< GPCR News < GPCRs in Oncology and Immunology Orphan receptor GPR50 attenuates inflammation and insulin L1 preadipocytes Published date November 1, 2022 Abstract Type 2 diabetes (T2DM) is characterized by insulin secretion deficiencies and systemic insulin resistance (IR) in adipose tissue, skeletal muscle, and Although the mechanism of T2DM is not yet fully known, inflammation and insulin resistance play a central The aim of this study was to investigate the effect of GPR50 on inflammation and insulin resistance in

Our results show that CB2 stimulation of ILC2s protects against insulin-resistance onset, ameliorates glucose tolerance, and reverses established insulin resistance. Immunology , CP: Metabolism , ILC2 , T2DM , adipose inflammation , glucose tolerance , immunotherapy , insulin resistance Source Contribute to the GPCR News Coming soon Become a Contributor Classified GPCR News

In insulin-resistant HF patients, AT2R autoantibodies were decreased (r = -.240, P < 0.05), and AT1R

and Type 2 Diabetes (T2D) by exploring metabolically important signaling pathways in immune cells and insulin-sensitive different cell culture systems, to understand the role of immune cell GPCRs and their cross-talk with other insulin-sensitive

Sponsors GPCR Retreat Program < Back to schedule Removing the GPCR-mediated brake on exocytosis enhances insulin

Previously, we identified potent positive crosstalk between insulin/IGF-1 receptors and G protein-coupled Here, we show that a combination of insulin and the GPCR agonist neurotensin induced rapid activation

Ottawa Read More Friday, November 3rd / 2:45 PM Removing the GPCR-mediated brake on exocytosis enhances insulin

in Oncology and Immunology S1P Signaling Genes as Prominent Drivers of BCR-ABL1-Independent Imatinib Resistance Although BCR-ABL1 mutation is a key cause of CML resistance, understanding mechanisms independent of phosphate (S1P) signaling-associated genes (SphK1 and S1PRs) and their role in BCR-ABL1-independent resistant Through comprehensive transcriptomic analysis of IM-sensitive and IM-resistant CML groups, we identified the differentially expressed genes and found a notable upregulation of SphK1, S1PR2, and S1PR5 in IM-resistant

in Oncology and Immunology Activation of PI3K/Akt pathway by G protein-coupled receptor 37 promotes resistance Most importantly, we investigated whether GPR37 affects cisplatin-induced drug resistance in NSCLC. positively regulates NSCLC cell invasion, migration, and proliferation, suppresses cell apoptosis, heightens resistance

Sponsor this event Register now to join the exclusive Adhesion GPCR Workshop group and stay updated with Join the AGPCR24 group How to register for the Adhesion GPCR workshop 2024? If you're a Dr. GPCR Ecosystem member 01 Register for the event 02 Accept the invitation to the private group If you're you mention "AGPCR24 Workshop" when you fill out the information Wait to be accepted in the Ecosystem Register

The objective of this study was to elucidate the genomic basis of drug resistance or sensitivity, identify Results: We detected genetic signatures associated with sensitivity or resistance to specific agents,

show that the elevated expression of UCA1 enhances cell proliferation, invasive migration, and therapy resistance High Grade Serous Ovarian Carcinoma , Let-7 miRNAs , Oncogenic Pathways , Ovarian Cancer , Therapy Resistance

March 2, 2024 Abstract " Background: Novel therapeutic targets are urgently needed for treating drug-resistant non-small cell lung cancer (NSCLC) and overcoming drug resistance to molecular-targeted therapies.

highly specific antibodies for complex targets, with implications for overcoming challenges like drug resistance

LOGO CONTEST Adhesion GPCR workshop 2024 CINVESTAV, Mexico City, Mexico October 23-25 Register Rules Artist-scientists must be registered to attend the adhesion GPCR workshop 2024 in Mexico City. Register for the Adhesion GPCR 2024 Learn more about the Adhesion GPCR workshop 2024 Up About the event

Adhesion GPCR workshop 2024 CINVESTAV, Mexico City, Mexico October 23-25 Register AGPCR Newsletter Dr Register for the Adhesion GPCR 2024 Learn more about the Adhesion GPCR workshop 2024 Up About the event

cells, promote tumor angiogenesis, and affect the tumor immune microenvironment (TIME) and tumor drug resistance

of AGPCR signaling and function Structural Determinants Of GAIN Domain Autoproteolysis And Cleavage Resistance ADGRL1 with QM/MM Florian Seufert Structural Determinants Of GAIN Domain Autoproteolysis And Cleavage Resistance structure of the human ADGRB2/BAI2 hormone receptor (HormR) and GAIN domains and found that this ADGR is resistant

RNAi of daf-7, jnk-1, mpk-1, and dcar-1 resulted in susceptibility, and nhr-8 RNAi caused resistance

LP2 is a 4, 7 D, L lanthionine-stabilized analog of angiotensin-(1-7), with an N-terminal D-lysine, resistant

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all thirteen glioblastoma cell lines tested, irrespective of genetic and phenotypic heterogeneity, or resistance

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