Gene interactions and pathways from curated databases and text-mining

◀ Back to LPA

LPA — SLC9A3

Text-mined interactions from Literome

Lee-Kwon et al., J Biol Chem 2003 : However, in OK cells exogenously expressing E3KARP, LPA stimulated NHE3 activity ... The LPA induced increases of NHE3 activity, surface NHE3 amounts, and exocytosis were completely inhibited by pretreatment with the PI 3-kinase inhibitor, LY294002 ... These results show that LPA stimulates NHE3 in the apical surface of OK cells by a mechanism that is dependent on both E3KARP and PI 3-kinase
Choi et al., Biochim Biophys Acta 2004 : Pretreatment with U73122, a PLC inhibitor, prevented the LPA induced NHE3 activation and the exocytic trafficking of NHE3 ... BAPTA-AM completely blocked the LPA induced increase of NHE3 activity and surface NHE3 amount by decreasing the LPA induced exocytic trafficking of NHE3 ... Pretreatment with GF109203X, a PKC inhibitor, did not affect the percent of LPA induced NHE3 activation and increase of surface NHE3 amount
Lin et al., Gastroenterology 2010 (Diarrhea...) : Expression of the LPA receptor LPA ( 5 ) was necessary for LPA induced stimulation of NHE3 activity in colonic epithelial cells ... Stimulation of NHE3 by the LPA-LPA ( 5 ) signaling required coexpression of NHERF2, which interacted with LPA ( 5 ) ... LPA stimulated NHE3 and fluid absorption in part by increasing NHE3 protein abundance at the brush border membrane of intestinal epithelial cells
Cha et al., J Cell Sci 2010 : LPA acutely stimulated NHE3 activity in OK cells stably expressing NHERF2
Murtazina et al., Am J Physiol Cell Physiol 2011 (Second Messenger Systems) : Luminal lysophosphatidic acid (LPA) stimulated NHE3 in wild-type but not in NHERF2-null ileum ... In conclusion, 1 ) there are subtle structural abnormalities in the small intestine of NHERF2-null mouse which include fewer villus epithelial cells ; 2 ) the decreased basal NHE3 activity and reduced brush border NHE3 amount in NHERF2-null mice show that NHERF2 is necessary for normal basal trafficking or retention of NHE3 in the apical domain ; 3 ) hyperosmolar inhibition of NHE3 occurs similarly in wild-type and NHERF2-null ileum, demonstrating that some inhibitory mechanisms of NHE3 are not NHERF2 dependent ; 4 ) cAMP inhibition of NHE3 is NHERF2 dependent at a step downstream of cAMP/PKAII phosphorylation of NHE3 at aa 552 ; 5 ) cGMP- and UTP induced inhibition of NHE3 are NHERF2 dependent at steps beyond cGKII and the UTP induced increase of intracellular Ca ( 2+ ) ; and 6 ) LPA stimulation of NHE3 is also NHERF2 dependent
Yoo et al., Am J Physiol Cell Physiol 2011 : We found that LPA ( 5 ) transactivated the epidermal growth factor receptor (EGFR) and that inhibition of EGFR blocked LPA ( 5 ) -dependent activation of NHE3 , suggesting an obligatory role of EGFR in the NHE3 regulation ... However, inhibition of apical EGFR, but not basolateral EGFR, abrogated LPA induced regulation of MEK and NHE3 , indicating that LPA ( 5 ) selectively activates apical EGFR ... Similarly to MEK inhibition, knockdown of Pyk2 blocked activation of NHE3 by LPA ... Together, these results unveil a pivotal role of apical EGFR in NHE3 regulation by LPA and show that the RhoA-ROCK-Pyk2 and MEK-ERK pathways converge onto NHE3
Yoo et al., Am J Physiol Gastrointest Liver Physiol 2012 : Similarly to Caco-2 cells, SK-CO15 cells lacked the expression of the LPA receptor LPA ( 5, ) but exogenous expression of LPA ( 5 ) resulted in acute stimulation of NHE3