IndraLab

Statements


| 5

sparser
"Neurofibromin sequesters CRMP2 from syntaxin 1A. On loss of neurofibromin, as observed in patients with NF1, the CRMP2/neurofibromin interaction is uncoupled, which liberates CRMP2 to interact with both syntaxin 1A and Cav2.2, culminating in increased release of the pronociceptive neurotransmitter CGRP."

sparser
"In the DII-DIII linker, PKC phosphorylates the sites identified in mouse brain as S773 and S892, and CaMKII at S783, and impacts syntaxin1ACav2.2 interaction ( xref )."

sparser
"Past efforts to harness uncoupling of the syntaxin 1A-Cav2.2 interaction for therapeutic use have not advanced despite an early report of success [ xref ]."

sparser
"Interactions between Cav2.2 and the synaptic protein syntaxin 1A then follow to produce fast, synchronous neurotransmitter release [ xref – xref ]."

sparser
"Neurofibromin uncouples CRMP2 from syntaxin 1A. Upon loss/mutation of neurofibromin, as seen in patients with NF1, the CRMP2/Neurofibromin interaction is uncoupled, which frees CRMP2 to interact with both syntaxin 1A and CaV2.2, culminating in increased release of the pro-nociceptive neurotransmitter calcitonin gene related peptide (CGRP)."