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Search Results to Andrew J. Henderson, PhD

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Research Expertise & Professional Interests My research focuses on cellular mechanisms that regulate HIV replication and transcription. Active projects in the lab include elucidating T cell costimulatory signal transduction cascades that positively and negatively regulate HIV transcription, determining mechanisms by which HIV circumvents anti-inflammatory signals to promote HIV replication and AIDS-associated inflammatory diseases and characterizing the transcriptional status of HIV provirus in T cell and macrophage subsets. Although, HIV is our primary experimental system, our research provides general insights into signal transduction, tissue-specific gene expression, immune cell function and mechanisms that contribute to inflammatory disorders and autoimmunity. Below highlights some of the current on-going projects in the lab: T cell signals regulate HIV replication. T cell activation through the T cell receptor and costimulatory molecules, including CD28, influences susceptibility of T cells to HIV infection as well as proviral transcription. Incomplete T cell receptor signaling has been proposed to be a mechanism that contributes to proviral latency. We hypothesize that CD28 engagement results in distinct signaling cascades that have very different consequences for HIV transcription. We are actively characterizing signaling events emanating from critical tyrosine residues within the cytoplasmic tail of CD28 that either inhibit or induce HIV transcription to fully appreciate how costimulatory signals impact HIV transcription. In addition, we are characterizing the transcriptional machinery that regulates HIV expression in response to T cell signals. Understanding mechanisms by which CD28 regulates HIV transcription will further define pathways associated with this receptor as well as identify putative upstream signal transduction events critical for controlling HIV expression. Related projects have suggested that non-receptor tyrosine kinases necessary for T cell activation and function, such as the Src kinase Lck and the Tec kinase Itk mediate efficient release of HIV. The mechanisms by which these kinases influence these late steps of HIV virus replication are actively being studied. Regulation of HIV transcription elongation. HIV provirus is regulated at the level of transcription and involves changes in transcription initiation, chromatin organization and elongation. In particular, transcription elongation has been demonstrated to be a limiting step for HIV expression and overcoming this block is the primary activity of the viral factor Tat, which through the recruitment of P-TEFb to the LTR, post-translationally modifies RNA polymerase II and associated factors to increase processive transcription. Whether this initial lack of RNA polymerase II processivity represents proximal paused RNA polymerase II, premature termination, or both has not been resolved. Recent work from our lab shows that negative elongation factor NELF and the transcription termination factor Pcf11 repress HIV transcription. We hypothesize that the coordinate control of RNA Polymerase II activity and premature transcription termination coupled with chromatin changes create key check-points for HIV transcription that directly contributes to proviral transcriptional latency. In addition, we posit that there are cellular signals that extinguish HIV expression by inducing promoter proximal pausing and premature termination. Using a receptor tyrosine kinase that represses HIV expression, we are mapping signaling pathways that are upstream of transcription initiation, elongation and termination. Understanding the regulation of HIV transcription elongation will provide novel cellular targets for controlling and purging HIV in different cellular reservoirs.
Self-Described Keywords transcription
Self-Described Keywords transcription factors

One or more keywords matched the following items that are connected to Henderson, Andrew

Item TypeName
Concept Transcription Factors
Concept Transcription, Genetic
Concept Transcriptional Activation
Concept Transcription Factor AP-1
Concept Reverse Transcription
Concept GATA3 Transcription Factor
Concept Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
Concept Transcription Elongation, Genetic
Concept Transcription Termination, Genetic
Academic Article Ig/EBP (C/EBP gamma) is a transdominant negative inhibitor of C/EBP family transcriptional activators.
Academic Article C/EBP proteins activate transcription from the human immunodeficiency virus type 1 long terminal repeat in macrophages/monocytes.
Academic Article GATA elements are necessary for the activity and tissue specificity of the T-cell receptor beta-chain transcriptional enhancer.
Academic Article Lessons in transcriptional regulation learned from studies on immunoglobulin genes.
Academic Article C/EBP activators are required for HIV-1 replication and proviral induction in monocytic cell lines.
Academic Article The absence of the transcription activator TFE3 impairs activation of B cells in vivo.
Academic Article Transcriptional regulation during B cell development.
Academic Article Interaction between CCAAT/enhancer binding protein and cyclic AMP response element binding protein 1 regulates human immunodeficiency virus type 1 transcription in cells of the monocyte/macrophage lineage.
Academic Article CCAAT/enhancer binding proteins are not required for HIV-1 entry but regulate proviral transcription by recruiting coactivators to the long-terminal repeat in monocytic cells.
Academic Article Melanoma cell migration to type IV collagen requires activation of NF-kappaB.
Academic Article Identification of binding sites for members of the CCAAT/enhancer binding protein transcription factor family in the simian immunodeficiency virus long terminal repeat.
Academic Article Recruitment of phosphatidylinositol 3-kinase to CD28 inhibits HIV transcription by a Tat-dependent mechanism.
Academic Article CD28-dependent HIV-1 transcription is associated with Vav, Rac, and NF-kappa B activation.
Academic Article RON receptor tyrosine kinase, a negative regulator of inflammation, inhibits HIV-1 transcription in monocytes/macrophages and is decreased in brain tissue from patients with AIDS.
Academic Article Signal transduction induced by apoptotic cells inhibits HIV transcription in monocytes/macrophages.
Academic Article Negative elongation factor NELF represses human immunodeficiency virus transcription by pausing the RNA polymerase II complex.
Academic Article Transcription termination factor Pcf11 limits the processivity of Pol II on an HIV provirus to repress gene expression.
Academic Article The receptor tyrosine kinase RON represses HIV-1 transcription by targeting RNA polymerase II processivity.
Academic Article Selective targeting of ITK blocks multiple steps of HIV replication.
Academic Article Thioredoxin reductase-1 negatively regulates HIV-1 transactivating protein Tat-dependent transcription in human macrophages.
Academic Article 15-Deoxy-Delta12,14-prostaglandin J2 inhibits HIV-1 transactivating protein, Tat, through covalent modification.
Academic Article Combinatorial signals from CD28 differentially regulate human immunodeficiency virus transcription in T cells.
Academic Article Celastrol inhibits Tat-mediated human immunodeficiency virus (HIV) transcription and replication.
Academic Article Mechanisms of HIV Transcriptional Regulation and Their Contribution to Latency.
Academic Article Negative elongation factor (NELF) coordinates RNA polymerase II pausing, premature termination, and chromatin remodeling to regulate HIV transcription.
Academic Article T Cell Transcription Factors and Their Impact on HIV Expression
Academic Article T Cell Transcription Factors and Their Impact on HIV Expression.
Academic Article Transcriptional regulation and T cell exhaustion.
Academic Article Blimp-1, an intrinsic factor that represses HIV-1 proviral transcription in memory CD4+ T cells.
Academic Article RNAP II processivity is a limiting step for HIV-1 transcription independent of orientation to and activity of endogenous neighboring promoters.
Academic Article Identification of benzazole compounds that induce HIV-1 transcription.

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