Where it comes from
- Made in
- Sensory and brain neurons that make the beta splice form of TAC1
- Sent out by
- With substance P and neurokinin A
- Acts on
- Airway and gut smooth muscle
- Vessels
What it does
In medicine
Beyond the body’s own use
- Nothing containing it is in trials, approved or obtainable outside the laboratory
- Its reason for existing is the splice: the beta form of the tachykinin gene puts a 26-residue extension in front of neurokinin A 1, and the product is slower to act and slower to be destroyed 3
- What is unknown is whether that matters in the body. No animal has been made that can make one splice form and not the other, so nothing shows what a tissue loses when it keeps substance P and loses neuropeptide K 2
Sources
- Tatemoto et al., Neuropeptide K, isolation, structure and biological activities of a novel brain tachykinin, Biochemical and Biophysical Research Communications 1985
- Takeda et al., Regional distribution of neuropeptide gamma and other tachykinins of the substance P gene, Regulatory Peptides 1990
- Michael-Titus et al., In vivo metabolism and clearance of substance P and co-expressed tachykinins in rat striatum, Neuroscience 2002
This card describes what a medicine is for and what the evidence says; it recommends nothing. Talk to your clinician about anything you read here.