Tadashi Inagami
Vanderbilt University
427 Papers
7.1K Citations
Tadashi Inagami is an academic researcher from Vanderbilt University. The author has contributed to research in topics: Angiotensin II & Renin–angiotensin system. The author has an hindex of 91, co-authored 426 publications. Previous affiliations of Tadashi Inagami include Yale University & Max Delbrück Center for Molecular Medicine.
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Papers
Domains for G-protein coupling in angiotensin II receptor type I: studies by site-directed mutagenesis.
TL;DR: Results suggest that polar residues in the second cytosolic loop, the carboxy terminal region of the third cytosol loop, and the car boxy terminal cytosoli tail are important for G-protein coupling of AT1 receptor.
Identification of a peptidase which processes atrial natriuretic factor precursor to its active form with 28 amino acid residues in particulate fractions of rat atrial homogenate
TL;DR: With the objective of identifying specific peptidase responsible for the processing of atrial natriuretic factor precursor pro-ANF to the circulating active form ANF (99-126), a fluorometric assay method was devised using synthetic fluorogenic substrate Boc-Ala-Gly-Pro-Arg-MCA(methylcoumarinamide) which contains the amino acid sequence immediately adjacent to the arginyl peptide bond.
Effect of Alkylguanidines on the Inactivation of Trypsin by Alkylation and Phosphorylation
TL;DR: The observed 7- fold increase in catalytic rate coupled with the concomitant 6-fold increase in the rate of alkylation strongly suggests that the binding of methylguanidine to the recognition site of the enzyme alters the reactivity of an imidazole group (groups).
Molecular cloning of a novel angiotensin II receptor isoform involved in phosphotyrosine phosphatase inhibition.
Yoshikazu Kambayashi,S. Bardhan,K. Takahashi,Satoshi Tsuzuki,H Inui,Takao Hamakubo,Tadashi Inagami +6 more
TL;DR: The expressed AT2 receptor mediated angiotensin II-induced inhibition of protein tyrosine phosphatase, an action that was dependent on a pertussis toxin-sensitive G-protein-coupled mechanism in COS-7 cells, and suggested novel functional roles of the renin-angiotens in system in cross-talk with phosphotyrosine signaling by modulating protein phosphotYrosine levels.
Hyporeninemic normoaldosteronism in severe autonomic failure
TL;DR: It is speculated that direct sympathetic innervation is essential for the maintenance of renin, perhaps by providing trophic stimuli.