PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
17884942-5	2007	Cytochalasin D, jasplakinolide, latrunculin B, and swinholide A altered the actin cytoskeleton of GH4 cells, as assessed by Alexa Fluor phalloidin staining, and inhibited insulin-increased prolactin gene transcription.	Cytochalasin D	0-14	insulin	Homo sapiens	171-178	
15466888-8	2004	Latrunculin B, cytochalasin D and jasplakinolide, which disrupt actin dynamics, prevented insulin- and PDGF-induced actin remodeling but significantly inhibited GLUT4myc translocation only in response to insulin (75-85%, P<0.05), not to PDGF (20-30% inhibition).	Cytochalasin D	15-29	insulin	Homo sapiens	90-97	
15466888-8	2004	Latrunculin B, cytochalasin D and jasplakinolide, which disrupt actin dynamics, prevented insulin- and PDGF-induced actin remodeling but significantly inhibited GLUT4myc translocation only in response to insulin (75-85%, P<0.05), not to PDGF (20-30% inhibition).	Cytochalasin D	15-29	insulin	Homo sapiens	204-211	
9607310-5	1998	We further show that wortmannin and the cytoskeleton disruptors cytochalasin D and latrunculin B completely blocked these insulin effects.	Cytochalasin D	64-78	insulin	Homo sapiens	122-129	
11786928-2	2002	In the present study, cytochalasin D, which failed to affect D-glucose uptake and metabolism by isolated islets, also augmented glucose-stimulated insulin release, but unexpectedly to a lesser extent than cytochalasin B.	Cytochalasin D	22-36	insulin	Homo sapiens	147-154	
11786928-5	2002	Nevertheless, even in the presence of forskolin, cytochalasin B was more efficient than cytochalasin D in augmenting glucose-stimulated insulin secretion.	Cytochalasin D	88-102	insulin	Homo sapiens	136-143	
11104665-5	2000	Withdrawal of cytochalasin D from the extracellular medium induced actin filament repolymerization, and reinstated both the recruitment of PH-GFP fusion proteins to the plasma membrane and PKB activation in response to insulin and PDGF.	Cytochalasin D	14-28	insulin	Homo sapiens	219-226	
11594774-2	2001	Insulin but not IGF-I or PDGF-induced ERK activation was abrogated by Ras inhibition, either by treatment with the farnesyl transferase inhibitor FTP III, or by actin disassembly by cytochalasin D, previously shown to inhibit Ras activation.	Cytochalasin D	182-196	insulin	Homo sapiens	0-7	
11466321-9	2001	A second inhibitor of endocytosis, cytochalasin D, also blocked insulin-dependent MAPK phosphorylation.	Cytochalasin D	35-49	insulin	Homo sapiens	64-71	
1719004-7	1991	Permeability coefficients for cyanocobalamin (9.66 x 10(-5) cm/s) and insulin (4.18 x 10(-5) cm/s) increased significantly during perfusion with thrombin (10 U/ml) or cytochalasin D (1 microgram/ml), whereas permeability to albumin (0.39 x 10(-5) cm/s) remained unchanged.	Cytochalasin D	167-181	insulin	Homo sapiens	70-77	
2168179-3	1990	Cytochalasin D potentiated insulin secretion in a dose-dependent manner, and the combination of theophylline and cytochalasin D resulted in an insulin secretory response no greater than that produced by either agent alone.	Cytochalasin D	0-14	insulin	Homo sapiens	27-34	
3115801-0	1987	Early stimulation by EGF plus insulin of rRNA, c-fos, and actin mRNA expression: inhibition by cytochalasin D.	Cytochalasin D	95-109	insulin	Homo sapiens	30-37	
3115801-3	1987	We observed that CD slightly increased rRNA synthesis in nonstimulated cells; conversely, it decreased rRNA synthesis in cells stimulated by EGF + insulin.	Cytochalasin D	17-19	insulin	Homo sapiens	147-154	
3115801-5	1987	The c-fos mRNA was not expressed in control cells and was accumulated in cells stimulated by the mixture of EGF + insulin; this accumulation was inhibited by CD.	Cytochalasin D	158-160	insulin	Homo sapiens	114-121