PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
19200052-0	2009	TNF-alpha induction by nickel compounds is specific through ERKs/AP-1-dependent pathway in human bronchial epithelial cells.	Nickel	23-29	tumor necrosis factor	Homo sapiens	0-9	
19200052-3	2009	The current study demonstrates that exposure of human bronchial epithelial cells (Beas-2B) to nickel compounds results in the induction of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) and transactivation of nuclear factor of activated T cells (NFAT), nuclear factor-kappaB (NF-kappaB), and activator protein-1 (AP-1).	Nickel	94-100	tumor necrosis factor	Homo sapiens	165-192	
19200052-3	2009	The current study demonstrates that exposure of human bronchial epithelial cells (Beas-2B) to nickel compounds results in the induction of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) and transactivation of nuclear factor of activated T cells (NFAT), nuclear factor-kappaB (NF-kappaB), and activator protein-1 (AP-1).	Nickel	94-100	tumor necrosis factor	Homo sapiens	194-203	
19200052-4	2009	Further studies show that neither overexpression of IKKbeta-KM, a kinase inactive mutant of IKKbeta, nor the ectopic expression of a dominant negative mutant of NFAT could inhibit the TNF-alpha induction by nickel exposure.	Nickel	207-213	tumor necrosis factor	Homo sapiens	184-193	
19200052-5	2009	Overexpression of TAM67, a dominant-negative mutant of c-Jun, dramatically reduced the TNF-alpha induction, suggesting that AP-1 is a mediator of TNF-alpha induction in nickel responses.	Nickel	169-175	tumor necrosis factor	Homo sapiens	87-96	
19200052-5	2009	Overexpression of TAM67, a dominant-negative mutant of c-Jun, dramatically reduced the TNF-alpha induction, suggesting that AP-1 is a mediator of TNF-alpha induction in nickel responses.	Nickel	169-175	tumor necrosis factor	Homo sapiens	146-155	
19200052-6	2009	Our results show that ERKs are AP-1 upstream kinases responsible for TNF-alpha induction by nickel exposure; although JNKs, ERKs, and p38K were all activated in the Beas-2B cells exposed to nickel compounds.	Nickel	92-98	tumor necrosis factor	Homo sapiens	69-78	
19200052-6	2009	Our results show that ERKs are AP-1 upstream kinases responsible for TNF-alpha induction by nickel exposure; although JNKs, ERKs, and p38K were all activated in the Beas-2B cells exposed to nickel compounds.	Nickel	190-196	tumor necrosis factor	Homo sapiens	69-78	
19200052-7	2009	Our results demonstrate that inflammatory TNF-alpha could be induced by nickel exposure in Beas-2B cells specifically through an ERKs/AP-1-dependent pathway.	Nickel	72-78	tumor necrosis factor	Homo sapiens	42-51