Hongjiang Wu

TL;DR: This small domain within chromogranin A may contribute to a novel, autocrine, homeostatic (negative-feedback) mechanism controlling catecholamine release from chromaffin cells and neurons.

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: It is demonstrated that chromogranin A is a substrate for the endogenous endoproteases PC1 and furin in vivo, and that such processing influences its trafficking into the regulated secretory pathway; furthermore, lack of change in chromoganin B and secretogran in II cleavage after diminution of PCl suggests that the action of PC1 on chromog Granin A may be specific within the chromog Cranin/secretogranIn protein family.

TL;DR: The results suggest that this complex gene is encoded by exon modules with evolutionary links to homologous modules in other chromogranin/secretogran in protein family members, and that the 5'-flanking region of the gene is sufficient to confer neuroendocrine tissue-specific expression of the chromogrannin A gene.

TL;DR: It is concluded that catestatin is cleaved extensively in vivo, and the peptide is released by exocytosis as demonstrated by radioimmunoassay of size-fractionated chromaffin granules.