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The atypical chemokine receptor ACKR3 has not too long ago been claimed to work as an opioid scavenger with distinctive negative regulatory properties to various family members of opioid peptides.
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We shown that, in contrast to classical opioid receptors, ACKR3 would not result in classical G protein signaling and is not modulated by the classical prescription or analgesic opioids, including morphine, fentanyl, or buprenorphine, or by nonselective opioid antagonists like naloxone. Instead, we recognized that LIH383, an ACKR3-selective subnanomolar competitor peptide, stops ACKR3’s negative regulatory function on opioid peptides in an ex vivo rat brain product and potentiates their exercise towards classical opioid receptors.
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Synthesis and stereochemical resolve of the antiparasitic pseudo-aminal variety monoterpene indole alkaloid Yoshihiko Noguchi
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