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< GPCR News < GPCRs in Oncology and Immunology DANGER Signals Activate G-Protein Receptor Kinases Suppressing Neutrophil Function and Predisposing to Infection After Tissue Trauma Published date May 8, 2023 Abstract "Objective: Surgery injures tissue and predisposes to local and systemic infections. We studied injury-induced immune dysfunction seeking novel means to reverse such predisposition. Background: Injury mobilizes primitive 'DANGER signals' (DAMPs) activating innate immunocyte (neutrophils, PMN) signaling and function. Mitochondrial (mt) formyl peptides (FP) activate G-protein coupled receptors (GPCR) like FPR1. mtDNA and heme activate toll-like receptors (TLR9, TLR2/4). GPCR kinases (GRKs) can regulate GPCR activation. Methods: We studied human and mouse PMN signaling elicited by mtDAMPs (GPCR surface expression; protein phosphorylation or acetylation; Ca2+ flux) and antimicrobial functions (cytoskeletal reorganization, chemotaxis (CTX), phagocytosis, bacterial killing) in cellular systems and clinical injury samples. Predicted rescue therapies were assessed in cell systems and mouse injury-dependent pneumonia models. Results: mtFPs activate GRK2, internalizing GPCRs and suppressing CTX. mtDNA suppresses CTX, phagocytosis and killing via TLR9 through a novel, non-canonical mechanism that lacks GPCR endocytosis. Heme also activates GRK2. GRK2 inhibitors like paroxetine restore functions. GRK2 activation via TLR9 prevented actin reorganization, implicating histone deacetylases (HDACs). Actin polymerization, CTX, bacterial phagocytosis and killing were also rescued therefore by the HDAC inhibitor valproate. Trauma repository PMN showed GRK2 activation and cortactin deacetylation which varied with severity and was most marked in patients developing infections. Either GRK2 or HDAC inhibition prevented loss of mouse lung bacterial clearance, but only the combination rescued clearance when given post-injury. Conclusions: Tissue injury-derived DAMPs suppress antimicrobial immunity via canonical GRK2 activation and a novel TLR-activated GRK2 pathway impairing cytoskeletal organization. Simultaneous GRK2/HDAC inhibition rescues susceptibility to infection after tissue injury. Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved." Authors Hyo In Kim , Jinbong Park , David Gallo , Sidharth Shankar , Barbora Konecna , Yohan Han , Valerie Banner-Goodspeed , Krystal R Capers , Seong-Gyu Ko , Leo E Otterbein , Kiyoshi Itagaki , Carl J Hauser. Source Contribute to the GPCR News Coming soon Become a Contributor Classified GPCR News Call for GPCR papers GPCR Industry News Adhesion GPCRs GPCR Events, Meetings, and Webinars Reviews, GPCRs, and more GPCR Binders, Drugs, and more Methods & Updates in GPCR Research GPCRs in Neuroscience GPCRs in Cardiology, Endocrinology, and Taste GPCRs in Oncology and Immunology Structural and molecular insights into GPCR function GPCR Activation and Signaling More from Dr. GPCR Create an account and get our contributors articles in your inbox Subscribe to the Dr. GPCR Monthly Newsletter today! Follow the Dr. GPCR News and get weekly notifications about the GPCR field Share < Previous Next >

< GPCR News < GPCRs in Oncology and Immunology High expression of GPR50 promotes the proliferation, migration and autophagy of hepatocellular carcinoma cells in vitro Published date June 26, 2023 ! Widget Didn’t Load Check your internet and refresh this page. If that doesn’t work, contact us. ! Widget Didn’t Load Check your internet and refresh this page. If that doesn’t work, contact us. ! Widget Didn’t Load Check your internet and refresh this page. If that doesn’t work, contact us. Source Contribute to the GPCR News Coming soon Become a Contributor Classified GPCR News Call for GPCR papers GPCR Industry News Adhesion GPCRs GPCR Events, Meetings, and Webinars Reviews, GPCRs, and more GPCR Binders, Drugs, and more Methods & Updates in GPCR Research GPCRs in Neuroscience GPCRs in Cardiology, Endocrinology, and Taste GPCRs in Oncology and Immunology Structural and molecular insights into GPCR function GPCR Activation and Signaling More from Dr. GPCR Create an account and get our contributors articles in your inbox Subscribe to the Dr. GPCR Monthly Newsletter today! Follow the Dr. GPCR News and get weekly notifications about the GPCR field Share < Previous Next >

