Results 181 to 190 of about 9,380 (213)

A heteromeric TRP channel that functions as a WNT-activated G protein-coupled receptor. [PDF]

Nat Commun
Hardy EP, Haider AN, Patel MM, Nesin V, Hoang HTM, Gostynska SE, Berry WL, Pioszak AA, Ahmad M, Parnell SC, Tsiokas L.   +10 more
europepmc   +1 more source

GRKs phosphorylate GPCR C-terminal peptides in a hierarchical manner

Löbbert A, Lorz N, Matthees ESF, Rößler P, Hoffmann C, Gossert AD.   +5 more
europepmc   +1 more source

P-Rex1 Limits the Agonist-Induced Internalisation of GPCRs Independently of its Rac-GEF Activity

Baker MJ, Hampson E, Islam P, Pelaez Moral R, Maunders EA, Hornigold K, Tsonou E, Hornigold DC, Hubbard RE, Massey AJ, Welch HCE.   +10 more
europepmc   +1 more source

Integrating GRK2 and NFkappaB in the Pathophysiology of Cardiac Hypertrophy

Journal of Cardiovascular Translational Research, 2015
G protein coupled receptor kinase type 2 (GRK2) plays an important role in the development and maintenance of cardiac hypertrophy and heart failure even if its exact role is still unknown. In this study, we assessed the effect of GRK2 on the regulation of cardiac hypertrophy.
Daniela Sorriento, Gaetano Santulli, Antonietta Franco   +2 more
exaly   +7 more sources

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Abstract 166: Identification of Grk2 as novel oncology target and development of potent Grk2 inhibitors

Cancer Research, 2022
Abstract G Protein-Coupled Receptor Kinase 2 (Grk2) is a serine-threonine kinase widely expressed in the human body. The GRK family of kinases is known for its role in GPCR phosphorylation and desensitization upon GPCR activation by agonists.
Alexandra Lantermann, Eugene Chekler, Bruce Lefker, Garmen Yuen, Vanessa Lam, Matthew Strickland, Justyne Pennacchio, Aaron Fulgham, Dara Bree, Thomas Perekslis, Grazia Piizzi, Hongyue Dai, Tim Zheng, John Wagner, Pearl Huang   +14 more
openaire   +1 more source

GRK2 at the Control Shaft of Cellular Metabolism

Current Pharmaceutical Design, 2012
G protein receptor kinase 2 (GRK2) has been for years mainly considered the negative regulator of the cardiac β adrenergic signaling. However GRK2 is a ubiquitous molecule and its kinase activity and scaffold properties brought to several investigations which have evidenced its involvement in pathophysiology of extra-cardiac diseases. Later discoveries,
CICCARELLI, Michele, E. Cipolletta, IACCARINO, Guido   +2 more
openaire   +5 more sources

GRK2 as a therapeutic target for heart failure

Expert Opinion on Therapeutic Targets, 2017
G protein-coupled receptor (GPCR) kinase-2 (GRK2) is a regulator of GPCRs, in particular β-adrenergic receptors (ARs), and as demonstrated by decades of investigation, it has a pivotal role in the development and progression of cardiovascular disease, like heart failure (HF).
Cannavo, Alessandro, Komici, Klara, Bencivenga, Leonardo, D’amico, Maria Loreta, Gambino, Giuseppina, Liccardo, Daniela, Ferrara, Nicola, Rengo, Giuseppe   +7 more
openaire   +4 more sources

An essential role for Grk2 in Hedgehog signalling downstream of Smoothened [PDF]

EMBO Reports, 2016
Abstract The G‐protein‐coupled receptor kinase 2 (adrbk2/ GRK 2) has been implicated in vertebrate Hedgehog (Hh) signalling based on the effects of its transient knock‐down in mammalian cells and zebrafish embryos.
Raymond Teck Ho Lee, Ganesh V Pusapati, Rajat Rohatgi   +2 more
exaly   +4 more sources

GRK2, a novel regulator of skeletal development

The FASEB Journal, 2022
STUDY OBJECTIVE During skeletal development, the cartilaginous growth plate (GP) allows for bone elongation, composed of chondrocytes organized into three histological zones: resting (RZ), proliferative (PZ), and hypertrophic (HZ).
Natalie K. Yoshioka, Vengadeshprabhu Karuppagounder, William J. Pinamont, Gina M. Deiter, Reyad A. Elbarbary, Maurizio Pacifici, Fadia Kamal   +6 more
openaire   +1 more source

GRK2 interacts with and phosphorylates Nedd4 and Nedd4-2

Biochemical and Biophysical Research Communications, 2007
Epithelial Na(+) channels (ENaC) mediate the transport of sodium (Na) across epithelia in the kidney, gut, and lungs and are required for blood pressure regulation. They are inhibited by ubiquitin protein ligases, such as Nedd4 and Nedd4-2, which bind to proline-rich motifs (PY motifs) present in the C-termini of ENaC subunits. Loss of inhibition leads
Sanchez-Perez, A., Kumar, S., Cook, D.
openaire   +3 more sources