Table 1.
Sequences of human apelin and Toddler/ELABELA, the endogenous peptide ligands of the AR. All isoforms of each ligand retain identical C-termini, and various lengths of peptide are presented based on biological detection or the presence of proposed dibasic proteolytic cleavage sites. Apelin-12 is most likely not produced endogenously, but is the shortest possible synthetic isoform that retains biological activity (Tatemoto et al. 2001).
| Apelin Peptide | Sequence |
|---|---|
| Preproapelin (Apelin-77) | MNLRLCVQALLLLWLSLTAVCGGSLMPLPDGNGLEDGNVRHLVQPRGSRNGPGPWQGGRRKFRRQRPRLSHKGPMPF |
| Proapelin (Apelin-55) | GSLMPLPDGNGLEDGNVRHLVQPRGSRNGPGPWQGGRRKFRRQRPRLSHKGPMPF |
| Apelin-36 | LVQPRGSRNGPGPWQGGRRKFRRQRPRLSHKGPMPF |
| Apelin-17 | KFRRQRPRLSHKGPMPF |
| Pyr-apelin-13 | Pyr–RPRLSHKGPMPF |
| Apelin-13 | QRPRLSHKGPMPF |
| Apelin-12 | RPRLSHKGPMPF |
| Toddler/ELABELA Peptide | Sequence |
| Preprotoddler (Toddler-54) | MRFQQFLFAFFIFIMSLLLISGQEPVNLTMRRKLRKHNCLQRRCMPLHSRVPFP |
| Protoddler (Toddler-32) | QEPVNLTMRRKLRKHNCLQRRCMPLHSRVPFP |
| Toddler-22a | KLRKHNCLQRRCMPLHSRVPFP |
| Toddler-11 | CMPLHSRVPFP |
a
Toddler-22 is shown by analogy to apelin-17; zebrafish Toddler-21 and the corresponding apelin-16 isoform were shown to be active by Pauli et al. (2014), with divergent sequences in the N-terminal region compared to the human peptides.