The Experts below are selected from a list of 34899 Experts worldwide ranked by ideXlab platform

Hans A.r. Bluyssen - One of the best experts on this subject based on the ideXlab platform.

  • a positive feedback Amplifier Circuit that regulates interferon ifn stimulated gene expression and controls type i and type ii ifn responses
    Frontiers in Immunology, 2018
    Co-Authors: Agata Michalska, Katarzyna Blaszczyk, Joanna Wesoly, Hans A.r. Bluyssen
    Abstract:

    IFN-I and IFN-II both induce IFN-stimulated gene (ISG) expression through Janus Kinase (Jak)-dependent phosphorylation of Signal Transducer and Activator of Transcription (STAT) 1 and STAT2. STAT1 homodimers, known as GAF, activate transcription in response to all types of IFNs by direct binding to IFN-II activation site (GAS)-containing genes. Association of interferon regulatory factor (IRF) 9 with STAT1-STAT2 heterodimers (known as ISGF3) or with STAT2 homodimers (STAT2/IRF9) in response to IFN-I, redirects these complexes to a distinct group of target genes harboring the interferon stimulated response element (ISRE). Similarly, IRF1 regulates expression of ISGs in response to IFN-I and IFN-II by directly binding the ISRE or IRF-responsive element (IRE). In addition, evidence is accumulating for an IFN-independent and -dependent role of unphosphorylated STAT1 and STAT2, with or without IRF9, and IRF1 in basal as well as long-term ISG expression. This review provides insight into the existence of an intracellular Amplifier Circuit regulating ISG expression and controlling long-term cellular responsiveness to IFN-I and IFN-II. The exact timely steps that take place during IFN-activated feedback regulation and the control of ISG transcription and long-term cellular responsiveness to IFN-I and IFN-II, is currently not clear. Based on existing literature and our novel data we predict the existence of a multifaceted intracellular Amplifier Circuit that depends on unphosphorylated and phosphorylated ISGF3 and GAF complexes and IRF1. In a combinatorial and timely fashion, these complexes mediate prolonged ISG expression and control cellular responsiveness to IFN-I and IFN-II. This proposed intracellular Amplifier Circuit also provides a molecular explanation for the existing overlap between IFN-I and IFN-II activated ISG expression.

  • a positive feedback Amplifier Circuit that regulates interferon ifn stimulated gene expression and controls type i and type ii ifn responses
    Frontiers in Immunology, 2018
    Co-Authors: Agata Michalska, Katarzyna Blaszczyk, Joanna Wesoly, Hans A.r. Bluyssen
    Abstract:

    Interferon (IFN)-I and IFN-II both induce IFN-stimulated gene (ISG) expression through Janus kinase (JAK)-dependent phosphorylation of signal transducer and activator of transcription (STAT) 1 and STAT2. STAT1 homodimers, known as γ-activated factor (GAF), activate transcription in response to all types of IFNs by direct binding to IFN-II activation site (γ-activated sequence)-containing genes. Association of interferon regulatory factor (IRF) 9 with STAT1-STAT2 heterodimers [known as interferon-stimulated gene factor 3 (ISGF3)] or with STAT2 homodimers (STAT2/IRF9) in response to IFN-I, redirects these complexes to a distinct group of target genes harboring the interferon-stimulated response element (ISRE). Similarly, IRF1 regulates expression of ISGs in response to IFN-I and IFN-II by directly binding the ISRE or IRF-responsive element. In addition, evidence is accumulating for an IFN-independent and -dependent role of unphosphorylated STAT1 and STAT2, with or without IRF9, and IRF1 in basal as well as long-term ISG expression. This review provides insight into the existence of an intracellular Amplifier Circuit regulating ISG expression and controlling long-term cellular responsiveness to IFN-I and IFN-II. The exact timely steps that take place during IFN-activated feedback regulation and the control of ISG transcription and long-term cellular responsiveness to IFN-I and IFN-II is currently not clear. Based on existing literature and our novel data, we predict the existence of a multifaceted intracellular Amplifier Circuit that depends on unphosphorylated and phosphorylated ISGF3 and GAF complexes and IRF1. In a combinatorial and timely fashion, these complexes mediate prolonged ISG expression and control cellular responsiveness to IFN-I and IFN-II. This proposed intracellular Amplifier Circuit also provides a molecular explanation for the existing overlap between IFN-I and IFN-II activated ISG expression.

Agata Michalska - One of the best experts on this subject based on the ideXlab platform.