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< GPCR News < GPCRs in Oncology and Immunology The EBI2 receptor is coexpressed with CCR5 in CD4+ T cells and boosts HIV-1 R5 replication Published date May 21, 2024 Abstract " Objective: CCR5, a G protein-coupled receptor (GPCR), is used by most HIV strains as a coreceptor. In this study, we looked for other GPCRs able to modify HIV-1 infection. Design: We analyzed the effects of one GPCR coexpressed with CCR5, EBI2, on HIV-1 replicative cycle. Methods: We identified GPCRs expressed in primary CD4+CCR5+ T cells by multi-RT-qPCR. We studied GPCR dimerization by FRET technology. Cell lines expressing EBI2 were established by transduction with HIV vectors. HIV-1 entry was quantified with virions harboring β-lactamase fused to the viral protein vpr, early and late HIV-1 transcriptions by qPCR, NFkB nuclear activation by immunofluorescence and transfection, and viral production by measuring p24 concentration in culture supernatant by ELISA. Results: We showed that EBI2 is naturally expressed in primary CD4+CCR5+ T cells, and that CCR5 and EBI2 heterodimerize. We observed that this coexpression reduced viral entry by 50%. The amount of HIV reverse transcripts was similar in cells expressing or not EBI2. Finally, the presence of EBI2 induced the translocation of NFkB and activated HIV-1 genome expression. Globally, the result was a drastic HIV-1 R5, but not X4, overproduction in EBI2-transduced cells. Conclusions: EBI2 expression in CD4+CCR5+ cells boosts HIV-1 R5 productive infection. As the natural ligand for EBI2 is present in blood and lymphoid tissues, the constant EBI2 activation might increase HIV replication in CD4+ T cells. It might be of interest to test the effect of EBI2 antagonists on the residual viral production persisting in patients aviremic under treatment." Authors Adeline Guigues , Sandrine Gimenez , Clément Mettling , Damien Maurel , Etienne Doumazane , Laurent Prézeau , Vincent François , Pierre Corbeau Source Classified GPCR News More from Dr. GPCR Share < Previous Next >

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< GPCR News < GPCRs in Oncology and Immunology Neutrophils are itching to specialize Published date February 13, 2024 Abstract "Neutrophils are heterogeneous, but the mechanisms underlying their ability to polarize remain unclear. In this issue of Immunity, Gour et al. demonstrate that the GPCR Mrgpra1 and the neuropeptide NPFF, molecules involved in pain and itch, direct neutrophil polarization that impacts host defense and pneumonia susceptibility." Authors Carlos H Hiroki , Bryan G Yipp Source Contribute to the GPCR News Coming soon Become a Contributor Classified GPCR News Call for GPCR papers GPCR Industry News Adhesion GPCRs GPCR Events, Meetings, and Webinars Reviews, GPCRs, and more GPCR Binders, Drugs, and more Methods & Updates in GPCR Research GPCRs in Neuroscience GPCRs in Cardiology, Endocrinology, and Taste GPCRs in Oncology and Immunology Structural and molecular insights into GPCR function GPCR Activation and Signaling More from Dr. GPCR Create an account and get our contributors articles in your inbox Subscribe to the Dr. GPCR Monthly Newsletter today! Follow the Dr. GPCR News and get weekly notifications about the GPCR field Share < Previous Next >

