ArticleBiochemistry2008
The trans-Golgi proteins SCLIP and SCG10 interact with chromogranin A to regulate neuroendocrine secretion.
Article in Biochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
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- Microtubules, Membranes, and Movement: New Roles for Stathmin-2 in Axon Integrity.Journal of neuroscience research · 2024Review
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- Stathmin-2 Mediates Glucagon Secretion From Pancreatic α-Cells.Frontiers in endocrinology · 2020Article
- Loss of YAP1 defines neuroendocrine differentiation of lung tumors.Cancer science · 2016Article
- Overexpression of SCLIP promotes growth and motility in glioblastoma cells.Cancer biology & therapy · 2015Article
- Cardiac electrical activity in a genomically "humanized" chromogranin a monogenic mouse model with hyperadrenergic hypertension.Journal of cardiovascular translational research · 2014Article
- Dynamic expression of Notch-dependent neurogenic markers in the chick embryonic nervous system.Frontiers in neuroanatomy · 2014Article
- Novel genes upregulated when NOTCH signalling is disrupted during hypothalamic development.Neural development · 2013Article
- HID-1, a new component of the peptidergic signaling pathway.Genetics · 2011Article
- Pro-hormone secretogranin II regulates dense core secretory granule biogenesis in catecholaminergic cells.The Journal of biological chemistry · 2010Article
- Chromogranin A: a novel susceptibility gene for essential hypertension.Cellular and molecular life sciences : CMLS · 2010Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Secretion of proteins and peptides from eukaryotic cells takes place by both constitutive and regulated pathways. Regulated secretion may involve interplay of proteins that are currently unknown. Recent studies suggest an important role of chromogranin A (CHGA) in the regulated secretory pathway in neuroendocrine cells, but the mechanism by which CHGA enters the regulated pathway, or even triggers the formation of the pathway, remains unclear. In this study, we used a transcriptome/proteome-wide approach, to discover binding partners for CHGA, by employing a phage display cDNA library method. Several proteins within or adjacent to the secretory pathway were initially detected as binding partners of recombinant human CHGA. We then focused on the trans-Golgi protein SCLIP (STMN3) and its stathmin paralog SCG10 (STMN2) for functional study. Co-immunoprecipitation experiments confirmed the interaction of each of these two proteins with CHGA in vitro. SCLIP and SCG10 were colocalized to the Golgi apparatus of chromaffin cells in vivo and shared localization with CHGA as it transited the Golgi. Downregulation of either SCLIP or SCG10 by synthetic siRNAs virtually abolished chromaffin cell secretion of a transfected CHGA-EAP chimera (expressing CHGA fused to an enzymatic reporter, and trafficked to the regulated pathway). SCLIP siRNA also decreased the level of secretion of endogenous CHGA and SCG2, as well as transfected human growth hormone, while SCG10 siRNA decreased the level of regulated secretion of endogenous CHGB. Moreover, a dominant negative mutant of SCG10 (Cys 22,Cys 24-->Ala 22,Ala 24) significantly blocked secretion of the transfected CHGA-EAP chimera. A decrease in the buoyant density of chromaffin granules was observed after downregulation of SCG10 by siRNA, suggesting participation of these stathmins in granule formation or maturation. We conclude that SCLIP and SCG10 interact with CHGA, share partial colocalization in the Golgi apparatus, and may be necessary for typical transmitter storage and release from chromaffin cells.
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