Tsonwin Hai
Affiliations: | Ohio State University, Columbus, Columbus, OH |
Area:
Molecular Biology, Cell BiologyGoogle:
"Tsonwin Hai"
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Publications
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| Bambouskova M, Gorvel L, Lampropoulou V, et al. (2018) Electrophilic properties of itaconate and derivatives regulate the IκBζ-ATF3 inflammatory axis. Nature |
| Wang Z, He Y, Deng W, et al. (2017) Atf3 deficiency promotes genome instability and spontaneous tumorigenesis in mice. Oncogene |
| Chang YS, Jalgaonkar SP, Middleton JD, et al. (2017) Stress-inducible gene Atf3 in the noncancer host cells contributes to chemotherapy-exacerbated breast cancer metastasis. Proceedings of the National Academy of Sciences of the United States of America |
| Kalfon R, Koren L, Aviram S, et al. (2016) ATF3 expression in cardiomyocytes preserves homeostasis in the heart and controls peripheral glucose tolerance. Cardiovascular Research |
| Fernández-Verdejo R, Vanwynsberghe AM, Essaghir A, et al. (2016) Activating transcription factor 3 attenuates chemokine and cytokine expression in mouse skeletal muscle after exercise and facilitates molecular adaptation to endurance training. Faseb Journal : Official Publication of the Federation of American Societies For Experimental Biology |
| Rau KK, Hill CE, Harrison BJ, et al. (2016) Cutaneous tissue damage induces long-lasting nociceptive sensitization and regulation of cellular stress- and nerve injury-associated genes in sensory neurons. Experimental Neurology |
| Brajkovic S, Ferdaoussi M, Pawlowski V, et al. (2016) Islet Brain 1 Protects Insulin Producing Cells against Lipotoxicity. Journal of Diabetes Research. 2016: 9158562 |
| Mallano T, Palumbo-Zerr K, Zerr P, et al. (2016) Activating transcription factor 3 regulates canonical TGFβ signalling in systemic sclerosis. Annals of the Rheumatic Diseases. 75: 586-92 |
| Barbarov Y, Timaner M, Alishekevitz D, et al. (2015) Host JDP2 expression in the bone marrow contributes to metastatic spread. Oncotarget. 6: 37737-49 |
| Koren L, Alishekevitz D, Elhanani O, et al. (2015) ATF3-dependent cross-talk between cardiomyocytes and macrophages promotes cardiac maladaptive remodeling. International Journal of Cardiology. 198: 232-40 |