Dr. GPCR Summit 2022 Dr. GPCR Ecosystem Partners Welcome to the official page of the 3rd edition of the Dr. GPCR Summit This year the Summit will be held between October 10th and 16th. You can join us for free when you become a Dr. GPCR Ecosystem site member, which is also free! The content of the Summit will only be available to site-members who must be approved to join us. You can participate: As an attendee by becoming a site member. It only takes a minute, and it's free With your pre-recorded talk By presenting a poster on Wonder By giving a live talk. Space is limited, and we will do our best to accommodate your request For Speakers and presenters: Make sure you are registered as a site member to get access to the entire Summit for Free! Verify that you talk data and time are in your calendar. You can verify it too by checking out the schedule on our website. Live talks should be 30 mins with 15 mins Q/A. Live trainee talks should be 15 mins with 5 mins Q/A. All live talks will be on Zoom, the link will be added to your calendar invite and will be available here on our website but only visible to registered site-members. Similar to previous years: The meeting will be virtual (on Zoom) to host as many participants as possible Live talks will be hosted on Zoom from October 10th to the 14th Trainees are invited to participate by presenting a trainee talk, a poster, or a pre-recorded talk Presentation prizes will be available for the best trainee talks and posters We are also trying out a few new things: Networking and poster sessions on Wonder A full day dedicated to trainee talks Workshops and panel discussions In case you'd like to present your work, you'll need: Become an Ecosystem site member Pick the correct form and submit it before September 30th, 2022 You'll need a 1-minute video abstract in addition to the written version You can always email us with any questions and comments at Hello@DrGPCR.com << Submit your live talk details >> << Submit a pre-recorded talk >> << Submit your poster >> << Live talk schedule >> << Pre-recorded talk list >> << Poster presentation list >> Tags Dr. GPCR Summit Dr. GPCR Summit 2022 Dr. GPCR Summit 2022 Schedule Dr. GPCR Summit 2022 Details Dr. GPCR Summit 2022 Pre-Recorded Talks Dr. GPCR Summit 2022 Live Talks Dr. GPCR Summit 2022 Poster Presentations Submit Pre-Recorded Talk Presentation for Dr. GPCR Summit 2022 Submit Live Talk Presentation for Dr. GPCR Summit 2022 Submit Poster Presentation for Dr. GPCR Summit 2022

< GPCR News < GPCRs in Oncology and Immunology G protein-coupled receptors: A target for microbial metabolites and a mechanistic link to microbiome-immune-brain interactions Published date October 1, 2023 ! Widget Didn’t Load Check your internet and refresh this page. If that doesn’t work, contact us. ! Widget Didn’t Load Check your internet and refresh this page. If that doesn’t work, contact us. ! Widget Didn’t Load Check your internet and refresh this page. If that doesn’t work, contact us. Source Contribute to the GPCR News Coming soon Become a Contributor Classified GPCR News Call for GPCR papers GPCR Industry News Adhesion GPCRs GPCR Events, Meetings, and Webinars Reviews, GPCRs, and more GPCR Binders, Drugs, and more Methods & Updates in GPCR Research GPCRs in Neuroscience GPCRs in Cardiology, Endocrinology, and Taste GPCRs in Oncology and Immunology Structural and molecular insights into GPCR function GPCR Activation and Signaling More from Dr. GPCR Create an account and get our contributors articles in your inbox Subscribe to the Dr. GPCR Monthly Newsletter today! Follow the Dr. GPCR News and get weekly notifications about the GPCR field Share < Previous Next >

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Principles of Pharmacology in Drug Discovery I Dr. Terry Kenakin Dates: October 3 to 24, 2024 Course duration: 4 Weeks Get Started Premium Members benefits: - Subscribe and save 25% on every GPCR Course - Early-bird access - Recordings will be available < Back to GPCR courses ! Widget Didn’t Load Check your internet and refresh this page. If that doesn’t work, contact us. Exciting News: Public Enrollment Now Open! Details Your Instructor Dr. Terry Kenakin After obtaining a BS in chemistry and PhD in Pharmacology at the University of Alberta, Edmonton Canada, I did a post doctoral Fellowship with Sir James Black in London U.K. I then worked at Burroughs-Wellcome in Research Triangle Park, NC (7 years) and then GlaxoSmithKline in RTP for 25 years. I then moved to the University of North Carolina School of Medicine where currently I am a Professor of Pharmacology. My interests are in receptor theory, pharmacology applied to drug discovery and allosteric protein function.

