Transcription Factor

14,000,000 Leading Edge Experts on the ideXlab platform

Scan Science and Technology

Contact Leading Edge Experts & Companies

Scan Science and Technology

Contact Leading Edge Experts & Companies

The Experts below are selected from a list of 532707 Experts worldwide ranked by ideXlab platform

Andrew D. Sharrocks - One of the best experts on this subject based on the ideXlab platform.

  • the ets domain Transcription Factor family
    Nature Reviews Molecular Cell Biology, 2001
    Co-Authors: Andrew D. Sharrocks
    Abstract:

    ETS-domain Transcription-Factor networks represent a model for how combinatorial gene expression is achieved. These Transcription Factors interact with a multitude of co-regulatory partners to elicit gene-specific responses and drive distinct biological processes. These proteins are controlled by a complex series of inter and intramolecular interactions, and signalling pathways impinge on these proteins to further regulate their action.

  • the mechanism of phosphorylation inducible activation of the ets domain Transcription Factor elk 1
    The EMBO Journal, 1999
    Co-Authors: Shenhsi Yang, Andrew D. Sharrocks, Paul Shore, Nicola Willingham, Jeremy H Lakey
    Abstract:

    Protein phosphorylation represents one of the major mechanisms for Transcription Factor activation. Here we demonstrate a molecular mechanism by which phosphorylation by mitogen-activated protein (MAP) kinases leads to changes in Transcription Factor activity. MAP kinases stimulate DNA binding and Transcriptional activation mediated by the mammalian ETS-domain Transcription Factor Elk-1. Phosphorylation of the C-terminal Transcriptional activation domain induces a conformational change in Elk-1, which accompanies the stimulation of DNA binding. C-terminal phosphorylation is coupled to activation of DNA binding by the N-terminal DNA-binding domain via an additional intermediary domain. Activation of DNA binding is mediated by an allosteric mechanism involving the key phosphoacceptor residues. Together, these results provide a molecular model for how phosphorylation induces changes in Elk-1 activity.

Brian Seed - One of the best experts on this subject based on the ideXlab platform.

  • the Transcription Factor mafb antagonizes antiviral responses by blocking recruitment of coactivators to the Transcription Factor irf3
    Nature Immunology, 2010
    Co-Authors: Brian Seed
    Abstract:

    Type I interferons (IFN-α and IFN-β) are key to antiviral immunity. Kim and Seed now demonstrate that the Transcription Factor MAFB acts as a metastable switch to control expression of IFN-β. Viral infection induces type I interferons (IFN-α and IFN-β) that recruit unexposed cells in a self-amplifying response. We report that the Transcription Factor MafB thwarts auto-amplification by a metastable switch activity. MafB acted as a weak positive basal regulator of Transcription at the IFNB1 promoter through activity at Transcription Factor AP-1–like sites. Interferon elicitors recruited the Transcription Factor IRF3 to the promoter, whereupon MafB acted as a Transcriptional antagonist, impairing the interaction of coactivators with IRF3. Mathematical modeling supported the view that prepositioning of MafB on the promoter allows the system to respond rapidly to fluctuations in IRF3 activity. Higher expression of MafB in human pancreatic islet beta cells might increase cellular vulnerability to viral infections associated with the etiology of type 1 diabetes.

  • the Transcription Factor mafb antagonizes antiviral responses by blocking recruitment of coactivators to the Transcription Factor irf3
    Nature Immunology, 2010
    Co-Authors: Hwijin Kim, Brian Seed
    Abstract:

    Viral infection induces type I interferons (IFN-alpha and IFN-beta) that recruit unexposed cells in a self-amplifying response. We report that the Transcription Factor MafB thwarts auto-amplification by a metastable switch activity. MafB acted as a weak positive basal regulator of Transcription at the IFNB1 promoter through activity at Transcription Factor AP-1-like sites. Interferon elicitors recruited the Transcription Factor IRF3 to the promoter, whereupon MafB acted as a Transcriptional antagonist, impairing the interaction of coactivators with IRF3. Mathematical modeling supported the view that prepositioning of MafB on the promoter allows the system to respond rapidly to fluctuations in IRF3 activity. Higher expression of MafB in human pancreatic islet beta cells might increase cellular vulnerability to viral infections associated with the etiology of type 1 diabetes.

Laurie H Glimcher - One of the best experts on this subject based on the ideXlab platform.

