Nutrient availability controls the landscape of nutrient transporters present at the plasma membrane, notably by regulating their ubiquitylation and subsequent endocytosis. In yeast, this involves the Nedd4 ubiquitin ligase Rsp5 and arrestin-related trafficking adaptors (ARTs). ARTs are targeted by signaling pathways and warrant that cargo ubiquitylation and endocytosis appropriately respond to nutritional inputs. Here, we show that glucose deprivation regulates the ART protein Csr2/Art8 at multiple levels to trigger high-affinity glucose transporter endocytosis. Csr2 is transcriptionally induced in these conditions through the AMPK orthologue Snf1 and downstream transcriptional repressors. Upon synthesis, Csr2 becomes activated by ubiquitylation. In contrast, glucose replenishment induces CSR2 transcriptional shutdown and switches Csr2 to an inactive, deubiquitylated form. This glucose-induced deubiquitylation of Csr2 correlates with its phospho-dependent association with 14-3-3 proteins and involves protein kinase A. Thus, two glucose signaling pathways converge onto Csr2 to regulate hexose transporter endocytosis by glucose availability. These data illustrate novel mechanisms by which nutrients modulate ART activity and endocytosis.

• MeSH
• arrestin genetika   metabolismus   MeSH
• časové faktory MeSH
• endocytóza * MeSH
• genetická transkripce MeSH
• glukosa nedostatek   MeSH
• jaderné proteiny genetika   metabolismus   MeSH
• mutace MeSH
• protein-serin-threoninkinasy metabolismus   MeSH
• proteinfosfatasa 1 metabolismus   MeSH
• proteinkinasy závislé na cyklickém AMP metabolismus   MeSH
• proteiny 14-3-3 metabolismus   MeSH
• proteiny přenášející monosacharidy genetika   metabolismus   MeSH
• regulace genové exprese u hub MeSH
• represorové proteiny metabolismus   MeSH
• Saccharomyces cerevisiae - proteiny genetika   metabolismus   MeSH
• Saccharomyces cerevisiae genetika   metabolismus   MeSH
• ubikvitinace MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• arrestin MeSH
• BMH1 protein, S cerevisiae MeSH Prohlížeč
• BMH2 protein, S cerevisiae MeSH Prohlížeč
• Csr2 protein, S cerevisiae MeSH Prohlížeč
• glukosa MeSH
• Hxt6 protein, S cerevisiae MeSH Prohlížeč
• HXT7 protein, S cerevisiae MeSH Prohlížeč
• jaderné proteiny MeSH
• MIG1 protein, S cerevisiae MeSH Prohlížeč
• Mig2 protein, S cerevisiae MeSH Prohlížeč
• protein-serin-threoninkinasy MeSH
• proteinfosfatasa 1 MeSH
• proteinkinasy závislé na cyklickém AMP MeSH
• proteiny 14-3-3 MeSH
• proteiny přenášející monosacharidy MeSH
• represorové proteiny MeSH
• Saccharomyces cerevisiae - proteiny MeSH
• SNF1-related protein kinases MeSH Prohlížeč

Regulation of G protein coupled receptors (GPCRs) looks to be not only classically lineary regulated but it is now discovered to be a complex network of interconnected proteins. Taking these in mind it is highly probable that there is multilevel system of regulation that is able to maintain control of signaling. We review here main mechanisms of GPCRs regulation.

• MeSH
• arrestin fyziologie   MeSH
• fosforylace MeSH
• lidé MeSH
• proteinkinasy fyziologie   MeSH
• proteiny RGS fyziologie   MeSH
• receptory spřažené s G-proteiny fyziologie   MeSH
• signální transdukce fyziologie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• anglický abstrakt MeSH
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• arrestin MeSH
• proteinkinasy MeSH
• proteiny RGS MeSH
• receptory spřažené s G-proteiny MeSH

The protein-protein interactions that underlie shut-off of the light-activated rhodopsin were studied using synthetic peptides derived from C-terminal region of the rhodopsin. The photoresponses were recorded in whole-cell voltage clamp from rod outer segments (ROS) that were internally dialyzed with an intracellular solution containing the synthetic peptides. This was the first time that synthetic peptides have been used in functionally intact ROS. None of the tested peptides promoted the shut-off of the photolyzed rhodopsin (R) by stimulating the binding of an activated arrestin to non-phosphorylated R, contrary to what was expected from in vitro experiments (Puig et al. FEBS Lett. 362: 185-188, 1995).

• MeSH
• adenosintrifosfát farmakologie   MeSH
• arrestin metabolismus   MeSH
• fosforylace MeSH
• fotolýza MeSH
• ještěři MeSH
• kalmodulin farmakologie   MeSH
• kinetika MeSH
• molekulární sekvence - údaje MeSH
• peptidové fragmenty chemie   farmakologie   MeSH
• rodopsin analogy a deriváty   chemie   metabolismus   farmakologie   MeSH
• sekvence aminokyselin MeSH
• sekvenční homologie MeSH
• skot MeSH
• světlo * MeSH
• zevní segment tyčinky fyziologie   účinky záření   MeSH
• zvířata MeSH
• Check Tag
• skot MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Research Support, U.S. Gov't, P.H.S. MeSH
• Názvy látek
• adenosintrifosfát MeSH
• arrestin MeSH
• kalmodulin MeSH
• metarhodopsins MeSH Prohlížeč
• peptidové fragmenty MeSH
• rodopsin MeSH