< GPCR News < GPCRs in Oncology and Immunology Mechanistic exploration of bioactive constituents in Gnetum gnemon for GPCR-related cancer treatment through network pharmacology and molecular docking Published date October 28, 2024 Abstract "G Protein-Coupled Receptors (GPCRs) are integral membrane proteins that have gained considerable attention as drug targets, particularly in cancer treatment. In this study, we explored the capacity of bioactive compounds derived from Gnetum gnemon (GG) for the development of of pharmaceuticals targeting GPCRs within the context of cancer therapy. Integrated approach combined network pharmacology and molecular docking to identify and validate the underlying pharmacological mechanisms. We retrieved targets for GG-derived compounds and GPCRs-related cancer from databases. Subsequently, we established a protein-protein interaction (PPI) network by mapping the shared targets. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were employed to predict the mechanism of action of these targets. Molecular docking was conducted to validate our findings. We identified a total of 265 targets associated with GG-derived bioactive compounds for the treatment of GPCRs-related cancer. Functional enrichment analysis revealed the promising therapeutic effects of these targets on GPCRs-related cancer pathways. The PPI network analysis identified hub targets, including MAPK3, SRC, EGFR, STAT3, ESR1, MTOR, CCND1, and PPARG, which demonstrate as treatment targets for GPCRs-related cancer using GG-derived compounds. Additionally, molecular docking experiments demonstrated the strong binding affinity of gnetin A, gnetin C, (-)-viniferin, and resveratrol dimer, thus inhibiting MAPK3, SRC, EGFR, and MTOR. Survival analysis established the clinical prognostic relevance of identified hub genes in cancer. This study presents a novel approach for comprehending the therapeutic mechanisms of GG-derived active compounds and thereby paving the way for their prospective clinical applications in the field of cancer treatment." Authors Moragot Chatatikun, Nawanwat C Pattaranggoon, Imran Sama-Ae, Onggan Ranteh, Manlika Poolpirom, Oranan Pantanakong, Pitchaporn Chumworadet, Fumitaka Kawakami, Motoki Imai, Aman Tedasen Tags ADME , Cancer , GPCRs , Molecular Docking , Network pharmacology Source Contribute to the GPCR News Coming soon Become a Contributor Classified GPCR News Call for GPCR papers GPCR Industry News Adhesion GPCRs GPCR Events, Meetings, and Webinars Reviews, GPCRs, and more GPCR Binders, Drugs, and more Methods & Updates in GPCR Research GPCRs in Neuroscience GPCRs in Cardiology, Endocrinology, and Taste GPCRs in Oncology and Immunology Structural and molecular insights into GPCR function GPCR Activation and Signaling More from Dr. GPCR Create an account and get our contributors articles in your inbox Subscribe to the Dr. GPCR Monthly Newsletter today! Follow the Dr. GPCR News and get weekly notifications about the GPCR field Share < Previous Next >

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Dr. GPCR Podcast << Back to podcast list Dr. Stephen Ferguson The History of the Great Lakes GPCR Retreat with Dr. Stephen Ferguson About Dr. Stephen Ferguson Dr. Stephen Ferguson is a Professor in the Department of Cellular and Molecular Medicine at the University of Ottawa. He did B.Sc. in biology at McGill University and received his Ph.D. under the mentorship of Dr. Brian Collier in the Department of Pharmacology and Therapeutics at McGill University (1994). He did his postdoctoral training with Dr. Marc G. Caron at Duke University (1994-1997), where he and his colleagues investigated the role of G protein-coupled receptor kinases and beta-arrestin in regulating G protein-coupled receptor endocytosis, trafficking, and signaling. He has held four Canada Research Chairs since 2001 and was previously a Heart and Stroke Foundation of Canada MacDonald Scholar (1998-2003) and Heart and Stroke Foundation of Ontario Career Investigator (2003-2016). He was a recipient of Canada's Top 40 under 40 award in 2004 and received Queen Elizabeth II, Diamond Jubilee Medal, in 2012. He has also received both Junior (2001) and Senior (2005) investigator awards from the Pharmacological Society of Canada. Most recently, in 2021, he was elected as a Fellow of the Canadian Academy of Health Science (FCAHS). His research career has focused on the investigation of the regulation of G protein-coupled receptors signaling mechanisms in health and disease. He currently holds multiple research grants from the Canadian Institutes of Health Research (CIHR) for his research investigating the role of metabotropic glutamate receptor signaling in Huntington’s and Alzheimer’s disease. Dr. Stephen Ferguson on the web Carlton University Canada Research Chairs Twitter ResearchGate LinkedIn Dr. GPCR Ecosystem Great Lakes GPCR Retreat on the web 21st Great Lakes GPCR Retreat More about previous GPCR Retreat meetings Dr. GPCR Ecosystem Listen and subscribe to where you get your podcasts. << Previous Podcast Episode Next Podcast Episode >>

