by the native parathyroid hormone-related protein 1 to 141 relative to its N-terminal fragment 1 to 36 PTH type 1 receptor (PTHR), is largely derived from studies done with its N-terminal fragment, PTHrP1-36 the native PTHrP1-141 displays biased agonist signaling properties that are not mimicked by PTHrP1-36 Although PTHrP1-36 induces transient cAMP production, acute intracellular Ca2+ (iCa2+) release and β-arrestin Furthermore, we show that the molecular basis for biased signaling differences between PTHrP1-36 and

We demonstrate that the chemoreceptor genes, srg-36 and srg-37 , which encode G protein-coupled receptors mutation in egl-30 encoding Gqα suppresses axon regeneration defective phenotype in acox-1.1 and srg-36 Here, we show that SRG-36 and SRG-37 act as upstream GPCRs that activate EGL-30. SRG-36 and SRG-37 are GPCRs for the dauer-inducing ascaroside, ascr#5. Consistent with this, we found that ascr#5 activates the axon regeneration pathway via SRG-36/SRG-37

Fischer – Facts - NobelPrize.org. https://www.nobelprize.org/prizes/medicine/1992/fischer/facts/. 36.

Science, 2020. 369(6503). 4.     

Check the original article at https://pubmed.ncbi.nlm.nih.gov/36719944/ #GPCR #DrGPCR#Ecosystem

Check the original article at https://pubmed.ncbi.nlm.nih.gov/36729338/ #GPCR #DrGPCR#Ecosystem

details of this study, you can consult the article at the following link https://pubmed.ncbi.nlm.nih.gov/36502633 PMID: 36502633. https://pubmed.ncbi.nlm.nih.gov/36502633/

Check the original article at https://pubmed.ncbi.nlm.nih.gov/36309016/ Bibliography 1.

mechanisms underlying this interaction, we conducted a host-directed CRISPR-Cas9 screen and identified 361

Interestingly, FLNA absence reduced the basal number of hetero-dimers (-36.8 ± 6.3% reduction of PLA

transcriptomic analysis, expression of GPER was correlated with clinicopathological variables and survival of 360 According to the cutoff value, 26.4% (95/360) of patients showed high GPER expression and significant