Molecular mechanisms of Kat6b in the differentiation of HSCs

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In: Student Reports, Summer 2019, The Jackson Laboratory


As hematopoietic stem cells (HSCs) age, they experience a multitude of changes that affect their epigenetic identity and ultimately their differentiation into erythroid, myeloid, and lymphoid progenitors [Geiger, 2013]. These changes are associated with epigenetic drift, stochastic alterations of epigenetics facilitated by cell division and regulator activity [Bernitz, 2016]. Kat6b is a known epigenetic regulator that acetylates the lysine 23 residue of histone H3 (H3K23ac) in small cell lung cancer [Sim6-Ruidalbas, 2015]. Work from our lab shows that Kat6b regulates differentiation of HSCs to myeloid and erythroid cell types and that the transcript and protein levels of this gene decrease with age in HSCs [Khokhar, 2019]. This study aimed to test the hypothesis that KAT6B is responsible for H3K23ac in murine HSCs. The first step goals of this study were to ensure the specificity of the KAT6B antibody and establish the relationship between KAT6B and H3K23ac in a murine cell line.

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