PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
16467108-10	2006	Lovastatin affected various IR-induced stress responses in HUVEC: It attenuated the increase in p53/p21 protein level and impaired the activation of nuclear factor-kappaB, Chk-1, and Akt kinase but did not inhibit extracellular signal-regulated kinase activation.	Lovastatin	0-10	H3 histone pseudogene 16	Homo sapiens	100-103	
22294184-6	2012	A marked rise in the cell-cycle inhibitor p21, together with reduction of aurora kinases A and B, cyclins B1 and D1 proteins was induced by lovastatin alone or in combination with docetaxel.	Lovastatin	140-150	H3 histone pseudogene 16	Homo sapiens	42-45	
21907187-4	2011	Western blot analysis revealed that lovastatin caused an increase of the protein level of p27 and cyclin-dependent kinase (CDK)4 and a decrease of the protein level of cyclin A2, cyclin D3, and phosphorylated Rb (pRb), but did not significantly change the protein levels of p21, cyclins D1 and E, and CDK2, in ARO cells.	Lovastatin	36-46	H3 histone pseudogene 16	Homo sapiens	274-295	
16985065-9	2006	All three statins (lovastatin, fluvastatin, and simvastatin) inhibited cyclin E/cdk2 kinase leading to hypophosphorylation of Rb, but this inhibition was correlated with a loss of the activating phosphorylation on Thr160 of cyclin E-associated cdk2 and not dependent on the cdk inhibitors p21 and p27.	Lovastatin	19-29	H3 histone pseudogene 16	Homo sapiens	289-292	
24556504-6	2014	Lovastatin supplementation arrested cells in the G0/G1 phase and enhanced expression levels of p21, whereas the conjugate did not demonstrate cell cycle arrest nor increased p21 expression.	Lovastatin	0-10	H3 histone pseudogene 16	Homo sapiens	95-98	
12434292-8	2002	In our previous report, we proved that lovastatin, a pharmacological inhibitor of p21(ras) function, also reversed the increase of cortisol level in mutant K-ras stably transfected human adrenocortical cells.	Lovastatin	39-49	H3 histone pseudogene 16	Homo sapiens	82-85	
10399961-4	1999	We show that p21 ras processing is blocked by lovastatin, suggesting that inhibition of isoprenylation may be important in lovastatin-induced apoptosis.	Lovastatin	46-56	H3 histone pseudogene 16	Homo sapiens	13-16	
11307620-3	2001	Lovastatin and phenylacetate promote p21 accumulation but fail to induce cell cycle arrest.	Lovastatin	0-10	H3 histone pseudogene 16	Homo sapiens	37-40	
10502413-4	1999	The induction of the CKIs by modulators of cAMP such as cholera toxin (CT) + 1-isobutyl-3-methylxanthine (IBMX) and lovastatin fluctuates with biphasic kinetics (although the kinetics of CKI induction with CT + IBMX treatment are different from that of lovastatin) and is depicted by the periodic accumulation of lower molecular weight forms of p21 and p27 which also correlate with fluctuations in CDK2 activity.	Lovastatin	116-126	H3 histone pseudogene 16	Homo sapiens	345-348	
10502413-9	1999	Last, treatment of MDA-MB-157 cells with lovastatin, another known cAMP modulator which also causes growth arrest, resulted in the induction of p21 and p27 without any increase in PKA activity.	Lovastatin	41-51	H3 histone pseudogene 16	Homo sapiens	144-147	
10399961-4	1999	We show that p21 ras processing is blocked by lovastatin, suggesting that inhibition of isoprenylation may be important in lovastatin-induced apoptosis.	Lovastatin	123-133	H3 histone pseudogene 16	Homo sapiens	13-16	
9811471-0	1998	Lovastatin mediated G1 arrest in normal and tumor breast cells is through inhibition of CDK2 activity and redistribution of p21 and p27, independent of p53.	Lovastatin	0-10	H3 histone pseudogene 16	Homo sapiens	124-127	
9811471-4	1998	However, the binding of p21 and p27 to CDK2 increases significantly following treatment of cells with lovastatin leading to inhibition of CDK2 activity and a subsequent arrest of cells in G1.	Lovastatin	102-112	H3 histone pseudogene 16	Homo sapiens	24-27	
