Fig. 1: Kinase activation is crucial in enhancing NHE1 activity in AML. | Leukemia

Fig. 1: Kinase activation is crucial in enhancing NHE1 activity in AML.

From: Regulation of proton partitioning in kinase-activating acute myeloid leukemia and its therapeutic implication

Fig. 1

A Volcano plot of kinase overexpression (–log(p value) against change in pHi in HEK293, each dot represents one kinase, red dots indicated those kinases that significantly raised the pHi (n = 3). B Heatmap showing pHi of HEK293 that increased with kinase overexpression and was reduced by HMA treatment in vitro (n = 3). C Thirteen kinases raised pHi of cord blood progenitors in vitro (n = 3). D, E NHE1 overexpression enhanced D pHi increase and E growth of cord blood progenitors upon leukemic alleles or kinases overexpression in vitro (FLT3-ITD, KRASG12D, and BTK), but not with MLL-AF9 or CDK4 (n = 3–5). F Representative western blot analysis of phosphoserine 14-3-3 (pSer 14-3-3) and NHE1 in NHE1 immunoprecipitation (IP) eluate from cord blood progenitors upon leukemic alleles or kinase overexpression. The numbers representing the level of NHE1 phosphorylation (intensity of pSer 14-3-3 signal normalized by NHE1 in NHE1 IP eluate) are summarized in panel G. G FLT3-ITD, KRASG12D, and BTK, but not MLL-AF9 or CDK4 increased the level of NHE1 phosphorylation in cord blood progenitors (n = 3).

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