PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
24811262-8	2014	Flavopiridol NPs significantly decreased inflammatory factor synthesis by astrocytes, including TNF-alpha, IL-1beta, and IL-6, while the IL-10 expression was elevated.	alvocidib	0-12	tumor necrosis factor	Homo sapiens	96-105	
12021392-0	2002	Synergistic induction of apoptosis in human myeloid leukemia cells by phorbol 12-myristate 13-acetate and flavopiridol proceeds via activation of both the intrinsic and tumor necrosis factor-mediated extrinsic cell death pathways.	alvocidib	106-118	tumor necrosis factor	Homo sapiens	169-190	
18287248-0	2008	Flavopiridol suppresses tumor necrosis factor-induced activation of activator protein-1, c-Jun N-terminal kinase, p38 mitogen-activated protein kinase (MAPK), p44/p42 MAPK, and Akt, inhibits expression of antiapoptotic gene products, and enhances apoptosis through cytochrome c release and caspase activation in human myeloid cells.	alvocidib	0-12	tumor necrosis factor	Homo sapiens	24-45	
18287248-2	2008	We have shown previously that flavopiridol abrogates tumor necrosis factor (TNF)-induced nuclear factor-kappaB (NF-kappaB) activation.	alvocidib	30-42	tumor necrosis factor	Homo sapiens	53-74	
18287248-2	2008	We have shown previously that flavopiridol abrogates tumor necrosis factor (TNF)-induced nuclear factor-kappaB (NF-kappaB) activation.	alvocidib	30-42	tumor necrosis factor	Homo sapiens	76-79	
18287248-4	2008	TNF is a potent inducer of activator protein-1 (AP-1), and flavopiridol abrogated this activation in a dose- and time-dependent manner.	alvocidib	59-71	tumor necrosis factor	Homo sapiens	0-3	
18287248-6	2008	When examined for its effect on other signaling pathways, flavopiridol inhibited TNF-induced activation of various mitogen-activated protein kinases, including c-Jun NH(2)-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), and p44/p42 MAPK.	alvocidib	58-70	tumor necrosis factor	Homo sapiens	81-84	
18287248-8	2008	Flavopiridol also inhibited the TNF-induced induction of intercellular adhesion molecule-1, c-Myc, and c-Fos, all known to mediate tumorigenesis.	alvocidib	0-12	tumor necrosis factor	Homo sapiens	32-35	
18287248-9	2008	Moreover, TNF-induced apoptosis was enhanced by flavopiridol through activation of the bid-cytochrome-caspase-9-caspase-3 pathway.	alvocidib	48-60	tumor necrosis factor	Homo sapiens	10-13	
18287248-10	2008	Overall, our results clearly suggest that flavopiridol interferes with the TNF cell-signaling pathway, leading to suppression of antiapoptotic mechanisms and enhancement of apoptosis.	alvocidib	42-54	tumor necrosis factor	Homo sapiens	75-78	
12566305-2	2003	We found that the combination treatment of flavopiridol (100-500 nM) with tumor necrosis factor (TNF)-alpha (10 ng/ml) induced a rapid and eminent apoptosis, 20 +/- 5% in 6-h treatment, in a human non-small cell lung carcinoma cell line, A549, as determined by the increase of sub-G(1) fraction in flow cytometry.	alvocidib	43-55	tumor necrosis factor	Homo sapiens	74-107	
12566305-9	2003	In contrast, flavopiridol was found to inhibit the NF-kappa B-dependent gene transcription, which might give an explanation for the synergistic effect of flavopiridol with TNF-alpha.	alvocidib	13-25	tumor necrosis factor	Homo sapiens	172-181	
12566305-9	2003	In contrast, flavopiridol was found to inhibit the NF-kappa B-dependent gene transcription, which might give an explanation for the synergistic effect of flavopiridol with TNF-alpha.	alvocidib	154-166	tumor necrosis factor	Homo sapiens	172-181