9811471-5	1998	The increased CKI binding to CDK2 is achieved by the redistribution of both p21 and p27 from CDK4 to CDK2 complexes subsequent to decreases in CDK4 and cyclin D3 expression following lovastatin treatment.	Lovastatin	183-193	H3 histone pseudogene 16	Homo sapiens	76-79	
9811471-2	1998	In the present study we have investigated the nature of the CKIs (p21 and p27) alterations resulting in G1 arrest in both normal and tumor breast cell lines by lovastatin.	Lovastatin	160-170	H3 histone pseudogene 16	Homo sapiens	66-69	
9811471-3	1998	We show that even though lovastatin treatment causes G1 arrest in a wide variety of normal and tumor breast cells irrespective of their p53 or pRb status, the p21 and p27 protein levels are not increased in all cell lines treated suggesting that the increase in p21 and p27 protein expression per se is not necessary for lovastatin mediated G1 arrest.	Lovastatin	25-35	H3 histone pseudogene 16	Homo sapiens	262-265	
2278880-3	1990	Lovastatin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, may prevent the farnesylation of de novo synthesized ras p21.	Lovastatin	0-10	H3 histone pseudogene 16	Homo sapiens	145-148	
8425769-5	1993	Under the experimental conditions used, lovastatin prevented the membrane association, but not the biosynthesis, of p21.	Lovastatin	40-50	H3 histone pseudogene 16	Homo sapiens	116-119	
33987937-0	2021	Lovastatin reduces PEL cell survival by phosphorylating ERK1/2 that blocks the autophagic flux and engages a cross-talk with p53 to activate p21.	Lovastatin	0-10	H3 histone pseudogene 16	Homo sapiens	141-144	
33987937-4	2021	At molecular level, Lovastatin by dephosphorylating STAT3, induced ERK1/2 activation that inhibited autophagy and phosphorylated p53ser15 that in turn maintained ERK1/2 activated and up-regulated p21.	Lovastatin	20-30	H3 histone pseudogene 16	Homo sapiens	196-199	
33987937-5	2021	However, p21 played a pro-survival role in this setting, as its inhibition by UC2288 further reduced cell survival in PEL cells undergoing Lovastatin treatment.	Lovastatin	139-149	H3 histone pseudogene 16	Homo sapiens	9-12	
33987937-6	2021	In conclusion, this study suggests that Lovastatin may represent a valid therapeutic alternative against PEL cells, especially if used in combination with p21 inhibitors.	Lovastatin	40-50	H3 histone pseudogene 16	Homo sapiens	155-158	
30939155-0	2019	Regulatory mechanisms of fluvastatin and lovastatin for the p21 induction in human cervical cancer HeLa cells.	Lovastatin	41-51	H3 histone pseudogene 16	Homo sapiens	60-63	
30939155-5	2019	Our data showed that the statins-fluvastatin and lovastatin-induced p21 expression as general histone deacetylase inhibitors in a p53-independent manner, which is mediated through various pathways, such as apoptosis, autophagy, cell cycle progression, and DNA damage, to be involved in the function of p21 in HeLa cells.	Lovastatin	49-59	H3 histone pseudogene 16	Homo sapiens	68-71	
30939155-5	2019	Our data showed that the statins-fluvastatin and lovastatin-induced p21 expression as general histone deacetylase inhibitors in a p53-independent manner, which is mediated through various pathways, such as apoptosis, autophagy, cell cycle progression, and DNA damage, to be involved in the function of p21 in HeLa cells.	Lovastatin	49-59	H3 histone pseudogene 16	Homo sapiens	302-305	
30939155-6	2019	The curative effect repositioning of digoxin, a cardiovascular medication, was combined with fluvastatin and lovastatin, and the results further implied that p21 induction is involved in a p53-dependent and p53-independent manner.	Lovastatin	109-119	H3 histone pseudogene 16	Homo sapiens	158-161	
26713523-7	2015	Treatment with 2.5mumol/L SAHA significantly up-regulated the expression of p21 protein in 48 h, while the protein expression was reduced in combined treatment with 5mumol/L lovastatin.	Lovastatin	174-184	H3 histone pseudogene 16	Homo sapiens	76-79