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Mouse Hemokinin-1 Decapeptide Subjected to a Brain-specific Post-translational Modification
Georgia Deliconstantinos1, Stephen Barton2, Mikhail Soloviev3
1School of Life Sciences, Kingston University, London, U.K. ginadeli@hotmail.com.
In Vivo (Athens, Greece)
|September 9, 2017
Summary
Researchers characterized mouse hemokinin-1, a tachykinin peptide. They discovered brain-specific N-terminal acetylation of hemokinin-1, enhancing its signaling potency.
Area of Science:
- Neuroscience
- Biochemistry
- Molecular Biology
Background:
- Mouse hemokinin-1 (HK1), encoded by the Tac4 gene, is a tachykinin peptide involved in pain signaling via the neurokinin 1 receptor.
- Processing of the TAC4 precursor differs from TAC1 (substance P precursor), necessitating HK1 sequence characterization.
Purpose of the Study:
- To characterize the sequence of mouse hemokinin-1 (HK1).
- To investigate the post-translational modifications of HK1 in the mouse brain and periphery.
Main Methods:
- Development of anti-tachykinin antibodies for immunoaffinity purification.
- Mass spectrometry (MALDI-ToF) for peptide identification and characterization.
Main Results:
- Mouse hemokinin-1 was identified as an amidated decapeptide present in both murine brain and periphery.
- A brain-specific post-translational modification, N-terminal acetylation, was observed for mouse hemokinin-1.
Conclusions:
- N-terminal acetylation of mouse hemokinin-1 is a brain-specific modification.
- This acetylation may enhance the peptide's potency in ligand-receptor interactions for neural signaling.
