Nitish R. Mahapatra

TL;DR: Loss of the physiological "brake" catestatin in Chga mice coupled with dysregulation of transmitter storage and release may act in concert to alter autonomic control of the circulation in vivo, eventuating in hypertension.

TL;DR: A surprising pattern of CHGA variants is shown that alter the expression and function of this gene, both in vivo and in vitro, including rare alleles that qualitatively change the encoded product to alter the signaling potency ofCHGA-derived catecholamine release-inhibitory catestatin peptides.

TL;DR: Rank order of variant inhibitory potency for all four nicotinic processes was identical, suggesting mediation by similar combinations of receptor α/β subunits and that crucial catestatin residues are likely to be identical across the four processes.

TL;DR: Nicotinic cholinergic stimulus-transcription coupling occurs in vivo and can be provoked either directly or indirectly (by vesicular transmitter depletion).

TL;DR: It is established that a CgA-GFP fusion protein expressed in neuroendocrine PC12 cells is trafficked to the dense core secretory granule and thereby sorted to the regulated pathway for exocytosis and the data reveal for the first time that the CGA77-115 domain of the mature protein may be necessary (though perhaps not sufficient) for trafficking C gA into the regulated pathways of secretion.