1) on tumor-infiltrating lymphocytes suppress anti-tumor immunity. In breast tumors, PD-L1 expression levels are the highest in estrogen receptor-negative, progesterone receptor-negative, and human epidermal growth factor receptor 2-negative (triple-negative) cancers. In this study, we show that a portion of PD-L1 exogenously expressed in several triple-negative breast cancer cell lines, as well as endogenous PD-L1, is proteolytically cleaved by cell surface metalloproteases. Read More

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January 2020

NMDA Receptors Regulate Neuregulin 2 Binding to ER-PM Junctions and Ectodomain Release by ADAM10 [corrected].

Mol Neurobiol 2019 12 25;56(12):8345-8363. Epub 2019 Jun 25.

Section on Molecular Neurobiology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, 35 Lincoln Drive, Room 2C-1000, Bethesda, MD, 20892, USA.

Unprocessed pro-neuregulin 2 (pro-NRG2) accumulates on neuronal cell bodies at junctions between the endoplasmic reticulum and plasma membrane (ER-PM junctions). NMDA receptors (NMDARs) trigger NRG2 ectodomain shedding from these sites followed by activation of ErbB4 receptor tyrosine kinases, and ErbB4 signaling cell-autonomously downregulates intrinsic excitability of GABAergic interneurons by reducing voltage-gated sodium channel currents. NMDARs also promote dispersal of Kv2. Read More

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December 2019

Functional Characterization of Colon Cancer-Associated Mutations in : Modifications in the Pro-Domain Interfere with Trafficking and Maturation.

Int J Mol Sci 2019 May 4;20(9). Epub 2019 May 4.

Institute of Biochemistry, Christian-Albrechts-Universität zu Kiel, 24118 Kiel, Germany.

Colorectal cancer is one of the most commonly diagnosed malignancies in the Western world and is associated with elevated expression and activity of epidermal growth factor receptors (EGF-R). The metalloproteinase ADAM17 is involved in EGF-R activation by processing EGF-R ligands from membrane-bound pro-ligands. Underlining the link between colon cancer and ADAM17, genetic intestinal cancer models in ADAM17-deficient mice show a reduced tumor burden. Read More

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KDEL Receptor 1 Contributes to Cell Surface Association of Protein Disulfide Isomerases.

Cell Physiol Biochem 2019 ;52(4):850-868

Centre of Biochemistry and Molecular Biology, Structural Biology, Kiel University, Kiel, Germany,

Background/aims: Endoplasmic reticulum (ER)-resident proteins with a C-terminal KDEL ERretention sequence are captured in the Golgi apparatus by KDEL receptors (KDELRs). The binding of such proteins to these receptors induces their retrograde transport. Nevertheless, some KDEL proteins, such as Protein Disulfide Isomerases (PDIs), are found at the cell surface. Read More

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Relation between Tetraspanin- Associated and Tetraspanin- Non- Associated Exosomal Proteases and Metabolic Syndrome in Colorectal Cancer Patients

Asian Pac J Cancer Prev 2019 03 26;20(3):809-815. Epub 2019 Mar 26.

Cancer Research Institute, Тomsk National Research Medical Center, Russian Academy of Science, Tomsk, Russia. Email:

Purpose: Exosomal proteases are important in regulation of molecular signaling from growth factor receptors and adhesion molecules and also the regulation of cell motility and protein folding. The aim of this study was to evaluate the level of ADAM10, ADAM17 and 20S proteasomes in exosomes isolated from colorectal cancer patients (CRCPs) in relation with clinical and histopathological parameters. Methods: Blood plasma exosomes of 60 CRCPs at stage T2-4N0-2M0-1 and 10 control subjects (CSs) with colorectal polyps were isolated using ultrafiltration in combination with ultracentrifugation. Read More

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ADAM8 in invasive cancers: links to tumor progression, metastasis, and chemoresistance.

Clin Sci (Lond) 2019 01 11;133(1):83-99. Epub 2019 Jan 11.

Department of Neurosurgery, Philipps University Marburg, Baldingerstrasse, Marburg D-35033, Germany

Ectodomain shedding of extracellular and membrane proteins is of fundamental importance for cell-cell communication in neoplasias. A Disintegrin And Metalloproteinase (ADAM) proteases constitute a family of multifunctional, membrane-bound proteins with traditional sheddase functions. Their protumorigenic potential has been attributed to both, essential (ADAM10 and ADAM17) and 'dispensable' ADAM proteases (ADAM8, 9, 12, 15, and 19). Read More

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January 2019

Nanoquinacrine sensitizes 5-FU-resistant cervical cancer stem-like cells by down-regulating Nectin-4 via ADAM-17 mediated NOTCH deregulation.

