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.

identified a positive association between predicted ONV + DAC response and mutations in splicing factors (SF In the phase 1b/2 trial, patients with SF mutations (SRSF2, SF3B1) had a higher CR/CRi rate (50%) compared to those without SF mutations (9%). be a potential therapy in R/R AML patients, particularly those with high OXPHOS gene expression and SF

Professor Christopoulos has over 360 publications, including in leading international journals such as

Professor Christopoulos has over 360 publications, including in leading international journals such as