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Lysine methylation of histone H3 and H4 has been identified as a promising therapeutic target in treating various cellular diseases.
Furthermore, the epigenetic mechanisms are believed to respond to different chemical and physical agents, and may lead to altered biological pathways associated with cellular diseases.
Post-translational addition of methyl groups to the amino terminal tails of histone proteins regulates cellular gene expression at various stages of development and the pathogenesis of cellular diseases, including cancer.
Further investigations by replacing Suv39H1 chromodomain with other domains from the royal family of proteins can improve the specificity of the H3 K9 sensor capable of detecting mono-, di-, and tri-methylation of the H3 K9 mark discretely to screen small molecule drugs altering a specific degree of H3 K9 methylation implicated in various cellular diseases.
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The fish have enabled scientists to gain a better understanding of gene therapy, cellular disease and molecular biology.
High-throughput imaging (HTI) is a powerful tool in the discovery of cellular disease mechanisms.
Cancer is a cellular disease characterized by the progressive, persistent, abnormal, purposeless, and uncontrolled proliferation of tissues.
To conceptually evaluate this strategy, we generated X-CGD patient-derived induced pluripotent stem cells (iPSCs), which recapitulate the cellular disease phenotype upon granulocytic differentiation.
To better understand functional interplay between trisomy 21 and GATA1 mutations in hematopoiesis, we constructed cellular disease models using human induced pluripotent stem cells (iPSCs) and genome-editing technologies.
Furthermore, expression of the relatively insoluble subunits of simple epithelial keratins carries the risk of protein aggregation induced cellular disease [30]in the event of mutation, imbalance of subunit expression, chemical induced aggregation or deficient degradation [31].
This emphasizes the challenges that lie ahead in translating pure genetic associations into cellular disease mechanism.
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