  • a positive feedback Amplifier Circuit that regulates interferon ifn stimulated gene expression and controls type i and type ii ifn responses
    Frontiers in Immunology, 2018
    Co-Authors: Agata Michalska, Katarzyna Blaszczyk, Joanna Wesoly, Hans A.r. Bluyssen
    Abstract:

    IFN-I and IFN-II both induce IFN-stimulated gene (ISG) expression through Janus Kinase (Jak)-dependent phosphorylation of Signal Transducer and Activator of Transcription (STAT) 1 and STAT2. STAT1 homodimers, known as GAF, activate transcription in response to all types of IFNs by direct binding to IFN-II activation site (GAS)-containing genes. Association of interferon regulatory factor (IRF) 9 with STAT1-STAT2 heterodimers (known as ISGF3) or with STAT2 homodimers (STAT2/IRF9) in response to IFN-I, redirects these complexes to a distinct group of target genes harboring the interferon stimulated response element (ISRE). Similarly, IRF1 regulates expression of ISGs in response to IFN-I and IFN-II by directly binding the ISRE or IRF-responsive element (IRE). In addition, evidence is accumulating for an IFN-independent and -dependent role of unphosphorylated STAT1 and STAT2, with or without IRF9, and IRF1 in basal as well as long-term ISG expression. This review provides insight into the existence of an intracellular Amplifier Circuit regulating ISG expression and controlling long-term cellular responsiveness to IFN-I and IFN-II. The exact timely steps that take place during IFN-activated feedback regulation and the control of ISG transcription and long-term cellular responsiveness to IFN-I and IFN-II, is currently not clear. Based on existing literature and our novel data we predict the existence of a multifaceted intracellular Amplifier Circuit that depends on unphosphorylated and phosphorylated ISGF3 and GAF complexes and IRF1. In a combinatorial and timely fashion, these complexes mediate prolonged ISG expression and control cellular responsiveness to IFN-I and IFN-II. This proposed intracellular Amplifier Circuit also provides a molecular explanation for the existing overlap between IFN-I and IFN-II activated ISG expression.

  • a positive feedback Amplifier Circuit that regulates interferon ifn stimulated gene expression and controls type i and type ii ifn responses
    Frontiers in Immunology, 2018
    Co-Authors: Agata Michalska, Katarzyna Blaszczyk, Joanna Wesoly, Hans A.r. Bluyssen
    Abstract:

    Interferon (IFN)-I and IFN-II both induce IFN-stimulated gene (ISG) expression through Janus kinase (JAK)-dependent phosphorylation of signal transducer and activator of transcription (STAT) 1 and STAT2. STAT1 homodimers, known as γ-activated factor (GAF), activate transcription in response to all types of IFNs by direct binding to IFN-II activation site (γ-activated sequence)-containing genes. Association of interferon regulatory factor (IRF) 9 with STAT1-STAT2 heterodimers [known as interferon-stimulated gene factor 3 (ISGF3)] or with STAT2 homodimers (STAT2/IRF9) in response to IFN-I, redirects these complexes to a distinct group of target genes harboring the interferon-stimulated response element (ISRE). Similarly, IRF1 regulates expression of ISGs in response to IFN-I and IFN-II by directly binding the ISRE or IRF-responsive element. In addition, evidence is accumulating for an IFN-independent and -dependent role of unphosphorylated STAT1 and STAT2, with or without IRF9, and IRF1 in basal as well as long-term ISG expression. This review provides insight into the existence of an intracellular Amplifier Circuit regulating ISG expression and controlling long-term cellular responsiveness to IFN-I and IFN-II. The exact timely steps that take place during IFN-activated feedback regulation and the control of ISG transcription and long-term cellular responsiveness to IFN-I and IFN-II is currently not clear. Based on existing literature and our novel data, we predict the existence of a multifaceted intracellular Amplifier Circuit that depends on unphosphorylated and phosphorylated ISGF3 and GAF complexes and IRF1. In a combinatorial and timely fashion, these complexes mediate prolonged ISG expression and control cellular responsiveness to IFN-I and IFN-II. This proposed intracellular Amplifier Circuit also provides a molecular explanation for the existing overlap between IFN-I and IFN-II activated ISG expression.

Joanna Wesoly - One of the best experts on this subject based on the ideXlab platform.