< GPCR News < GPCRs in Oncology and Immunology The GPCR adaptor protein Norbin controls the trafficking of C5aR1 and CXCR4 in mouse neutrophils Published date October 28, 2024 Abstract "Norbin (Neurochondrin, NCDN) is a GPCR adaptor protein known for its importance in neuronal function. Norbin works by binding to numerous GPCRs, controlling their steady state trafficking and sometimes their agonist-induced internalisation, as well as their signalling. We recently showed that Norbin is expressed in neutrophils, limits the surface levels of the GPCRs C5aR1 and CXCR4 in neutrophils, and suppresses neutrophil-mediated innate immunity. Here, we identify C5aR1 and CXCR4 as direct Norbin interactors and used mice with myeloid-Norbin deficiency to investigate the role of Norbin in the trafficking of endogenous C5aR1 and CXCR4 in primary neutrophils by flow cytometry and cell fractionation. We show that Norbin mediates the agonist-induced internalisation of C5aR1 through a β-arrestin-dependent mechanism and limits the recycling of internalised C5aR1 and CXCR4 back to the cell surface. Norbin does not control the constitutive internalisation of C5aR1 and CXCR4, nor does it affect the agonist-induced internalisation of CXCR4. Norbin suppresses C5aR1 signalling in mouse neutrophils by limiting the C5a-stimulated membrane translocation of Tiam1, Vav, and PKCδ, and activation of Erk and p38 Mapk pathways, as well as Gαi-dependent ROS production. Our study demonstrates how Norbin suppresses C5aR1 and CXCR4 function in neutrophils and increases our understanding of the mechanisms through which Norbin regulates GPCR trafficking generally, by identifying its importance in β-arrestin recruitment, β-arrestin dependent agonist-induced receptor internalisation, and receptor recycling." Authors Stephen A Chetwynd, Richard J Ward, Graeme Milligan, Heidi C E Welch Tags C5aR1 , CXCR4 , G protein-coupled receptor (GPCR) , GPCR trafficking , Ncdn , Neurochondrin , P-Rex1 , agonist-induced internalisation , receptor desensitization , receptor endocytosis , receptor recycling , β-arrestin Source Contribute to the GPCR News Coming soon Become a Contributor Classified GPCR News Call for GPCR papers GPCR Industry News Adhesion GPCRs GPCR Events, Meetings, and Webinars Reviews, GPCRs, and more GPCR Binders, Drugs, and more Methods & Updates in GPCR Research GPCRs in Neuroscience GPCRs in Cardiology, Endocrinology, and Taste GPCRs in Oncology and Immunology Structural and molecular insights into GPCR function GPCR Activation and Signaling More from Dr. GPCR Create an account and get our contributors articles in your inbox Subscribe to the Dr. GPCR Monthly Newsletter today! Follow the Dr. GPCR News and get weekly notifications about the GPCR field Share < Previous Next >

< GPCR News < GPCRs in Oncology and Immunology Chemokine Physiology in Cancer Published date November 1, 2022 Abstract Chemokines are chemotactic cytokines whose canonical functions govern movement of receptor expressing cells along chemical gradients. Chemokines are a physiologic system that is finely tuned by ligand and receptor expression, ligand or receptor oligomerization, redundancy, expression of atypical receptors and non-GPCR binding partners that cumulatively influence discrete pharmacological signaling responses and cellular functions. In cancer, chemokines play paradoxical roles in both the directed emigration of metastatic, receptor-expressing cancer cells out of the tumor as well as immigration of tumor infiltrating immune cells that culminate in a tumor unique immune microenvironment. In the age of precision oncology strategies to effectively harness the power of immunotherapy requires consideration of chemokine gradients within the unique spatial topography and temporal influences within heterogenous tumors. In this article we review current literature on the diversity of chemokine ligands and their cellular receptors that detect and process chemotactic gradients and illustrate how differences between ligand recognition and receptor activation influence the signaling machinery that drive cellular movement into and out of the tumor microenvironment. Facets of chemokine physiology across discrete cancer immune phenotypes are contrasted to existing chemokine-centered therapies in cancer. Authors Donovan Drouillard, Brian T Craig, Michael B Dwinell Tags Chemokine receptor; cell migration; immuno-oncology; metastasis; tumorigenesis. Source Contribute to the GPCR News Coming soon Become a Contributor Classified GPCR News Call for GPCR papers GPCR Industry News Adhesion GPCRs GPCR Events, Meetings, and Webinars Reviews, GPCRs, and more GPCR Binders, Drugs, and more Methods & Updates in GPCR Research GPCRs in Neuroscience GPCRs in Cardiology, Endocrinology, and Taste GPCRs in Oncology and Immunology Structural and molecular insights into GPCR function GPCR Activation and Signaling More from Dr. GPCR Create an account and get our contributors articles in your inbox Subscribe to the Dr. GPCR Monthly Newsletter today! Follow the Dr. GPCR News and get weekly notifications about the GPCR field Share < Previous Next >

