PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 7996788-5 1994 Despite causing increased Ang II receptor number, dexamethasone preincubation prevented Ang II-induced PLC activation, as indicated by phosphatidylinositol 4,5-bisphosphate degradation and inositol trisphosphate formation. Phosphatidylinositol 4,5-Diphosphate 135-172 angiotensinogen Rattus norvegicus 88-94 7920381-2 1994 As in RIE-1 cells, treatment of IEC-6 or IEC-18 cells with angiotensin II (AII) activated phosphatidylinositol-4,5-bisphosphate (PIP2) hydrolysis although (in contrast to RIE-1 cells) the magnitude of AII-induced PIP2 hydrolysis was small and not associated with a mitogenic response in either IEC cell line. Phosphatidylinositol 4,5-Diphosphate 90-127 angiotensinogen Rattus norvegicus 59-73 7920381-2 1994 As in RIE-1 cells, treatment of IEC-6 or IEC-18 cells with angiotensin II (AII) activated phosphatidylinositol-4,5-bisphosphate (PIP2) hydrolysis although (in contrast to RIE-1 cells) the magnitude of AII-induced PIP2 hydrolysis was small and not associated with a mitogenic response in either IEC cell line. Phosphatidylinositol 4,5-Diphosphate 90-127 angiotensinogen Rattus norvegicus 75-78 7920381-2 1994 As in RIE-1 cells, treatment of IEC-6 or IEC-18 cells with angiotensin II (AII) activated phosphatidylinositol-4,5-bisphosphate (PIP2) hydrolysis although (in contrast to RIE-1 cells) the magnitude of AII-induced PIP2 hydrolysis was small and not associated with a mitogenic response in either IEC cell line. Phosphatidylinositol 4,5-Diphosphate 129-133 angiotensinogen Rattus norvegicus 59-73 7920381-2 1994 As in RIE-1 cells, treatment of IEC-6 or IEC-18 cells with angiotensin II (AII) activated phosphatidylinositol-4,5-bisphosphate (PIP2) hydrolysis although (in contrast to RIE-1 cells) the magnitude of AII-induced PIP2 hydrolysis was small and not associated with a mitogenic response in either IEC cell line. Phosphatidylinositol 4,5-Diphosphate 129-133 angiotensinogen Rattus norvegicus 75-78 7920381-2 1994 As in RIE-1 cells, treatment of IEC-6 or IEC-18 cells with angiotensin II (AII) activated phosphatidylinositol-4,5-bisphosphate (PIP2) hydrolysis although (in contrast to RIE-1 cells) the magnitude of AII-induced PIP2 hydrolysis was small and not associated with a mitogenic response in either IEC cell line. Phosphatidylinositol 4,5-Diphosphate 213-217 angiotensinogen Rattus norvegicus 59-73 7920381-2 1994 As in RIE-1 cells, treatment of IEC-6 or IEC-18 cells with angiotensin II (AII) activated phosphatidylinositol-4,5-bisphosphate (PIP2) hydrolysis although (in contrast to RIE-1 cells) the magnitude of AII-induced PIP2 hydrolysis was small and not associated with a mitogenic response in either IEC cell line. Phosphatidylinositol 4,5-Diphosphate 213-217 angiotensinogen Rattus norvegicus 75-78 3024736-2 1987 Stimulation of the glomeruli pulse-chase labeled with [3H]glycerol by angiotensin II caused a rapid (within 15 s) breakdown of phosphatidylinositol 4,5-bisphosphate (PIP2) with a concurrent production of 1,2-diacylglycerol. Phosphatidylinositol 4,5-Diphosphate 166-170 angiotensinogen Rattus norvegicus 70-84 7509802-3 1994 Thrombin and angiotensin II stimulated the hydrolysis of phosphatidylinositol (PI) 4,5-bisphosphate and the formation of several cytosolic species of inositol phosphates without the activation of PI 3-hydroxykinase. Phosphatidylinositol 4,5-Diphosphate 57-99 angiotensinogen Rattus norvegicus 13-27 1689113-4 1990 Preincubation of MCs with ANF significantly inhibited ANG II-induced release of inositol trisphosphate (IP3) resulting from hydrolysis of phosphatidylinositol 4, 5-bisphosphate. Phosphatidylinositol 4,5-Diphosphate 138-176 angiotensinogen Rattus norvegicus 54-60 3152162-5 1988 In AII-stimulated glomerulosa cells, hydrolysis of phosphatidylinositol (4,5)-bisphosphate (PIP2) by phospholipase C yields diacylglycerol and inositol 1,4,5-trisphosphate (Ins-P3), which act as second messengers by activating calcium-calmodulin and calcium-phospholipid dependent protein kinase pathways. Phosphatidylinositol 4,5-Diphosphate 51-90 angiotensinogen Rattus norvegicus 3-6 3152162-5 1988 In AII-stimulated glomerulosa cells, hydrolysis of phosphatidylinositol (4,5)-bisphosphate (PIP2) by phospholipase C yields diacylglycerol and inositol 1,4,5-trisphosphate (Ins-P3), which act as second messengers by activating calcium-calmodulin and calcium-phospholipid dependent protein kinase pathways. Phosphatidylinositol 4,5-Diphosphate 92-96 angiotensinogen Rattus norvegicus 3-6 3024736-2 1987 Stimulation of the glomeruli pulse-chase labeled with [3H]glycerol by angiotensin II caused a rapid (within 15 s) breakdown of phosphatidylinositol 4,5-bisphosphate (PIP2) with a concurrent production of 1,2-diacylglycerol. Phosphatidylinositol 4,5-Diphosphate 127-164 angiotensinogen Rattus norvegicus 70-84 3024736-5 1987 The change in phospholipid metabolism by angiotensin II was similar when the glomeruli were labeled with [32P]orthophosphate: the decrease in the labeling of PIP2 and the increase in the labeling of phosphatidic acid after 15 s. In addition, 32P labeling of PI increased after 2 min. Phosphatidylinositol 4,5-Diphosphate 158-162 angiotensinogen Rattus norvegicus 41-55 3024736-6 1987 These results suggest that angiotensin II, after binding to glomerular receptors, induces initial PIP2 hydrolysis to diacylglycerol and subsequent resynthesis of PIP2 through phosphoinositide turnover. Phosphatidylinositol 4,5-Diphosphate 98-102 angiotensinogen Rattus norvegicus 27-41 3024736-6 1987 These results suggest that angiotensin II, after binding to glomerular receptors, induces initial PIP2 hydrolysis to diacylglycerol and subsequent resynthesis of PIP2 through phosphoinositide turnover. Phosphatidylinositol 4,5-Diphosphate 162-166 angiotensinogen Rattus norvegicus 27-41 2997197-1 1985 Angiotensin II acts on cultured rat aortic vascular smooth muscle cells (VSMC) to induce the rapid, phospholipase C-mediated generation of inositol trisphosphate from phosphatidylinositol 4,5-bisphosphate and mobilization of intracellular Ca2+. Phosphatidylinositol 4,5-Diphosphate 167-204 angiotensinogen Rattus norvegicus 0-14 2826911-10 1987 AII-induced breakdown of phosphatidylinositol bisphosphate (PIP2) and phosphatidylinositol phosphate (PIP) leads to formation of inositol 1,4,5-trisphosphate (IP3) and inositol 1,4-bisphosphate (IP2). Phosphatidylinositol 4,5-Diphosphate 60-64 angiotensinogen Rattus norvegicus 0-3 3024620-1 1986 Incubation of rat renal mesangial cells with angiotensin II (0.1 microM) resulted in transient breakdown of phosphatidylinositol 4,5-bisphosphate, rapid generation of diacylglycerol and phosphatidic acid, increased 45Ca2+ influx, increased intracellular [Ca2+] as measured by quin 2, and increased prostaglandin E2 synthesis. Phosphatidylinositol 4,5-Diphosphate 108-145 angiotensinogen Rattus norvegicus 45-59 2996937-2 1985 Furthermore, it was shown that angiotensin II (AII) (10(-6)M) induced rapid hydrolysis of phosphatidylinositol 4,5-bisphosphate, leading to production of diacylglycerol rich in arachidonic acid, in the cultured rat mesangial cells. Phosphatidylinositol 4,5-Diphosphate 90-127 angiotensinogen Rattus norvegicus 31-45 2996937-2 1985 Furthermore, it was shown that angiotensin II (AII) (10(-6)M) induced rapid hydrolysis of phosphatidylinositol 4,5-bisphosphate, leading to production of diacylglycerol rich in arachidonic acid, in the cultured rat mesangial cells. Phosphatidylinositol 4,5-Diphosphate 90-127 angiotensinogen Rattus norvegicus 47-50 2822466-4 1987 Phorbol esters, which are tumor promoters, can stimulate