  • a positive feedback Amplifier Circuit that regulates interferon ifn stimulated gene expression and controls type i and type ii ifn responses
    Frontiers in Immunology, 2018
    Co-Authors: Agata Michalska, Katarzyna Blaszczyk, Joanna Wesoly, Hans A.r. Bluyssen
    Abstract:

    IFN-I and IFN-II both induce IFN-stimulated gene (ISG) expression through Janus Kinase (Jak)-dependent phosphorylation of Signal Transducer and Activator of Transcription (STAT) 1 and STAT2. STAT1 homodimers, known as GAF, activate transcription in response to all types of IFNs by direct binding to IFN-II activation site (GAS)-containing genes. Association of interferon regulatory factor (IRF) 9 with STAT1-STAT2 heterodimers (known as ISGF3) or with STAT2 homodimers (STAT2/IRF9) in response to IFN-I, redirects these complexes to a distinct group of target genes harboring the interferon stimulated response element (ISRE). Similarly, IRF1 regulates expression of ISGs in response to IFN-I and IFN-II by directly binding the ISRE or IRF-responsive element (IRE). In addition, evidence is accumulating for an IFN-independent and -dependent role of unphosphorylated STAT1 and STAT2, with or without IRF9, and IRF1 in basal as well as long-term ISG expression. This review provides insight into the existence of an intracellular Amplifier Circuit regulating ISG expression and controlling long-term cellular responsiveness to IFN-I and IFN-II. The exact timely steps that take place during IFN-activated feedback regulation and the control of ISG transcription and long-term cellular responsiveness to IFN-I and IFN-II, is currently not clear. Based on existing literature and our novel data we predict the existence of a multifaceted intracellular Amplifier Circuit that depends on unphosphorylated and phosphorylated ISGF3 and GAF complexes and IRF1. In a combinatorial and timely fashion, these complexes mediate prolonged ISG expression and control cellular responsiveness to IFN-I and IFN-II. This proposed intracellular Amplifier Circuit also provides a molecular explanation for the existing overlap between IFN-I and IFN-II activated ISG expression.

  • a positive feedback Amplifier Circuit that regulates interferon ifn stimulated gene expression and controls type i and type ii ifn responses
    Frontiers in Immunology, 2018
    Co-Authors: Agata Michalska, Katarzyna Blaszczyk, Joanna Wesoly, Hans A.r. Bluyssen
    Abstract:

    Interferon (IFN)-I and IFN-II both induce IFN-stimulated gene (ISG) expression through Janus kinase (JAK)-dependent phosphorylation of signal transducer and activator of transcription (STAT) 1 and STAT2. STAT1 homodimers, known as γ-activated factor (GAF), activate transcription in response to all types of IFNs by direct binding to IFN-II activation site (γ-activated sequence)-containing genes. Association of interferon regulatory factor (IRF) 9 with STAT1-STAT2 heterodimers [known as interferon-stimulated gene factor 3 (ISGF3)] or with STAT2 homodimers (STAT2/IRF9) in response to IFN-I, redirects these complexes to a distinct group of target genes harboring the interferon-stimulated response element (ISRE). Similarly, IRF1 regulates expression of ISGs in response to IFN-I and IFN-II by directly binding the ISRE or IRF-responsive element. In addition, evidence is accumulating for an IFN-independent and -dependent role of unphosphorylated STAT1 and STAT2, with or without IRF9, and IRF1 in basal as well as long-term ISG expression. This review provides insight into the existence of an intracellular Amplifier Circuit regulating ISG expression and controlling long-term cellular responsiveness to IFN-I and IFN-II. The exact timely steps that take place during IFN-activated feedback regulation and the control of ISG transcription and long-term cellular responsiveness to IFN-I and IFN-II is currently not clear. Based on existing literature and our novel data, we predict the existence of a multifaceted intracellular Amplifier Circuit that depends on unphosphorylated and phosphorylated ISGF3 and GAF complexes and IRF1. In a combinatorial and timely fashion, these complexes mediate prolonged ISG expression and control cellular responsiveness to IFN-I and IFN-II. This proposed intracellular Amplifier Circuit also provides a molecular explanation for the existing overlap between IFN-I and IFN-II activated ISG expression.

Katarzyna Blaszczyk - One of the best experts on this subject based on the ideXlab platform.

  • a positive feedback Amplifier Circuit that regulates interferon ifn stimulated gene expression and controls type i and type ii ifn responses
    Frontiers in Immunology, 2018
    Co-Authors: Agata Michalska, Katarzyna Blaszczyk, Joanna Wesoly, Hans A.r. Bluyssen
    Abstract:

