PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9176147-5 1997 Incubation of permeabilized VSMC with anti-PLC-beta 1 or anti-Gq alpha antibodies inhibited ANG II-dependent inositol polyphosphate (IP) formation, while anti-PLC-gamma 1 antibodies did not inhibit ANG II-regulated IP formation. Phytic Acid 109-131 angiotensinogen Homo sapiens 92-98 2547768-8 1989 Treatment with 50 microM cycloheximide abolished the ACTH-induced increases in inositol polyphosphate responses during AII stimulation, but had no effect on the responses of untreated cells to AII. Phytic Acid 79-101 angiotensinogen Homo sapiens 119-122 8255989-4 1993 Angiotensin II (Ang II) and ATP induced the inositol polyphosphate accumulation without 45Ca2+ uptake. Phytic Acid 44-66 angiotensinogen Homo sapiens 0-14 8255989-4 1993 Angiotensin II (Ang II) and ATP induced the inositol polyphosphate accumulation without 45Ca2+ uptake. Phytic Acid 44-66 angiotensinogen Homo sapiens 16-22 8255989-8 1993 12-O-tetradecanoylphorbol-13-acetate inhibited the Ang II-induced inositol polyphosphate accumulation but failed to inhibit the high K(+)-induced one. Phytic Acid 80-102 angiotensinogen Homo sapiens 65-71 2560344-5 1989 There is evidence emerging, but not discussed here, that angiotensin II may also mediate some of its effects on the mammalian proximal tubule via the inositol polyphosphate second messenger system. Phytic Acid 150-172 angiotensinogen Homo sapiens 57-71 12065659-2 2002 The up-regulation of endogenous TH protein or a transfected TH promoter-luciferase construct by AII, veratridine, or PMA (but not by forskolin) is abolished by transfection with a dominant negative FGFR1TK-mutant which localizes to the nucleus and plasma membrane, but not by extracellularly acting FGFR1 antagonists suramin and inositolhexakisphosphate (IP6). Phytic Acid 329-353 angiotensinogen Homo sapiens 96-99 12065659-2 2002 The up-regulation of endogenous TH protein or a transfected TH promoter-luciferase construct by AII, veratridine, or PMA (but not by forskolin) is abolished by transfection with a dominant negative FGFR1TK-mutant which localizes to the nucleus and plasma membrane, but not by extracellularly acting FGFR1 antagonists suramin and inositolhexakisphosphate (IP6). Phytic Acid 355-358 angiotensinogen Homo sapiens 96-99