@article{rivera-serrano_fritch_scholl_sherry_2017, title={A Cytoplasmic RNA Virus Alters the Function of the Cell Splicing Protein SRSF2}, volume={91}, ISSN={["1098-5514"]}, DOI={10.1128/jvi.02488-16}, abstractNote={ABSTRACT}, number={7}, journal={JOURNAL OF VIROLOGY}, author={Rivera-Serrano, Efrain E. and Fritch, Ethan J. and Scholl, Elizabeth H. and Sherry, Barbara}, year={2017}, month={Apr} }
 @article{rivera-serrano_sherry_2017, title={NF-kappa B activation is cell type-specific in the heart}, volume={502}, ISSN={["0042-6822"]}, DOI={10.1016/j.virol.2016.12.022}, abstractNote={Viral myocarditis is common and can progress to cardiac failure. Cardiac cell pro-inflammatory responses are critical for viral clearance, however sustained inflammatory responses contribute to cardiac damage. The transcription factor NF-κB regulates expression of many pro-inflammatory cytokines, but basal and induced activation of NF-κB in different cardiac cell types have not been compared. Here, we used primary cultures of cardiac myocytes and cardiac fibroblasts to identify cardiac cell type-specific events. We show that while viral infection readily stimulates activation of NF-κB in cardiac fibroblasts, cardiac myocytes are largely recalcitrant to activation of NF-κB. Moreover, we show that cardiac myocyte subpopulations differ in their NF-κB subcellular localization and identify the cis-Golgi as a cardiac myocyte-specific host compartment. Together, results indicate that NF-κB-dependent signaling in the heart is cardiac cell type-specific, likely reflecting mechanisms that have evolved to balance responses that can be either protective or damaging to the heart.}, journal={VIROLOGY}, author={Rivera-Serrano, Efrain E. and Sherry, Barbara}, year={2017}, month={Feb}, pages={133–143} }
 @article{rivera-serrano_deangelis_sherry_2017, title={Spontaneous activation of a MAVS-dependent antiviral signaling pathway determines high basal interferon-beta expression in cardiac myocytes}, volume={111}, DOI={10.1016/j.yjmcc.2017.08.008}, abstractNote={Viral myocarditis is a leading cause of sudden death in young adults as the limited turnover of cardiac myocytes renders the heart particularly vulnerable to viral damage. Viruses induce an antiviral type I interferon (IFN-α/β) response in essentially all cell types, providing an immediate innate protection. Cardiac myocytes express high basal levels of IFN-β to help pre-arm them against viral infections, however the mechanism underlying this expression remains unclear. Using primary cultures of murine cardiac and skeletal muscle cells, we demonstrate here that the mitochondrial antiviral signaling (MAVS) pathway is spontaneously activated in unstimulated cardiac myocytes but not cardiac fibroblasts or skeletal muscle cells. Results suggest that MAVS association with the mitochondrial-associated ER membranes (MAM) is a determinant of high basal IFN-β expression, and demonstrate that MAVS is essential for spontaneous high basal expression of IFN-β in cardiac myocytes and the heart. Together, results provide the first mechanism for spontaneous high expression of the antiviral cytokine IFN-β in a poorly replenished and essential cell type.}, journal={Journal of Molecular and Cellular Cardiology}, author={Rivera-Serrano, E. E. and DeAngelis, N. and Sherry, B.}, year={2017}, pages={102–113} }
 @article{stebbing_irvin_rivera-serrano_boehme_ikizler_yoder_dermody_sherry_lyles_2013, title={An ITAM in a Nonenveloped Virus Regulates Activation of NF- B, Induction of Beta Interferon, and Viral Spread}, volume={88}, ISSN={0022-538X}, url={http://dx.doi.org/10.1128/JVI.02573-13}, DOI={10.1128/jvi.02573-13}, abstractNote={ABSTRACT}, number={5}, journal={Journal of Virology}, publisher={American Society for Microbiology}, author={Stebbing, R. E. and Irvin, S. C. and Rivera-Serrano, E. E. and Boehme, K. W. and Ikizler, M. and Yoder, J. A. and Dermody, T. S. and Sherry, B. and Lyles, D. S.}, year={2013}, month={Dec}, pages={2572–2583} }
 @article{rivera-serrano_rodriguez-welsh_hicks_rojas-pierce_2012, title={A Small Molecule Inhibitor Partitions Two Distinct Pathways for Trafficking of Tonoplast Intrinsic Proteins in Arabidopsis}, volume={7}, ISSN={["1932-6203"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-84866026793&partnerID=MN8TOARS}, DOI={10.1371/journal.pone.0044735}, abstractNote={Tonoplast intrinsic proteins (TIPs) facilitate the membrane transport of water and other small molecules across the plant vacuolar membrane, and members of this family are expressed in specific developmental stages and tissue types. Delivery of TIP proteins to the tonoplast is thought to occur by vesicle–mediated traffic from the endoplasmic reticulum to the vacuole, and at least two pathways have been proposed, one that is Golgi-dependent and another that is Golgi-independent. However, the mechanisms for trafficking of vacuolar membrane proteins to the tonoplast remain poorly understood. Here we describe a chemical genetic approach to unravel the mechanisms of TIP protein targeting to the vacuole in Arabidopsis seedlings. We show that members of the TIP family are targeted to the vacuole via at least two distinct pathways, and we characterize the bioactivity of a novel inhibitor that can differentiate between them. We demonstrate that, unlike for TIP1;1, trafficking of markers for TIP3;1 and TIP2;1 is insensitive to Brefeldin A in Arabidopsis hypocotyls. Using a chemical inhibitor that may target this BFA-insensitive pathway for membrane proteins, we show that inhibition of this pathway results in impaired root hair growth and enhanced vacuolar targeting of the auxin efflux carrier PIN2 in the dark. Our results indicate that the vacuolar targeting of PIN2 and the BFA-insensitive pathway for tonoplast proteins may be mediated in part by common mechanisms.}, number={9}, journal={PLOS ONE}, publisher={Public Library of Science (PLoS)}, author={Rivera-Serrano, Efrain E. and Rodriguez-Welsh, Maria F. and Hicks, Glenn R. and Rojas-Pierce, Marcela}, editor={Damme, Els J. M.Editor}, year={2012}, month={Sep} }