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Posts (12)

  • The Quiet Power of RGS Proteins: Rethinking Pain Pathways through GPCR Biology

    Venetia Zachariou  introduced him to the power of RGS proteins — particularly RGS4  — in modulating pain RGS4 and the Unexpected Recovery Phenomenon One of the most compelling findings in Serafini’s experience was the spontaneous recovery observed in RGS4 knockout mice . mouse was starting to enter what we consider the chronic pain range, the mice that were constitutively RGS4 Serafini noted that RGS4 was especially intriguing because it was expressed robustly both in the peripheral

  • Regulators of G-protein signaling: essential players in GPCR signaling

    Another signaling pathway related to RGS4 involves the regulation of the immune response. RGS4 is expressed in various immune cells, including T cells and B cells, and has been shown to modulate RGS4 acts as a negative regulator of T cell activation, and its expression is upregulated in response Traynor, Differential modulation of mu- and delta-opioid receptor agonists by endogenous RGS4 protein Avrampou, K., et al., RGS4 Maintains Chronic Pain Symptoms in Rodent Models.

  • 📰 GPCR Weekly News, February 26 to March 3, 2024

    protein-coupled receptor regulates ischaemia-reperfusion injury GPCRs in Cardiology, Endocrinology, and Taste RGS4

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Other Pages (2)

  • GPCRs and the Science Behind Pain and Recovery with Dr. Alex Serafini | Dr. GPCR Ecosystem

    The lab’s work with RGS4 led to unexpected results: knockout mice spontaneously recovered from chronic in vivo-first strategies, combined with RNA-seq and behavioral analysis, revealed nuanced roles of RGS4 , RGS9, and RGSZ — not just as modulators but as potential therapeutic linchpins. GPCR ecosystem, GPCR drug discovery, GPCR podcast, GPCR data platform, GPCR training program, RGS4, chronic

  • Dr. Nariman Balenga | Dr. GPCR Ecosystem

    Kirk Druey at NIAID/NIH, where I characterized the role of RGS4 and RGS5 in airway hyperresponsiveness I studied the function of RGS5, calcium-sensing receptor, and an orphan adhesion GPCR, GPR64/ADGRG2 in

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