< GPCR News < GPCRs in Oncology and Immunology Phase 1/2 study of sorafenib added to cladribine, high-dose cytarabine, G-CSF, and mitoxantrone in untreated AML Published date September 12, 2023 ! Widget Didn’t Load Check your internet and refresh this page. If that doesn’t work, contact us. ! Widget Didn’t Load Check your internet and refresh this page. If that doesn’t work, contact us. ! Widget Didn’t Load Check your internet and refresh this page. If that doesn’t work, contact us. Source Contribute to the GPCR News Coming soon Become a Contributor Classified GPCR News Call for GPCR papers GPCR Industry News Adhesion GPCRs GPCR Events, Meetings, and Webinars Reviews, GPCRs, and more GPCR Binders, Drugs, and more Methods & Updates in GPCR Research GPCRs in Neuroscience GPCRs in Cardiology, Endocrinology, and Taste GPCRs in Oncology and Immunology Structural and molecular insights into GPCR function GPCR Activation and Signaling More from Dr. GPCR Create an account and get our contributors articles in your inbox Subscribe to the Dr. GPCR Monthly Newsletter today! Follow the Dr. GPCR News and get weekly notifications about the GPCR field Share < Previous Next >

< GPCR News < GPCRs in Oncology and Immunology GPR4 in the pH-dependent migration of melanoma cells in the tumor microenvironment Published date December 23, 2022 Abstract Due to its high metastatic potential, malignant melanoma is one of the deadliest skin cancers. In melanoma as well as in other cancers, acidification of the tumor microenvironment (= TME, inverse pH-gradient) is a well-known driver of tumor progression and metastasis. Membrane-bound receptors, such as the proton-sensitive GPCR (pH-GPCR) GPR4, are considered as potential initiators of the signaling cascades relevant to malignant transformation. In this study, we investigated the pH-dependent migration of GPR4 wildtype/overexpressing SK-Mel-28 cells by using an impedance-based electrical wounding and migration assay and classical Boyden chamber experiments. Migration of GPR4 overexpressing SK-Mel-28 cells was enhanced in a range of pH 6.5 - pH 7.5 as compared to controls in the impedance-based electrical wounding and migration assay. In Boyden chamber experiments, GPR4 overexpression only increased migration at pH 7.5 in a Matrigel-free setup, but not at pH 6.5. Results indicate that GPR4 is involved in the migration of melanoma cells, especially in the tumor periphery, and that this process is affected by pH in the TME. Authors Judith Anthea Stolwijk , Susanne Wallner , Judith Heider , Bernadett Kurz , Lisa Pütz , Stefanie Michaelis , Barbara Goricnik , Julia Erl , Linda Frank , Mark Berneburg , Frank Haubner , Joachim Wegener , Stephan Schreml Tags Boyden chamber , ECIS , GPR4 , impedance , malignant melanoma , migration , pH-GPCR. Source Contribute to the GPCR News Coming soon Become a Contributor Classified GPCR News Call for GPCR papers GPCR Industry News Adhesion GPCRs GPCR Events, Meetings, and Webinars Reviews, GPCRs, and more GPCR Binders, Drugs, and more Methods & Updates in GPCR Research GPCRs in Neuroscience GPCRs in Cardiology, Endocrinology, and Taste GPCRs in Oncology and Immunology Structural and molecular insights into GPCR function GPCR Activation and Signaling More from Dr. GPCR Create an account and get our contributors articles in your inbox Subscribe to the Dr. GPCR Monthly Newsletter today! Follow the Dr. GPCR News and get weekly notifications about the GPCR field Share < Previous Next >