    IFN-I and IFN-II both induce IFN-stimulated gene (ISG) expression through Janus Kinase (Jak)-dependent phosphorylation of Signal Transducer and Activator of Transcription (STAT) 1 and STAT2. STAT1 homodimers, known as GAF, activate transcription in response to all types of IFNs by direct binding to IFN-II activation site (GAS)-containing genes. Association of interferon regulatory factor (IRF) 9 with STAT1-STAT2 heterodimers (known as ISGF3) or with STAT2 homodimers (STAT2/IRF9) in response to IFN-I, redirects these complexes to a distinct group of target genes harboring the interferon stimulated response element (ISRE). Similarly, IRF1 regulates expression of ISGs in response to IFN-I and IFN-II by directly binding the ISRE or IRF-responsive element (IRE). In addition, evidence is accumulating for an IFN-independent and -dependent role of unphosphorylated STAT1 and STAT2, with or without IRF9, and IRF1 in basal as well as long-term ISG expression. This review provides insight into the existence of an intracellular Amplifier Circuit regulating ISG expression and controlling long-term cellular responsiveness to IFN-I and IFN-II. The exact timely steps that take place during IFN-activated feedback regulation and the control of ISG transcription and long-term cellular responsiveness to IFN-I and IFN-II, is currently not clear. Based on existing literature and our novel data we predict the existence of a multifaceted intracellular Amplifier Circuit that depends on unphosphorylated and phosphorylated ISGF3 and GAF complexes and IRF1. In a combinatorial and timely fashion, these complexes mediate prolonged ISG expression and control cellular responsiveness to IFN-I and IFN-II. This proposed intracellular Amplifier Circuit also provides a molecular explanation for the existing overlap between IFN-I and IFN-II activated ISG expression.

  • a positive feedback Amplifier Circuit that regulates interferon ifn stimulated gene expression and controls type i and type ii ifn responses
    Frontiers in Immunology, 2018
    Co-Authors: Agata Michalska, Katarzyna Blaszczyk, Joanna Wesoly, Hans A.r. Bluyssen
    Abstract:

    Interferon (IFN)-I and IFN-II both induce IFN-stimulated gene (ISG) expression through Janus kinase (JAK)-dependent phosphorylation of signal transducer and activator of transcription (STAT) 1 and STAT2. STAT1 homodimers, known as γ-activated factor (GAF), activate transcription in response to all types of IFNs by direct binding to IFN-II activation site (γ-activated sequence)-containing genes. Association of interferon regulatory factor (IRF) 9 with STAT1-STAT2 heterodimers [known as interferon-stimulated gene factor 3 (ISGF3)] or with STAT2 homodimers (STAT2/IRF9) in response to IFN-I, redirects these complexes to a distinct group of target genes harboring the interferon-stimulated response element (ISRE). Similarly, IRF1 regulates expression of ISGs in response to IFN-I and IFN-II by directly binding the ISRE or IRF-responsive element. In addition, evidence is accumulating for an IFN-independent and -dependent role of unphosphorylated STAT1 and STAT2, with or without IRF9, and IRF1 in basal as well as long-term ISG expression. This review provides insight into the existence of an intracellular Amplifier Circuit regulating ISG expression and controlling long-term cellular responsiveness to IFN-I and IFN-II. The exact timely steps that take place during IFN-activated feedback regulation and the control of ISG transcription and long-term cellular responsiveness to IFN-I and IFN-II is currently not clear. Based on existing literature and our novel data, we predict the existence of a multifaceted intracellular Amplifier Circuit that depends on unphosphorylated and phosphorylated ISGF3 and GAF complexes and IRF1. In a combinatorial and timely fashion, these complexes mediate prolonged ISG expression and control cellular responsiveness to IFN-I and IFN-II. This proposed intracellular Amplifier Circuit also provides a molecular explanation for the existing overlap between IFN-I and IFN-II activated ISG expression.

Paul Larsen - One of the best experts on this subject based on the ideXlab platform.

  • Modeling investigation of an ultrawideband terahertz sheet beam traveling-wave tube Amplifier Circuit
    IEEE Transactions on Electron Devices, 2011
    Co-Authors: Young-min Shin, John Pasour, Anisullah Baig, Larry R. Barnett, Neville C. Luhmann, Paul Larsen
    Abstract:

    Extensive numerical analysis has demonstrated that a terahertz (H-band) sheet beam traveling-wave tube (TWT) Amplifier Circuit, composed of a staggered double grating array waveguide, has very broad bandwidth ( $\sim$30%) of the fundamental passband (TE mode) with a 7 : 1 aspect ratio sheet beam without excitation of $n = \hbox{1}$ space harmonic backward-wave modes. Particle-in-cell (PIC) simulations utilizing MAGIC3D and CST PS predict that the designed Circuit produces $\sim$150–300-W output power, corresponding to $\sim$3%–5.5% intrinsic electronic efficiency ($\sim$35–38-dB saturated gain from 50-mW input driving power), over $\sim$25% bandwidth, which is in good agreement with CHRISTINE 1-D code predictions. Simulations, using a perfectly matched layer boundary ( $\sim -$30-dB return loss), show that the Circuit stably operates without noticeable oscillation. With a more realistic matching condition ($\sim-$ 9.5-dB return loss), it becomes unstable. However, simulations show that the incorporation of an attenuating sever with tapered conductivity suppresses the instability in tube operation.