Protein sequence alignment shows that calponin 1 is highly conserved in mammals but more diverged among lower vertebrates.
The expression of CNN1 is specific to differentiated mature smooth muscle cells, suggesting a role in contractile functions.
This feature is consistent with the hypothesis that the second actin-binding site plays a regulatory role in the binding of calponin to the actin filament.
The variable lengths and amino acid sequences of the C-terminal segment produce the size and charge differences among the calponin isoforms.
Deletion of the C-terminal tail strongly enhanced the actin-binding and bundling activities of all three isoforms of calponin.
[24] Numerous in vitro experimental data indicate that calponin 1 functions as an inhibitory regulator of smooth muscle contractility through inhibiting actomyosin interactions.
[6][25][26] In this regulation, binding of Ca2+-calmodulin and PKC phosphorylation dissociate calponin 1 from the actin filament and facilitate smooth muscle contraction.
While aortic smooth muscle of adult Wistar Kyoto rats, which naturally lacks calponin 1, is fully contractile, it has a decreased sensitivity to norepinephrine activation.
[30] Vas deferens smooth muscle from calponin 1 knockout mice showed faster maximum shortening velocity.