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Jacek Ostrowski

Researcher at Howard Hughes Medical Institute

Publications -  17
Citations -  645

Jacek Ostrowski is an academic researcher from Howard Hughes Medical Institute. The author has contributed to research in topics: Retinoic acid receptor & G protein-coupled receptor. The author has an hindex of 10, co-authored 17 publications receiving 637 citations. Previous affiliations of Jacek Ostrowski include Bristol-Myers Squibb.

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A small region of the beta-adrenergic receptor is selectively involved in its rapid regulation.

TL;DR: A small, hitherto unappreciated region of the receptor molecule may selectively subserve its rapid regulation, and with the demonstration that beta 2AR does not have to be phosphorylated or sequestered in order to enter the down-regulation pathway, the results suggest that the classical receptor endocytosis model may not be appropriate for Beta 2AR regulation.
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Antagonism of Catecholamine Receptor Signaling by Expression of Cytoplasmic Domains of the Receptors

TL;DR: Coexpression of the third intracellular loop of the alpha 1B-adrenergic receptor with its parent receptor inhibited receptor-mediated activation of phospholipase C, suggesting that the receptor-G protein interface may represent a target for receptor antagonist drugs.
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Cell-type and promoter-context dependent retinoic acid receptor (RAR) redundancies for RAR beta 2 and Hoxa-1 activation in F9 and P19 cells can be artefactually generated by gene knockouts

TL;DR: It is demonstrated that the expression of RARbeta2 is auto-inducible in RARgamma-/- but not in wild-type F9 cells, indicating that the functional redundancies observed between RARs in gene disruption studies can be artefactually generated.
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Molecular characterization of the cysJIH promoters of Salmonella typhimurium and Escherichia coli: regulation by cysB protein and N-acetyl-L-serine.

TL;DR: In strains carrying plasmids containing the S. typhimurium cysJIH region, the highest levels of primer extension products were found with RNA from cells grown on L-cystine, even though levels of the proteins encoded by cysj and cysI were normally repressed.
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Cloning and sequence analysis of the human β1-adrenergic receptor 5′-flanking promoter region

TL;DR: These putative hormone response elements support physiological evidence that thyroid and glucocorticoid hormones regulate beta 1AR function by affecting receptor expression in tissues such as heart and adipose, where beta 1-adrenergic receptors are important regulators of heart rate and lipolysis, respectively.