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Marco Conti

Researcher at University of California, San Francisco

Publications -  262
Citations -  23964

Marco Conti is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Phosphodiesterase & Oocyte. The author has an hindex of 88, co-authored 250 publications receiving 22421 citations. Previous affiliations of Marco Conti include University of California, Berkeley & University of California.

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Biochemistry and Physiology of Cyclic Nucleotide Phosphodiesterases: Essential Components in Cyclic Nucleotide Signaling

TL;DR: Some of the major concepts related to the understanding of PDE function and regulation are reviewed including the structure of catalytic and regulatory domains and arrangement in holoenzymes, the nature and function of negative and positive feedback circuits that have been conserved in PDEs from prokaryotes to human, and the emerging association of mutant PDE alleles with inherited diseases.
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EGF-like growth factors as mediators of LH action in the ovulatory follicle.

TL;DR: It is demonstrated that LH stimulation induces the transient and sequential expression of the epidermal growth factor (EGF) family members amphiregulin, epire gulin, and beta-cellulin, which are paracrine mediators that propagate the LH signal throughout the follicle.
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Phosphodiesterase 4D Deficiency in the Ryanodine-Receptor Complex Promotes Heart Failure and Arrhythmias

TL;DR: It is shown that PDE4D gene inactivation in mice results in a progressive cardiomyopathy, accelerated heart failure after myocardial infarction, and cardiac arrhythmias, and data suggest that reduced PDE 4D activity causes defective RyR2-channel function associated with heart failure and arrh rhythmias.
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Targeting of Cyclic AMP Degradation to β2-Adrenergic Receptors by β-Arrestins

TL;DR: It is shown that β-arrestins coordinate both processes by recruiting PDEs to activated β2-adrenergic receptors in the plasma membrane of mammalian cells by simultaneously slowing the rate of cAMP production through receptor desensitization and increasing the rates of its degradation at the membrane.