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Ryan T. Kendall

Researcher at Medical University of South Carolina

Publications -  9
Citations -  964

Ryan T. Kendall is an academic researcher from Medical University of South Carolina. The author has contributed to research in topics: Signal transduction & Angiotensin II. The author has an hindex of 7, co-authored 9 publications receiving 721 citations. Previous affiliations of Ryan T. Kendall include University of Tennessee Health Science Center.

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Fibroblasts in fibrosis: novel roles and mediators

TL;DR: Many common fibroblast-related features across various physiological and pathological protracted processes are recognized and a new appreciation has emerged for the role of non-cancerous fibro Blast interactions with tumors in cancer progression.
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The β-Arrestin Pathway-selective Type 1A Angiotensin Receptor (AT1A) Agonist [Sar1,Ile4,Ile8]Angiotensin II Regulates a Robust G Protein-independent Signaling Network

TL;DR: The findings suggest that AT1A receptors regulate a robust G protein-independent signaling network that affects protein phosphorylation and autocrine/paracrine prostaglandin production and that these pathways can be selectively modulated by biased ligands that antagonize G protein activation.
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Diversity in arrestin function.

TL;DR: The termination of heptahelical receptor signaling is a multilevel process coordinated, in large part, by members of the arrestin family of proteins, and growing evidence suggests that signalsomes regulate such diverse processes as endocytosis and exocythesis, cell migration, survival, and contractility.
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Arrestin-dependent angiotensin AT1 receptor signaling regulates Akt and mTor-mediated protein synthesis

TL;DR: The results suggest that in vivo, arrestin pathway-selective AT1 receptor agonists may promote cell growth or hypertrophy through arrestin-mediated mechanisms despite their antagonism of G protein signaling.
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Angiotensin II activates NF-κB through AT1A receptor recruitment of β-arrestin in cultured rat vascular smooth muscle cells.

TL;DR: The purpose of the present study was to examine the interrelationship between AT1AR activation, β-arrestin recruitment, and NF-κB activation in the ability of ANG II to increase COX-2 protein synthesis in RASMC.