Conditional deletion of IPR1 by Islet1-Cre in mice reveals a critical role of IPR1 in interstitial cells of Cajal in regulating GI motility.

Background And Aims: Inositol 1,4,5-trisphosphate receptor type 1 (IPR1) has been proposed to play a physiological role in regulating gastrointestinal (GI) motility, but the underlying cell-dependent mechanism remains unclear. Here, we utilized cell-specific IPR1 deletion strategies to address this question in mice.

Methods: Conditional IPR1 knockout mice using Wnt1-Cre, Islet1-Cre mice, and smMHC-Cre were generated.

Deletion of IPR1 by Pdgfrb-Cre in mice results in intestinal pseudo-obstruction and lethality.

Background: Inositol 1,4,5-trisphosphate receptors (IPRs) are a family of intracellular Ca release channels located on the membrane of endoplasmic reticulum, which have been shown to play critical roles in various cellular and physiological functions. However, their function in regulating gastrointestinal (GI) tract motility in vivo remains unknown. Here, we investigated the physiological function of IPR1 in the GI tract using genetically engineered mouse models.