Polycystin-1 is required for insulin-like growth factor 1-induced cardiomyocyte hypertrophy

Cardiac hypertrophy is the result of responses to various physiological or pathological stimuli. Recently, we showed that polycystin-1 participates in cardiomyocyte hypertrophy elicited by pressure overload and mechanical stress. Interestingly, polycystin-1 knockdown does not affect phenylephrine-in...

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Veröffentlicht in:	PloS one 2021-08, Vol.16 (8), p.e0255452
Hauptverfasser:	Fernández, Carolina, Torrealba, Natalia, Altamirano, Francisco, Garrido-Moreno, Valeria, Vásquez-Trincado, César, Flores-Vergara, Raúl, López-Crisosto, Camila, Ocaranza, María Paz, Chiong, Mario, Pedrozo, Zully, Lavandero, Sergio
Format:	Artikel
Sprache:	eng
Schlagworte:	AKT protein Analysis Animals Antibodies Biology and Life Sciences Cardiology Cardiomegaly - genetics Cardiomegaly - metabolism Cardiomegaly - pathology Cardiomyocytes Cells, Cultured Chronic illnesses Deregulation Diagnosis Gene expression Gene Knockdown Techniques Growth factors Health aspects Heart enlargement Hypertrophy Insulin Insulin-like growth factor 1 Insulin-like growth factor I Insulin-Like Growth Factor I - metabolism Insulin-like growth factors Insulin-Like Peptides Internal medicine Kinases Laboratory animals Medical research Medicine Medicine and Health Sciences Metabolism Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Pharmaceutical sciences Phenylephrine Phosphatase Phosphorylation Physical Sciences Physiology Polycystic kidney disease 1 protein Protein Tyrosine Phosphatase, Non-Receptor Type 1 - genetics Protein Tyrosine Phosphatase, Non-Receptor Type 1 - metabolism Protein-tyrosine-phosphatase Proteins Proto-Oncogene Proteins c-akt - metabolism Rats Receptor, IGF Type 1 - genetics Receptor, IGF Type 1 - metabolism Receptors Signal Transduction TRPP Cation Channels - genetics TRPP Cation Channels - metabolism Tyrosine
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