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Knockdown of Clk4 leads to pathological cardiomyocyte hypertrophy, but overexpression of Clk4 grants countermeasures to phenylephrine-induced cardiomyocyte hypertrophy. The direct substrate of CLK4's CLK4 cells, nexilin, has been identified as the direct substrate of CLK4, and the overexpression of a phosphorylation-mimic mutant of NEXN is sufficient to reverse cardiomyocytes' hypertrophic growth triggered by Clk4 knockdown. We conclude that CLK4 controls cardiac function by phosphorylation of NEXN, and that a lack of NEXN may cause pathological cardiac hypertrophy.
Source link: https://europepmc.org/article/MED/35907876
By Cdc42, we investigated baseline and left ventricular pressure overload responses in a MLK3 CRIB mutant mouse with point mutations in the CRIB domain, disrupting MLK3 transcription by Cdc42. Compared to wild type littermate controls, male and female MLK3 C/C mice's increased invasively measured blood pressure. MLK3 C/C mice, map3k11 mRNA, which codes for MLK3, and MLK3 protein were reduced by 74 % and 77 percent, respectively. JNK activation was also reduced in MLK3 C/C TAC mice's LV tissue, which was also reduced. MLK3 translocation was determined by TAC and membrane fraction in LV tissue from MLK3 +/+ but not MLK3 C/C mice. MLK3 CRIB domain is involved in MLK3's regulation of basal blood pressure and cardiac morphology, as well as promoting LV response to pressure overload, according to these results.
Source link: https://europepmc.org/article/MED/35867711
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