Cell Oncol (Dordr) 2019 Apr 3;42(2):157-171. Epub 2019 Jan 3.

Cancer Biology Division, KIIT School of Biotechnology, KIIT University, Campus-11, Patia, Bhubanesar, Odisha, 751024, India.

Purpose: Cervical cancer is a major cause of cancer-related death in women world-wide. Although the anti-metabolite 5-FU is widely used for its treatment, its clinical utility is limited due to the frequent occurrence of drug resistance during metastasis. Cancer stem-like cells (CSCs), present in the heterogeneous population of CC cells, are thought to contribute to this resistance. Read More

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Expression of a Recombinant High Affinity IgG Fc Receptor by Engineered NK Cells as a Docking Platform for Therapeutic mAbs to Target Cancer Cells.

Front Immunol 2018 6;9:2873. Epub 2018 Dec 6.

Department of Veterinary and Biomedical Sciences, University of Minnesota, St. Paul, MN, United States.

Anti-tumor mAbs are the most widely used and characterized cancer immunotherapy. Despite having a significant impact on some malignancies, most cancer patients respond poorly or develop resistance to this therapy. A known mechanism of action of these therapeutic mAbs is antibody-dependent cell-mediated cytotoxicity (ADCC), a key effector function of human NK cells. Read More

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October 2019

Renal ADAM10 and 17: Their Physiological and Medical Meanings.

Front Cell Dev Biol 2018 6;6:153. Epub 2018 Nov 6.

Department of Pathology, Kindai University School of Medicine, Osakasayama, Japan.

A disintegrin and metalloproteinases (ADAMs) are a Zn-dependent transmembrane and secreted metalloprotease superfamily, so-called "molecular scissors," and they consist of an N-terminal signal sequence, a prodomain, zinc-binding metalloprotease domain, disintegrin domain, cysteine-rich domain, transmembrane domain and cytoplasmic tail. ADAMs perform proteolytic processing of the ectodomains of diverse transmembrane molecules into bioactive mediators. This review summarizes on their most well-known members, ADAM10 and 17, focusing on the kidneys. Read More

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November 2018

Structural and Functional Analyses of the Shedding Protease ADAM17 in HoxB8-Immortalized Macrophages and Dendritic-like Cells.

J Immunol 2018 11 24;201(10):3106-3118. Epub 2018 Oct 24.

Institute of Biochemistry, Christian-Albrechts-University of Kiel, 24118 Kiel, Germany;

A disintegrin and metalloproteinase (ADAM) 17 has been implicated in many shedding processes. Major substrates of ADAM17 are TNF-α, IL-6R, and ligands of the epidermal growth factor receptor. The essential role of the protease is emphasized by the fact that ADAM17 deficiency is lethal in mice. Read More

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November 2018

Human rhomboid family-1 modulates clathrin coated vesicle-dependent pro-transforming growth factor α membrane trafficking to promote breast cancer progression.

EBioMedicine 2018 Oct 29;36:229-240. Epub 2018 Sep 29.

State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy, Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Tianjin 300071, China.; Collaborative Innovation Center for Biotherapy and School of Medicine, Nankai University, Tianjin, 300071, China. Electronic address:

Background: Epidermal growth factor receptor (EGFR) signalling is critical in epithelial cancer development. Human rhomboid family-1 (RHBDF1) facilitates the secretion of TGFα, an EGFR ligand, in breast cancer; however, the underlying mechanism remains unclear. We evaluated the role for RHBDF1 in clathrin-coated vesicle (CCV)-dependent pro-TGFα membrane trafficking in breast cancer cells upon stimulation by G-protein coupled receptor (GPCR) agonists. Read More

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October 2018

Expression of the ectodomain-releasing protease ADAM17 is directly regulated by the osteosarcoma and bone-related transcription factor RUNX2.

J Cell Biochem 2018 11 19;119(10):8204-8219. Epub 2018 Jun 19.

Program of Cellular and Molecular Biology, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago, Chile.

Osteoblast differentiation is controlled by transcription factor RUNX2 which temporally activates or represses several bone-related genes, including those encoding extracellular matrix proteins or factors that control cell-cell, and cell-matrix interactions. Cell-cell communication in the many skeletal pericellular micro-niches is critical for bone development and involves paracrine secretion of growth factors and morphogens. This paracrine signaling is in part regulated by "A Disintegrin And Metalloproteinase" (ADAM) proteins. Read More

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November 2018

FRMD8 promotes inflammatory and growth factor signalling by stabilising the iRhom/ADAM17 sheddase complex.

Elife 2018 06 13;7. Epub 2018 Jun 13.

Sir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom.

