PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
9442036-2	1998	In these cells, dexamethasone, a synthetic glucocorticoid, stimulated a rapid and selective increase in expression of the p21 cyclin-dependent kinase (CDK) inhibitor mRNA and protein and virtually abolished CDK2 phosphorylation of the retinoblastoma protein.	Dexamethasone	16-29	KRAS proto-oncogene, GTPase	Rattus norvegicus	122-125	
9442036-4	1998	Dexamethasone stimulated p21 promoter activity in a p53-independent manner that required functional glucocorticoid receptors.	Dexamethasone	0-13	KRAS proto-oncogene, GTPase	Rattus norvegicus	25-28	
9442036-6	1998	Analysis of 5" deletions of the p21 promoter uncovered a glucocorticoid responsive region between nucleotides -1481 and -1184, which does not contain a canonical glucocorticoid response element but which can confer dexamethasone responsiveness to a heterologous promoter.	Dexamethasone	215-228	KRAS proto-oncogene, GTPase	Rattus norvegicus	32-35	
9442036-8	1998	Finally, ectopic expression of p21 had no effect on hepatoma cell growth in the absence of glucocorticoids but facilitated the ability of dexamethasone to inhibit cell proliferation.	Dexamethasone	138-151	KRAS proto-oncogene, GTPase	Rattus norvegicus	31-34