Physician
Family Medicine
Dr. Michael J. Gale, MD
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Michael J. Gale practices Family Medicine. He went to medical school at Wake Forest School of Medicine. Michael Gale is also a published doctor. He has 99 paper published. The most recent paper is: Pathogen-Associated Molecular Pattern Recognition of Hepatitis C Virus Transmitted/Founder Variants by RIG-I Is Dependent on U-Core Length. Michael Gale accepts Medicare payments and is listed with Medicare.gov.
Publications
- Pathogen-Associated Molecular Pattern Recognition of Hepatitis C Virus Transmitted/Founder Variants by RIG-I Is Dependent on U-Core Length.
- RIG-I in RNA virus recognition.
- Hepatitis C Virus Infection Induces Autocrine Interferon Signaling by Human Liver Endothelial Cell and Release of Exosomes, Which Inhibits Viral Replication.
- Cytosolic Double-Stranded RNA Activates the NLRP3 Inflammasome via MAVS-Induced Membrane Permeabilization and K+ Efflux.
- In vitro and in vivo characterization of a West Nile virus MAD78 infectious clone.
- Interferon regulatory factor 5 (IRF5)-dependent immune responses in the draining lymph node protect against West Nile virus infection.
- Pushing to a cure by harnessing innate immunity against hepatitis C virus.
- Deficient IFN Signaling by Myeloid Cells Leads to MAVS-Dependent Virus-Induced Sepsis.
- Rapid generation of a mouse model for Middle East respiratory syndrome.
- Antiviral innate immunity: editorial overview.
- Innate Antiviral Immune Signaling, Viral Evasion and Modulation by HIV-1.
- Direct, Interferon-Independent Activation of the CXCL10 Promoter by NF-κB and IRF3 During Hepatitis C Virus Infection.
- The favorable IFNL3 genotype escapes mRNA decay mediated by AU-rich elements and hepatitis C virus-induced microRNAs.
- The essential, non-redundant roles of RIG-I and MDA5 in detecting and controlling West Nile virus infection.
- Regulation of hepatic innate immunity by hepatitis C virus.
- IL-1β Production through the NLRP3 Inflammasome by Hepatic Macrophages Links Hepatitis C Virus Infection with Liver Inflammation and Disease.
- Differential innate immune response programs in neuronal subtypes determine susceptibility to infection in the brain by positive-stranded RNA viruses.
- IFITM1 is a tight junction protein that inhibits hepatitis C virus entry.
- A Systems Biology Approach Reveals that Tissue Tropism to West Nile Virus Is Regulated by Antiviral Genes and Innate Immune Cellular Processes.
- IRF-3, IRF-5, and IRF-7 coordinately regulate the type I IFN response in myeloid dendritic cells downstream of MAVS signaling.
- Effects of the hepatitis C virus core protein on innate cellular defense pathways.
- Inactivation of the PKR protein kinase and stimulation of mRNA translation by the cellular co-chaperone P58(IPK) does not require J domain function.
- Proteomic Analysis of Mitochondrial-Associated ER Membranes (MAM) during RNA Virus Infection Reveals Dynamic Changes in Protein and Organelle Trafficking.
- Hepatitis C Virus Core Protein Inhibits Interferon Production by a Human Plasmacytoid Dendritic Cell Line and Dysregulates Interferon Regulatory Factor-7 and Signal Tr...
- IL-1β signaling promotes CNS-intrinsic immune control of West Nile virus infection.
- Uridine composition of the poly-U/UC tract of HCV RNA defines non-self recognition by RIG-I.
- Viral and therapeutic control of IFN-beta promoter stimulator 1 during hepatitis C virus infection.
- Cell-specific IRF-3 responses protect against West Nile virus infection by interferon-dependent and -independent mechanisms.
- Molecular clones of hepatitis C virus: applications to animal models.
- Evasion of intracellular host defence by hepatitis C virus.
- The role of innate immunity in chronic hepatitis C viral infection.
- Shared and unique functions of the DExD/H-box helicases RIG-I, MDA5, and LGP2 in antiviral innate immunity.
- Beta interferon controls West Nile virus infection and pathogenesis in mice.
- Coexpressed RIG-I agonist enhances humoral immune response to influenza virus DNA vaccine.
- Toll-like receptor 3 has a protective role against West Nile virus infection.
- Unveiling viral enablers.
- Regulation of innate immunity against hepatitis C virus infection.
- Fighting the flu with inflammasome signaling.
- Autoimmunity Initiates in Nonhematopoietic Cells and Progresses via Lymphocytes in an Interferon-Dependent Autoimmune Disease.
- RIG-I like receptors in antiviral immunity and therapeutic applications.
- Recognition of viruses by cytoplasmic sensors.
- Immune signaling by RIG-I-like receptors.
- Nonself RNA-sensing mechanism of RIG-I helicase and activation of antiviral immune responses.
- HIV infection of dendritic cells subverts the IFN induction pathway via IRF-1 and inhibits type 1 IFN production.
- Measure and countermeasure: type I IFN (IFN-alpha/beta) antiviral response against West Nile virus.
- Small self-RNA generated by RNase L amplifies antiviral innate immunity.
- RalB GTPase-mediated activation of the IkappaB family kinase TBK1 couples innate immune signaling to tumor cell survival.
- Hepatitis C virus production by human hepatocytes dependent on assembly and secretion of very low-density lipoproteins.
- Interferon regulatory factor IRF-7 induces the antiviral alpha interferon response and protects against lethal West Nile virus infection.
- Regulation of innate antiviral defenses through a shared repressor domain in RIG-I and LGP2.
- Dynamics of innate immunity are key to chronic immune activation in AIDS.
- The accelerating pace of HCV research: a summary of the 15th International Symposium on Hepatitis C Virus And Related Viruses.
