PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
8006078-12	1994	The Glu MTs formed after either CS or TGF-beta 1 treatment showed enhanced resistance to nocodazole, confirming that both treatments increased the level of stable MTs in cells.	Nocodazole	89-99	transforming growth factor beta 1	Homo sapiens	38-48	
10678166-5	2000	Destabilization of the MT network by nocodazole, colchicine, or a tubulin mutant disrupts the complex between Smads and MTs and increases TGF beta-induced Smad2 phosphorylation and transcriptional response in CCL64 cells.	Nocodazole	37-47	transforming growth factor beta 1	Homo sapiens	138-146	
21868450-9	2011	In addition, disruption of beta2-tubulin with the microtubule depolymerizers nocodazole and colchicine promoted Smad3 dissociation from beta2-tubulin, increased both TGF-beta1-induced Smad3 nuclear translocation and PAI-1 mRNA expression, and abolished the inhibitory effects of cGMP on these processes.	Nocodazole	77-87	transforming growth factor beta 1	Homo sapiens	166-175	
12746475-7	2003	The profibrogenic response was dependent upon apoptotic body engulfment, because nocodazole, a microtubule-inhibiting agent, blocked both the engulfment and the increase of TGF-beta1 and collagen alpha1(I) mRNA.	Nocodazole	81-91	transforming growth factor beta 1	Homo sapiens	173-182	
17452325-6	2007	Disruption of microtubule networks by nocodazole activates Mps1 and promotes TGF-beta-independent activation of Smad signaling.	Nocodazole	38-48	transforming growth factor beta 1	Homo sapiens	77-85