Many intercellular signals are synthesised as transmembrane precursors that are released by proteolytic cleavage ('shedding') from the cell surface. ADAM17, a membrane-tethered metalloprotease, is the primary shedding enzyme responsible for the release of the inflammatory cytokine TNFα and several EGF receptor ligands. ADAM17 exists in complex with the rhomboid-like iRhom proteins, which act as cofactors that regulate ADAM17 substrate shedding. Read More

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iTAP, a novel iRhom interactor, controls TNF secretion by policing the stability of iRhom/TACE.

Elife 2018 06 13;7. Epub 2018 Jun 13.

Membrane Traffic Lab, Instituto Gulbenkian de Ciência, Oeiras, Portugal.

The apical inflammatory cytokine TNF regulates numerous important biological processes including inflammation and cell death, and drives inflammatory diseases. TNF secretion requires TACE (also called ADAM17), which cleaves TNF from its transmembrane tether. The trafficking of TACE to the cell surface, and stimulation of its proteolytic activity, depends on membrane proteins, called iRhoms. Read More

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Excessive Glutamate Stimulation Impairs ACE2 Activity Through ADAM17-Mediated Shedding in Cultured Cortical Neurons.

Cell Mol Neurobiol 2018 Aug 15;38(6):1235-1243. Epub 2018 May 15.

Department of Pharmacology & Experimental Therapeutics, School of Medicine, Louisiana State University Health Sciences Center, 1901 Perdido Street, Room 5218, New Orleans, LA, 70112, USA.

The excitotoxicity of glutamate plays an important role in the progression of various neurological disorders via participating in inflammation and neuronal damage. In this study, we identified the role of excessive glutamate stimulation in the modulation of angiotensin-converting enzyme type 2 (ACE2), a critical component in the compensatory axis of the renin-angiotensin system (RAS). In primary cultured cortical neurons, high concentration of glutamate (100 µM) significantly reduced the enzymatic activity of ACE2. Read More

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Activation of stimulator of interferon genes (STING) induces ADAM17-mediated shedding of the immune semaphorin SEMA4D.

J Biol Chem 2018 05 4;293(20):7717-7726. Epub 2018 Apr 4.

From the Division of Cell Signaling, Fujii Memorial Institute of Medical Sciences, Tokushima University, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.

Stimulator of interferon genes (STING) is an endoplasmic reticulum-resident membrane protein that mediates cytosolic pathogen DNA-induced innate immunity and inflammatory responses in host defenses. STING is activated by cyclic di-nucleotides and is then translocated to the Golgi apparatus, an event that triggers STING assembly with the downstream enzyme TANK-binding kinase 1 (TBK1). This assembly leads to the phosphorylation of the transcription factor interferon regulatory factor 3 (IRF3), which in turn induces expression of type-I interferon (IFN) and chemokine genes. Read More

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Cullin 3 regulates ADAMs-mediated ectodomain shedding of amphiregulin.

Biochem Biophys Res Commun 2018 04 21;499(1):17-23. Epub 2018 Mar 21.

Division of Cell Growth and Tumor Regulation, Proteo-Science Center, Ehime University, Ehime, Japan; Department of Biochemistry and Molecular Genetics, Ehime University Graduate School of Medicine, Toon, Shitsukawa, Ehime 791-0295, Japan. Electronic address:

A disintegrin and metalloproteinase (ADAM) family are crucial enzymes for ectodomain shedding of multiple substrates and are involved in diverse biologic and pathologic processes. However, the molecular mechanism underlying substrate selectivity of ADAMs is poorly understood. In this study, we observed that disruption of actin polymerization by pharmacological inhibitors, latrunculin A (LatA) and cytochalasin D (CyD), induced ectodomain shedding of epidermal growth factor (EGF) family ligands. Read More

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[Effect of paraquat on the expression of a disintegrin and metalloproteinase-17 in A549 cells].

Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi 2018 Jan;36(1):12-17

Graduate School of Luzhou Southwest Medical University, Luzhou 646000, China.

Construct a paraquat (PQ) cell fibrosis model in vitro, observe the effect of PQ on the expression of a disintegrin and metalloproteinase-17 (ADAM17) in A549 cells, and explore the role of ADAM17 in the pulmonary fibrosis induced by PQ poisoning. A549 cells are divided into normal control group, different concentration of PQ groups, CCK-8 is used to detect cell viability, screening concentration and time of PQ, cell morphology is observed under microscope; Enzyme-linked immunosorbent assay (ELISA) detectes fibrosis markers of collagen type I (Col I) and fibronectin (FN) expression. Establishment of cell model of fibrosis; distribution by immunocytochemical detection of ADAM17 in A549 cells, Reverse transcription-polymerase chain reaction and Western blot are used to detect the expression of ADAM17 mRNA and protein. Read More

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January 2018