- Induction of IFN-beta and the innate antiviral response in myeloid cells occurs through an IPS-1-dependent signal that does not require IRF-3 and IRF-7.
- Innate immune evasion by hepatitis C virus and West Nile virus.
- Distinct poly(I-C) and virus-activated signaling pathways leading to interferon-beta production in hepatocytes.
- Viral regulation and evasion of the host response.
- The innate immune adaptor molecule MyD88 restricts West Nile virus replication and spread in neurons of the central nervous system.
- Disruption of hepatitis C virus RNA replication through inhibition of host protein geranylgeranylation.
- Translational control of viral gene expression in eukaryotes.
- Identification of FBL2 as a geranylgeranylated cellular protein required for hepatitis C virus RNA replication.
- Control of innate immune signaling and membrane targeting by the hepatitis C virus NS3/4A protease are governed by the NS3 helix ?0.
- Effector genes of interferon action against hepatitis C virus.
- Hepatitis C Virus Evasion from RIG-I-Dependent Hepatic Innate Immunity.
- Differential recognition of double-stranded RNA by RIG-I-like receptors in antiviral immunity.
- Reemergence of hepatitis C virus after 8.5 years in a patient with hypogammaglobulinemia: evidence for an occult viral reservoir.
- [RIG-I mediated hepatic innate immune signaling that controls HCV infection].
- Functional and therapeutic analysis of hepatitis C virus NS3.4A protease control of antiviral immune defense.
- Antiviral potency analysis and functional comparison of consensus interferon, interferon-alpha2a and pegylated interferon-alpha2b against hepatitis C virus infection.
- Regulation of interferon regulatory factor-3 by the hepatitis C virus serine protease.
- Control of antiviral defenses through hepatitis C virus disruption of retinoic acid-inducible gene-I signaling.
- Pegylated interferon and ribavirin promote early evolution of nonstructural 5A protein in individuals with hepatitis C who demonstrate a response to treatment.
- West Nile virus evades activation of interferon regulatory factor 3 through RIG-I-dependent and -independent pathways without antagonizing host defense signaling.
- Strategies for hepatitis C therapeutic intervention: now and next.
- Blockade of virus infection by human CD4+ T cells via a cytokine relay network.
- Apolipoprotein E on hepatitis C virion facilitates infection through interaction with low-density lipoprotein receptor.
- Immune evasion by hepatitis C virus NS3/4A protease-mediated cleavage of the Toll-like receptor 3 adaptor protein TRIF.
- Inhibition of retinoic acid-inducible gene I-mediated induction of beta interferon by the NS1 protein of influenza A virus.
- Viral evasion of the interferon system.
- Regulation of PKR and IRF-1 during hepatitis C virus RNA replication.
- Evasion and disruption of innate immune signalling by hepatitis C and West Nile viruses.
- New ways of initiating translation in eukaryotes.
- Viruses and interferon: a fight for supremacy.
- Establishment and maintenance of the innate antiviral response to West Nile Virus involves both RIG-I and MDA5 signaling through IPS-1.
- Activation of the interferon-beta promoter during hepatitis C virus RNA replication.
- Evolution of hepatitis C virus NS5A region in breakthrough patients during pegylated interferon and ribavirin therapy*.
- Mechanisms of action of interferon and ribavirin in chronic hepatitis C: Summary of a workshop.
- Nitric oxide controls an inflammatory-like Ly6C(hi)PDCA1+ DC subset that regulates Th1 immune responses.
- PKR and RNase L contribute to protection against lethal West Nile Virus infection by controlling early viral spread in the periphery and replication in neurons.
- Resistance to alpha/beta interferon is a determinant of West Nile virus replication fitness and virulence.
- Regulating intracellular antiviral defense and permissiveness to hepatitis C virus RNA replication through a cellular RNA helicase, RIG-I.
- Innate immunity induced by composition-dependent RIG-I recognition of hepatitis C virus RNA.
- Tissue specific expression of PKR protein kinase in aging B6D2F1 mice.
- Interferon regulatory factor-3 activation, hepatic interferon-stimulated gene expression, and immune cell infiltration in hepatitis C virus patients.
- A summary of the 18th International Symposium on Hepatitis C Virus and Related Viruses.
- IPS-1 is essential for the control of West Nile virus infection and immunity.
- Long double-stranded RNA induces an antiviral response independent of IFN regulatory factor 3, IFN-beta promoter stimulator 1, and IFN.
- Mitochondrial-associated endoplasmic reticulum membranes (MAM) form innate immune synapses and are targeted by hepatitis C virus.
- Viral evolution and interferon resistance of hepatitis C virus RNA replication in a cell culture model.
Schools
Wake Forest University
Ut Valley Regl Med Center
Doctors Specialties
- Family Medicine
Accepted Insurances
- Choice Plus POS II
- Cigna PPO
- Great West Healthcare-Cigna PPO
- Commercial Insurance Company
- Humana
- Medicare MCR
- Old Surety Life Insurance CompanyMedicare MCR
- Tricare
- Choice Plus POS
- Navigate HMO
- Navigate POS
- Options PPO
- United Healthcare
Education
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Wake Forest School of Medicine
Drug Facts
| NPI NUMBER | 1821003138 | |
| NPPES Provider LastName | GALE | |
| NPPES Provider FirstName | MICHAEL | |
| NPPES Provider ZIPCode | 84663 | |
| NPPES Provider State | UT | |
| Specialty Description | Family Practice | |
| Total Claim Count | 6385.0 | |
| Distinct Opioid Count | 4.0 | |
| Opioid Claim Count | 275.0 | |
| Percent Opioid Claims | 4.31 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1821003138 |
| Last Name Of The Provider | GALE |
| First Name Of The Provider | MICHAEL |
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