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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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
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
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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