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We have examined whether antisense morpholino oligonucleotides (morpholinos) can be used as a tool to suppress or 'knockdown' the expression of ion channels during development of the zebrafish.
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In mutation and knockout models of the voltage-gated sodium channels, perturbation of channel function during development impairs nervous system structure and function, underlining the importance of these channels in neurodevelopment.
Because of the importance of voltage-activated K+ channels during embryonic development and in cell proliferation, we present here the first description of these channels in E15 rat embryonic neural progenitor cells derived from the subventricular zone (SVZ).
The exception was a case of SWOPP accompanied by bifid tail of the pancreas [ 11], which is a congenital anomaly where the primitive pancreatic channels fail to fuse into a single main duct during development of the pancreas.
Significant changes of sodium channel expression during development were detected.
These data are consistent with previous reports of the Kcnq1 channel expressed during development [ 22].
Ion channel expression alters during development.
Additional functional experiments are required to characterize the roles of calcium channels during avian skin development.
Fig. 3 shows co-localization of both hybrid constructs in cytoplasmic vesicles (likely representing ER vesicles) and at the membrane, suggesting that Cx26 and Cx32 were in principle able to form heteromeric channels during early frog development.
Together, these results provide new insights into the role of voltage-gated Ca2+ channels in nonexcitable cells during development.
The loss or inactivation of these channels during ageing and/or hypertension development could be seen as a pathological mechanism.
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