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We have investigated Ca2+ signalling generated by aldosterone-induced T-type current (ICaT), the effects of ICaT in neonatal cardiomyocytes, and a putative role for ICaT in cardiomyocytes during cardiac pathology induced by stenosis in an adult rat.
The parameter analysis revealed the critical role of ICaT in assuring the robustness of mouse SAN pacemaking activities.
The reappearance of ICaT in adult cardiomyocytes was reported, in association with several aetiologies of ventricular hypertrophy.
These findings implicate ICaT in the regulation of CREB-dependent gene expression and ICaT/PP2A/CREB signalling in promoting apoptosis.
The time kinetics of ICaT were derived from experimental data (22) in previous models of ICaT in the rabbit SAN.
Of these, 511 proteins were labeled by both the light and heavy isoform of ICAT, in both biological replicates.
Similar(48)
Therefore, ICAT depletion in NSCs in ECM by transfection with miR-29b or siICAT predominantly promotes differentiation toward intermediate progenitor cells via nuclear β-catenin.
2DE or SELDI-TOF was used in the previous studies while we adapted ICAT strategy in this study.
We only considered cysteine residues that were labeled with both light and heavy ICAT labels in at least three biological replicates out of five.
To test the quantitative performance on our complex protein samples, we analyzed peptides, labeled with either heavy or light cleavable ICAT, mixed in different defined ratios.
We show here that, in neonatal cardiomyocytes, aldosterone-induced increase in ICaT density results mostly from an increase in Cav3.1 expression.
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