LMK-235 induces the differentiation of odontoblasts in dental pulp cells. It plays an important role in the regeneration of dental tissue.[1]
LMK235 is a histone deacetylase (HDAC) inhibitor with greater potency against HDAC4 and HDAC5 (IC50 = 11.9 and 4.2 nM, respectively) than other HDAC family members (IC50 values = HDAC1 320 nM, HDAC2 881 nM, HDAC6 55.7 nM, and HDAC8 1278 nM). LMK235 potentiates the cytotoxic effects of cisplatin, and sensitizes platinum-drug resistant tumor cell lines to cisplatin toxicity.
LMK235 is a histone deacetylase (HDAC) inhibitor; HDAC4- and HDAC5-preferring.
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Brain research bulletin, 162, 151-165 (2020-06-28)
Epigenetic processes play important roles in brain responses to ischemic injury. We studied effects of photothrombotic stroke (PTS, a model of ischemic stroke) on the intracellular level and cellular localization of histone deacetylases HDAC3, HDAC4 and HDAC6 in the rat
Human hematopoietic stem cells (HSCs) exhibit attrition of their self-renewal capacity when cultured ex vivo, a process that is partially reversed upon treatment with epigenetic modifiers, most notably inhibitors of histone deacetylases (HDACs) or lysine-specific demethylase LSD1. A recent study showed
The causative agent of the coronavirus disease 2019 (COVID-19) pandemic, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has infected millions and killed hundreds of thousands of people worldwide, highlighting an urgent need to develop antiviral therapies. Here we present a
Bone marrow failure (BMF) in Fanconi anemia (FA) patients results from dysfunctional hematopoietic stem and progenitor cells (HSPCs). To identify determinants of BMF, we performed single-cell transcriptome profiling of primary HSPCs from FA patients. In addition to overexpression of p53
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