protein kinase C. Angiotensin II and alpha 1-agonists activate protein kinase C via diacylglycerol release from phosphatidylinositol-4,5-diphosphate. Phosphatidylinositol 4,5-Diphosphate 169-205 angiotensinogen Rattus norvegicus 75-101 3084474-8 1986 Thus, angiotensin II induces rapid transient breakdown of PIP and PIP2 and delayed hydrolysis of PI. Phosphatidylinositol 4,5-Diphosphate 66-70 angiotensinogen Rattus norvegicus 6-20 3083411-2 1986 Ten of the 11 cytosolic proteins altered by EGF are identical to those affected by angiotensin II, a hormone that stimulates the breakdown of phosphatidylinositol 4,5-bisphosphate. Phosphatidylinositol 4,5-Diphosphate 142-179 angiotensinogen Rattus norvegicus 83-97 3458463-4 1986 Angiotensin II, noradrenaline and AGEPC caused a rapid breakdown of phosphatidylinositol 4,5-bisphosphate with a concomitant increase of 1,2-diacylglycerol and inositol trisphosphate, indicating an activation of phospholipase C by these hormones. Phosphatidylinositol 4,5-Diphosphate 68-105 angiotensinogen Rattus norvegicus 0-14 3004470-6 1986 Phosphorylation of angiotensin II by tyrosine kinase was inhibited by 0.2 mg/ml phosphatidyl inositol 4 phosphate or phosphatidyl inositol 4,5-bisphosphate. Phosphatidylinositol 4,5-Diphosphate 117-155 angiotensinogen Rattus norvegicus 19-33 6477952-4 1984 Angiotensin II, phenylephrine and parathyroid hormone (PTH) stimulate 32P incorporation into PC by 25, 29 and 26% and into PI by 189, 328 and 33% above control rates, respectively, whereas phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate labeling was not affected. Phosphatidylinositol 4,5-Diphosphate 226-263 angiotensinogen Rattus norvegicus 0-14 2987120-1 1985 Angiotensin II stimulated the breakdown of phosphatidylinositol-4,5-bisphosphate (PIP2) and the generation of inositol trisphosphate (IP3) in cultured rat aortic smooth muscle cells. Phosphatidylinositol 4,5-Diphosphate 43-80 angiotensinogen Rattus norvegicus 0-14 2987120-1 1985 Angiotensin II stimulated the breakdown of phosphatidylinositol-4,5-bisphosphate (PIP2) and the generation of inositol trisphosphate (IP3) in cultured rat aortic smooth muscle cells. Phosphatidylinositol 4,5-Diphosphate 82-86 angiotensinogen Rattus norvegicus 0-14 6477952-5 1984 However, when phospholipids were prelabeled with [32P]Pi, addition of angiotensin II led to a significant decrease in phosphatidylinositol 4,5-bisphosphate labeling in the first 2 min with no effect on the other phospholipid fractions. Phosphatidylinositol 4,5-Diphosphate 118-155 angiotensinogen Rattus norvegicus 70-84 24448808-0 2014 Phosphoinositide kinases play key roles in norepinephrine- and angiotensin II-induced increase in phosphatidylinositol 4,5-bisphosphate and modulation of cardiac function. Phosphatidylinositol 4,5-Diphosphate 98-135 angiotensinogen Rattus norvegicus 63-77 24448808-3 2014 The results demonstrated that activation of membrane receptors related to NE or Ang II caused an initial increase and a later fall in phosphatidylinositol 4,5-bisphosphate (PIP2) levels in the primary cultured cardiomyocytes from adult rats. Phosphatidylinositol 4,5-Diphosphate 134-171 angiotensinogen Rattus norvegicus 74-86 24448808-3 2014 The results demonstrated that activation of membrane receptors related to NE or Ang II caused an initial increase and a later fall in phosphatidylinositol 4,5-bisphosphate (PIP2) levels in the primary cultured cardiomyocytes from adult rats. Phosphatidylinositol 4,5-Diphosphate 173-177 angiotensinogen Rattus norvegicus 74-86 24448808-5 2014 When the systolic functions of the NE/Ang II-treated cells were measured, a maintained or failed contractility was found to be correlated with a rise or fall in corresponding PIP2 levels. Phosphatidylinositol 4,5-Diphosphate 175-179 angiotensinogen Rattus norvegicus 38-44