10 research outputs found

    Rare germline mutations in African American men diagnosed with earlyâ onset prostate cancer

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    Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142420/1/pros23464_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/142420/2/pros23464.pd

    MAVS-Mediated Apoptosis and Its Inhibition by Viral Proteins

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    BACKGROUND: Host responses to viral infection include both immune activation and programmed cell death. The mitochondrial antiviral signaling adaptor, MAVS (IPS-1, VISA or Cardif) is critical for host defenses to viral infection by inducing type-1 interferons (IFN-I), however its role in virus-induced apoptotic responses has not been elucidated. PRINCIPAL FINDINGS: We show that MAVS causes apoptosis independent of its function in initiating IFN-I production. MAVS-induced cell death requires mitochondrial localization, is caspase dependent, and displays hallmarks of apoptosis. Furthermore, MAVS(-/-) fibroblasts are resistant to Sendai virus-induced apoptosis. A functional screen identifies the hepatitis C virus NS3/4A and the Severe Acute Respiratory Syndrome coronavirus (SARS-CoV) nonstructural protein (NSP15) as inhibitors of MAVS-induced apoptosis, possibly as a method of immune evasion. SIGNIFICANCE: This study describes a novel role for MAVS in controlling viral infections through the induction of apoptosis, and identifies viral proteins which inhibit this host response

    Virtual Care Module Canvas Course

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    Medical Schoolhttp://deepblue.lib.umich.edu/bitstream/2027.42/170641/1/DanielLiesman_1.docxhttp://deepblue.lib.umich.edu/bitstream/2027.42/170641/2/DanielLiesman_2.docxhttp://deepblue.lib.umich.edu/bitstream/2027.42/170641/3/DanielLiesman_3.pptxhttp://deepblue.lib.umich.edu/bitstream/2027.42/170641/4/DanielLiesman_4.pptxhttp://deepblue.lib.umich.edu/bitstream/2027.42/170641/5/DanielLiesman_5.docxhttp://deepblue.lib.umich.edu/bitstream/2027.42/170641/6/DanielLiesman_6.doc

    An Investigation of Gene Regulatory Network State Space Variability

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    Genes are segments of DNA that provide a blueprint for cells and organisms to effectively control processes and regulations within individuals. There have been many attempts to quantify these processes, as a greater understanding of how genes operate could have large impacts on both personalized and precision medicine. Current biological methods cannot easily reveal the details of gene interactions. Therefore, we use gene expression data to infer networks of interactions, which are called gene regulatory networks or GRNs. These methods are designed to bypass the need for large amounts of data and extensive knowledge about a network. In this work, we extend previous work by investigating additional ways to incorporate stochasticity into gene regulatory networks
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