TRAVELING TIPS Adhesion GPCR workshop 2024 CINVESTAV, Mexico City, Mexico October 23-25 Register DO's and DONT's for travelers in Mexico Mexico travel advice *Travelers are encouraged to consult their country's embassy advisories as they may differ from the one posted above. The Canadian embassy provides a comprehensive list. We highly suggest reserving accommodations in the city's center as the housing around the venue is scarce, and some may not be suitable for a convenient stay. Do not hesitate to contact us if you have inquiries regarding the neighborhood of your choice. We suggest the following neighborhoods: Roma Norte, Juárez, Zona Rosa, Condesa, Cuauhtémoc, San Rafael Apart from the numerous Airbnb options in these neighborhoods, here are our recommendations for affordable hotels in order of preference: 1. Hotel Carlota : An industrial chic experience at economical pricing. It can include breakfasts. 2. Hotel Exe Suites Reforma 3. Hotel Maria Cristina : Old School “hacienda”-type hotel. 4. Hotel Laila 5. City Express by Marriott EBC Reforma 6. Hoteles PF Zona Rosa MAP AIR TRAVEL Mexico City is accessible by two major airports. Transportation options, approximate travel times, and approximate fares to and from the airports are listed. Fares are subject to change. Airfare and other travel arrangements are the full responsibility of aGPCR Workshop 2024 attendees. Aeropuerto Internacional de la Ciudad de México (AICM) Benito Juárez is located 15 km from the “Angel de la Independencia” and 13 km from Cinvestav. This airport is the best option for international travel. Time/Distance : Approximate 35-minute drive. Taxis : Taxis are available at the lower levels (outside of baggage claim) at each terminal. Fares are based on traffic conditions, but an average fare is $20-$30. Subway : The subway is only available at Terminal 1. If your flight arrives at Terminal 2, there is a shuttle to Terminal 1. At the subway station you can purchase a “Movilidad Integrada” card in order to access public transportation (subway, metrobus, bikes, bus, etc). Information from public transportation can be followed through Google Maps or City Mapper apps. Uber and Didi apps : Uber type applications are available in Mexico City and a safe option for transportation. Aeropuerto Internacional Felipe Ángeles (AIFA) is located 53 km from the “Angel de la Independencia” and 33 km from Cinvestav. Time/Distance : Approximate 60-minute drive. Taxis : Taxis are available at the lower levels (outside of baggage claim) at each terminal. Fares are based on traffic conditions, but an average fare is $30-$50. Public Transportation : We recommend taking a shuttle (available for travelers) from AIFA to AICM Terminal 1. TRAVEL & VISA INFORMATION We look forward to welcoming attendees. Please check if you need a visa or permit to enter Mexico. After identifying that a visa or permit is needed, foreign travelers should contact their country's Mexican Embassy Consular Section. To request a Letter of Invitation for visa purposes, contact us. MONEY EXCHANGE Mexican pesos are the currency of Mexico. Reliable exchange booths are available at airports, banks, and hotels. However, many businesses accept credit/debit cards. POSTER PRINTING Poster printing is the full responsibility of aGPCR Workshop 2024 attendees. Office Depot and Office Max offer services for poster printing. Close to Cinvestav, on “Instituto Politécnico Nacional” avenue, there are several small local businesses offering poster printing services. The average fare for poster printing is $10-$12. SIM CARD AND WIFI SIM cards can be easily purchased at the airport and Oxxo stores around the city. The average fare is $10-$12. Public Wi-Fi is available around the city, including at airports and subway stations, and just outside of Cinvestav. FOOD RESTRICTIONS Please share any food restrictions you might have (allergies, dietary, etc). We will try to accommodate you as best we can. GETTING TO THE VENUE UBER is the most recommended as it is a highly economical and safe way to reach Cinvestav from your housing accommodation. We recommend carpooling with others to reduce individual costs and to be environmentally friendly. Typical costs are $8 USD one way ($2 USD / person carpooling with four people). Register for the Adhesion GPCR 2024 Learn more about the Adhesion GPCR workshop 2024 Up About the event Learn more about the Adhesion GPCR workshop 2024 and its preliminary program. Up About the venue Discover Cinvestav, the host venue for the upcoming workshop. Up Abstract Submission Submit your research abstracts following our guidelines to present at the conference. Up Logo Contest Enter our logo contest for a chance to have your design represent the upcoming event.

