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Santhana G. T. Devaraj

Researcher at Houston Methodist Hospital

Publications -  20
Citations -  1563

Santhana G. T. Devaraj is an academic researcher from Houston Methodist Hospital. The author has contributed to research in topics: Panobinostat & Histone deacetylase inhibitor. The author has an hindex of 10, co-authored 20 publications receiving 1376 citations. Previous affiliations of Santhana G. T. Devaraj include University of Texas Medical Branch.

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Regulation of IRF-3-dependent Innate Immunity by the Papain-like Protease Domain of the Severe Acute Respiratory Syndrome Coronavirus *

TL;DR: It is shown here that infection of SARS-CoV triggers a weak IFN response in cultured human lung/bronchial epithelial cells without inducing the phosphorylation of IFN-regulatory factor 3 (IRF-3), a latent cellular transcription factor that is pivotal for type I IFN synthesis.
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Highly effective combination of LSD1 (KDM1A) antagonist and pan-histone deacetylase inhibitor against human AML cells

TL;DR: The combination of LSD1 antagonist and pan-HDI is a promising therapy warranting further testing against AML, and co-treatment with SP2509 and PS significantly improved the survival of the mice engrafted with the human AML cells, without exhibiting any toxicity.
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Toll-Like Receptor 3 Mediates Establishment of an Antiviral State against Hepatitis C Virus in Hepatoma Cells

TL;DR: It is shown that primary human hepatocytes express TLR3 and robustly upregulate ISGs upon poly(I·C) stimulation and thatTLR3 senses hepatitis C virus (HCV) infection when expressed in permissive hepatoma cells, acting independently of retinoic acid-inducible gene I and inducing IRF-3 activation and the synthesis of ISGs that restrict virus replication.
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Highly Active Combination of BRD4 Antagonist and Histone Deacetylase Inhibitor against Human Acute Myelogenous Leukemia Cells

TL;DR: The sensitizing effects of the histone hyperacetylation-inducing pan–histone deacetylase (HDAC) inhibitor panobinostat on human acute myelogenous leukemia (AML) blast progenitor cells (BPC) to the BET protein antagonist JQ1 are demonstrated.
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Histone deacetylase inhibitor treatment induces ‘BRCAness’ and synergistic lethality with PARP inhibitor and cisplatin against human triple negative breast cancer cells

TL;DR: Findings presented here demonstrate that by attenuating the levels of DNA damage response and homologous recombination proteins, pan-histone deacetylase inhibitor (HDI) treatment induces ‘BRCAness’ and sensitizes TNBC cells lacking BRCA1 to lethal effects of PARP inhibitor or cisplatin.