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L. Ercolani

Researcher at Harvard University

Publications -  36
Citations -  1735

L. Ercolani is an academic researcher from Harvard University. The author has contributed to research in topics: G protein & Heterotrimeric G protein. The author has an hindex of 20, co-authored 36 publications receiving 1719 citations. Previous affiliations of L. Ercolani include University of Iowa Hospitals and Clinics & United States Department of Veterans Affairs.

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Isolation and complete sequence of a functional human glyceraldehyde-3-phosphate dehydrogenase gene.

TL;DR: The isolated and sequenced 5.4 kilobase pairs of a 12-kilobase pair human genomic clone encoding a functional GAPDH gene strongly suggest that the human genome encodes a single functional GAPSH gene.
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A heterotrimeric G protein, G alpha i-3, on Golgi membranes regulates the secretion of a heparan sulfate proteoglycan in LLC-PK1 epithelial cells.

TL;DR: Evidence is provided for a novel role for the pertussis toxin sensitive G alpha i-3 protein in Golgi trafficking of a constitutively secreted protein in epithelial cells.
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An insulin response element in the glyceraldehyde-3-phosphate dehydrogenase gene binds a nuclear protein induced by insulin in cultured cells and by nutritional manipulations in vivo.

TL;DR: Two independent cis-acting insulin response elements in the gene encoding glyceraldehyde-3-phosphate dehydrogenase are sufficient to direct insulin-inducible gene expression and may represent a sequence recognized by at least one class of insulin-sensitive transcription factor(s).
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Membrane localization of the pertussis toxin-sensitive G-protein subunits alpha i-2 and alpha i-3 and expression of a metallothionein-alpha i-2 fusion gene in LLC-PK1 cells.

TL;DR: The findings suggest that alpha i subunit specificity for effectors may be achieved in polarized renal epithelial cells by their geographic segregation to different cellular membranes.
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Heterotrimeric G proteins, vesicle trafficking, and CFTR Cl- channels

TL;DR: The hypothesis that heterotrimeric G proteins regulate vesicle trafficking and exocytosis and that these events are critical for cAMP activation of CFTR-mediated Cl- secretion is tested and inhibition of G alpha i-2 may be a useful therapeutic approach to target mutant delta F508 CFTR Cl- channels from an intracellular vesicular pool to the plasma membrane.