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< GPCR News < GPCRs in Oncology and Immunology Stretch regulates alveologenesis and homeostasis via mesenchymal Gαq/11-mediated TGFβ2 activation Published date April 27, 2023 Abstract " Alveolar development and repair require tight spatiotemporal regulation of numerous signalling pathways that are influenced by chemical and mechanical stimuli. Mesenchymal cells play key roles in numerous developmental processes. Transforming growth factor-β (TGFβ) is essential for alveologenesis and lung repair, and the G protein α subunits Gαq and Gα11 (Gαq/11) transmit mechanical and chemical signals to activate TGFβ in epithelial cells. To understand the role of mesenchymal Gαq/11 in lung development, we generated constitutive (Pdgfrb-Cre+/-;Gnaqfl/fl;Gna11-/-) and inducible (Pdgfrb-Cre/ERT2+/-;Gnaqfl/fl;Gna11-/-) mesenchymal Gαq/11 deleted mice. Mice with constitutive Gαq/11 gene deletion exhibited abnormal alveolar development, with suppressed myofibroblast differentiation, altered mesenchymal cell synthetic function, and reduced lung TGFβ2 deposition, as well as kidney abnormalities. Tamoxifen-induced mesenchymal Gαq/11 gene deletion in adult mice resulted in emphysema associated with reduced TGFβ2 and elastin deposition. Cyclical mechanical stretch-induced TGFβ activation required Gαq/11 signalling and serine protease activity, but was independent of integrins, suggesting an isoform-specific role for TGFβ2 in this model. These data highlight a previously undescribed mechanism of cyclical stretch-induced Gαq/11-dependent TGFβ2 signalling in mesenchymal cells, which is imperative for normal alveologenesis and maintenance of lung homeostasis. " Authors Amanda T Goodwin , Alison E John , Chitra Joseph , Anthony Habgood , Amanda L Tatler , Katalin Susztak , Matthew Palmer , Stefan Offermanns , Neil C Henderson , R Gisli Jenkins . Tags Alveologenesis , Cyclical mechanical stretch , GPCR , Gαq/11 , Lung development , TGFβ . Source Contribute to the GPCR News Coming soon Become a Contributor Classified GPCR News Call for GPCR papers GPCR Industry News Adhesion GPCRs GPCR Events, Meetings, and Webinars Reviews, GPCRs, and more GPCR Binders, Drugs, and more Methods & Updates in GPCR Research GPCRs in Neuroscience GPCRs in Cardiology, Endocrinology, and Taste GPCRs in Oncology and Immunology Structural and molecular insights into GPCR function GPCR Activation and Signaling More from Dr. GPCR Create an account and get our contributors articles in your inbox Subscribe to the Dr. GPCR Monthly Newsletter today! Follow the Dr. GPCR News and get weekly notifications about the GPCR field Share < Previous Next >

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< GPCR News < GPCRs in Oncology and Immunology G protein-coupled estrogen receptor (GPER)/GPR30 forms a complex with the β1-adrenergic receptor, a membrane-associated guanylate kinase (MAGUK) scaffold protein, and protein kinase A anchoring protein (AKAP) 5 in MCF7 breast cancer cells Published date January 10, 2024 Abstract "G protein-coupled receptor 30 (GPR30), also named G protein-coupled estrogen receptor (GPER), and the β1-adrenergic receptor (β1AR) are G protein-coupled receptors (GPCR) that are implicated in breast cancer progression. Both receptors contain PSD-95/Discs-large/ZO-1 homology (PDZ) motifs in their C-terminal tails through which they interact in the plasma membrane with membrane-associated guanylate kinase (MAGUK) scaffold proteins, and in turn protein kinase A anchoring protein (AKAP) 5. GPR30 constitutively and PDZ-dependently inhibits β1AR-mediated cAMP production. We hypothesized that this inhibition is a consequence of a plasma membrane complex of these receptors. Using co-immunoprecipitation, confocal immunofluorescence microscopy, and bioluminescence resonance energy transfer (BRET), we show that GPR30 and β1AR reside in close proximity in a plasma membrane complex when transiently expressed in HEK293. Deleting the GPR30 C-terminal PDZ motif (-SSAV) does not interfere with the receptor complex, indicating that the complex is not PDZ-dependent. MCF7 breast cancer cells express GPR30, β1AR, MAGUKs, and AKAP5 in the plasma membrane, and co-immunoprecipitation revealed that these proteins exist in close proximity also under native conditions. Furthermore, expression of GPR30 in MCF7 cells constitutively and PDZ-dependently inhibits β1AR-mediated cAMP production. AKAP5 also inhibits β1AR-mediated cAMP production, which is not additive with GPR30-promoted inhibition. These results argue that GPR30 and β1AR form a PDZ-independent complex in MCF7 cells through which GPR30 constitutively and PDZ-dependently inhibits β1AR signaling via receptor interaction with MAGUKs and AKAP5." Authors Julia Tutzauer , D Stephen Serafin , Tobias Schmidt , Björn Olde , Kathleen M Caron , L M Fredrik Leeb-Lundberg Tags Breast cancer , GPER , GPR30 , PDZ domain , Protein complex , β(1)-adrenergic receptor Source Classified GPCR News More from Dr. GPCR Share < Previous Next >