Regulating cellular cyclic adenosine monophosphate: "Sources," "sinks," and now, "tunable valves".
cyclic AMP
guanine exchange modulators (GEMs)
noncanonical
phosphodiesterases
trimeric GTPases
Journal
Wiley interdisciplinary reviews. Systems biology and medicine
ISSN: 1939-005X
Titre abrégé: Wiley Interdiscip Rev Syst Biol Med
Pays: United States
ID NLM: 101516550
Informations de publication
Date de publication:
09 2020
09 2020
Historique:
received:
01
09
2019
revised:
31
01
2020
accepted:
31
03
2020
pubmed:
24
4
2020
medline:
21
10
2021
entrez:
24
4
2020
Statut:
ppublish
Résumé
A number of hormones and growth factors stimulate target cells via the second messenger pathways, which in turn regulate cellular phenotypes. Cyclic adenosine monophosphate (cAMP) is a ubiquitous second messenger that facilitates numerous signal transduction pathways; its production in cells is tightly balanced by ligand-stimulated receptors that activate adenylate cyclases (ACs), that is, "source" and by phosphodiesterases (PDEs) that hydrolyze it, that is, "sinks." Because it regulates various cellular functions, including cell growth and differentiation, gene transcription and protein expression, the cAMP signaling pathway has been exploited for the treatment of numerous human diseases. Reduction in cAMP is achieved by blocking "sources"; however, elevation in cAMP is achieved by either stimulating "source" or blocking "sinks." Here we discuss an alternative paradigm for the regulation of cellular cAMP via GIV/Girdin, the prototypical member of a family of modulators of trimeric GTPases, Guanine nucleotide Exchange Modulators (GEMs). Cells upregulate or downregulate cellular levels of GIV-GEM, which modulates cellular cAMP via spatiotemporal mechanisms distinct from the two most often targeted classes of cAMP modulators, "sources" and "sinks." A network-based compartmental model for the paradigm of GEM-facilitated cAMP signaling has recently revealed that GEMs such as GIV serve much like a "tunable valve" that cells may employ to finetune cellular levels of cAMP. Because dysregulated signaling via GIV and other GEMs has been implicated in multiple disease states, GEMs constitute a hitherto untapped class of targets that could be exploited for modulating aberrant cAMP signaling in disease states. This article is categorized under: Models of Systems Properties and Processes > Mechanistic Models Biological Mechanisms > Cell Signaling.
Identifiants
pubmed: 32323924
doi: 10.1002/wsbm.1490
pmc: PMC7581534
mid: NIHMS1586042
doi:
Substances chimiques
Phosphodiesterase Inhibitors
0
Cyclic AMP
E0399OZS9N
ErbB Receptors
EC 2.7.10.1
Phosphoric Diester Hydrolases
EC 3.1.4.-
GTP Phosphohydrolases
EC 3.6.1.-
Adenylyl Cyclases
EC 4.6.1.1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
e1490Subventions
Organisme : NIBIB NIH HHS
ID : T32 EB009380
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA160911
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI141630
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA238042
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK099226
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA100768
Pays : United States
Organisme : NIDDK NIH HHS
ID : T32 DK007202
Pays : United States
Informations de copyright
© 2020 Wiley Periodicals LLC.
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