4q12

According to Stolle et al., RASL11B expression is induced during maturation of THP-1 monocytic cells into macrophages and in coronary artery smooth muscle cells after treatment with TGF-beta1 suggesting that RASL11B may play a role in developmental processes or in pathophysiologies such as inflammation or cancer.
Pezeron et al. demonstrated that Rasl11b modulates function of the EGF-CFC coreceptor one-eyed-pinhead (oep) in zebrafish independently of the TGFbeta/Nodal pathway, which is crucial for germ layer formation. Down regulation of Rasl11b partially rescued endodermal and prechordal plate defects of zygotic homozygous oep zebrafish mutants. Rasl11b inhibitory action was observed only in animals with oep-deficient backgrounds, suggesting that normal oep expression prevents function of Rasl11b. On the other hand, Rasl11b down regulation did not rescue mesendodermal defects in other Nodal pathway mutants.