  • the Transcription Factor xbp1 is selectively required for eosinophil differentiation
    Nature Immunology, 2015
    Co-Authors: Sarah E Bettigole, Raphael Lis, Stanley Adoro, Annhwee Lee, Lisa A Spencer, Peter F Weller, Laurie H Glimcher
    Abstract:

    The Transcription Factor XBP1 is associated with endoplasmic reticulum stress. Glimcher and colleagues show that XBP1 is expressed during eosinophil differentiation and is uniquely required for the production of granule proteins and eosinophil survival.

  • plasma cell differentiation requires the Transcription Factor xbp 1
    Nature, 2001
    Co-Authors: Andreas M Reimold, Daniel S Friend, Neal N Iwakoshi, John P Manis, Prashanth Vallabhajosyula, Eva Szomolanyitsuda, Ellen M Gravallese, Michael J Grusby, Laurie H Glimcher
    Abstract:

    Considerable progress has been made in identifying the Transcription Factors involved in the early specification of the B-lymphocyte lineage. However, little is known about Factors that control the transition of mature activated B cells to antibody-secreting plasma cells. Here we report that the Transcription Factor XBP-1 is required for the generation of plasma cells. XBP-1 transcripts were rapidly upregulated in vitro by stimuli that induce plasma-cell differentiation, and were found at high levels in plasma cells from rheumatoid synovium. When introduced into B-lineage cells, XBP-1 initiated plasma-cell differentiation. Mouse lymphoid chimaeras deficient in XBP-1 possessed normal numbers of activated B lymphocytes that proliferated, secreted cytokines and formed normal germinal centres. However, they secreted very little immunoglobulin of any isotype and failed to control infection with the B-cell-dependent polyoma virus, because plasma cells were markedly absent. XBP-1 is the only Transcription Factor known to be selectively and specifically required for the terminal differentiation of B lymphocytes to plasma cells.

Valentina Echeverria - One of the best experts on this subject based on the ideXlab platform.

  • Transcription Factor sp1 dysregulation in alzheimer s disease
    Journal of Neuroscience Research, 2008
    Co-Authors: Bruce A Citron, John S Dennis, Ross Zeitlin, Valentina Echeverria
    Abstract:

    Altered gene expression occurs in central nervous system disorders, including Alzheimer’s disease (AD). Transcription Factor Sp1 may be involved insofar as it can regulate the expression of several AD-related proteins, including amyloid precursor protein (APP) and tau. Sp1 could itself be regulated by inflammatory and other Factors associated with AD, such as interleukin-1b .W e measured an almost threefold elevation in the number of mRNA molecules of this cytokine in the AD frontal cortex. Sp1 mRNA was found to be up-regulated in these AD brains (along with Sp1-regulated COX-2), and the Sp1 increase was also seen at the protein level by Western immunoblotting. To determine whether this would also occur in transgenic mice developing AD pathology, we examined the expression of Sp1 in the cortex and hippocampus and observed higher levels of Sp1 mRNA and protein. These results indicate that elements of regulatory pathways involving Transcription Factor Sp1 may be useful targets for therapeutic intervention to prevent or reverse AD. V C 2008 Wiley-Liss, Inc.

Sungeun Chang - One of the best experts on this subject based on the ideXlab platform.

  • increased expression of activating Transcription Factor 3 is related to the biologic behavior of cutaneous squamous cell carcinomas
    Human Pathology, 2011
    Co-Authors: Myoung Shin Kim, Oun Jae Park, Chong Hyun Won, Mi Woo Lee, Jee Ho Choi, Chan Woong Kim, Sung Eun Kim, Kee Chan Moon, Sungeun Chang
    Abstract:

    Activating Transcription Factor 3, a member of the activating Transcription Factor/cyclic adenosine monophosphate response element-binding family of Transcription Factors, is an adaptive response gene that plays an oncogenic role in the development of various cancers. To our knowledge, few information are available on the possible role of activating Transcription Factor 3 in skin cancer. In this study, we investigated the expression of activating Transcription Factor 3 in basal cell carcinomas (n = 5), actinic keratoses (n = 7), squamous cell carcinomas (n = 19), and Bowen disease (n = 14) by immunohistochemistry. In results, activating Transcription Factor 3 was significantly expressed in squamous cell carcinomas (15/19), suggesting that it is involved in the pathogenesis of squamous cell carcinomas but not in basal cell carcinomas (0/5). In addition, higher expression of activating Transcription Factor 3 was observed in squamous cell carcinomas that were metastatic (P < .01) or arose in organ transplant recipients (P < .05). Therefore, activating Transcription Factor 3 appears to play an oncogenic role in the development of squamous cell carcinomas and may be related to the biologic behavior of them.