Background: MRGPR-X1 are exclusively expressed in primary sensory neurons, provoke the sensation of pain, and are considered as promising targets for pain therapy. Results: MRGPR-X1 sensitize TRPV1 for protons and heat via PKC and directly activate TRPV1 via DAG and PIP 2 . Conclusion: MRGPR-X1 modulate TRPV1 activity via multiple mechanisms. Significance: Interrupting the functional interaction between MRGPR-X1 and TRPV1 is a promising approach to diminish pain.
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