PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
8983024-5	1996	Significantly, in the absence of the valine-12 activating mutation, tryptophan-28-ras ([W28]p21) was weakly transforming while, in contrast, [V12D28]p21 was unable to transform Rat-1 cells and retarded cell growth.	Tryptophan	68-78	KRAS proto-oncogene, GTPase	Rattus norvegicus	92-95
8983024-7	1996	The dissociation rate of both GTP and GDP bound to [W28]p21 is increased, suggesting a mechanism for its transforming potential in Rat-1 cells.	Guanosine Triphosphate	30-33	KRAS proto-oncogene, GTPase	Rattus norvegicus	56-59
8983024-7	1996	The dissociation rate of both GTP and GDP bound to [W28]p21 is increased, suggesting a mechanism for its transforming potential in Rat-1 cells.	Guanosine Diphosphate	38-41	KRAS proto-oncogene, GTPase	Rattus norvegicus	56-59
8825387-7	1996	At P21, Ki of bilirubin was significantly lower than at P10 and ranged from 0.03-0.06 microL/g/min in most brain areas.	Bilirubin	14-23	KRAS proto-oncogene, GTPase	Rattus norvegicus	3-6
8825387-10	1996	At P21, hyperbilirubinemia induced increases in blood-to-brain transfer of bilirubin of 50-200% in 16 brain areas, except in the hippocampus, sensory-motor cortex, and thalamic nuclei where they reached 200-433%.	Bilirubin	13-22	KRAS proto-oncogene, GTPase	Rattus norvegicus	3-6
8545279-15	1996	An activating point mutation was detected in codon 12 of the Ki-ras oncogene in the MNU-induced primary prostate tumors (8/10 examined), and metastases arising from these prostate tumors (2/3) but was absent in normal prostate tissue (0/6).	Methylnitrosourea	84-87	KRAS proto-oncogene, GTPase	Rattus norvegicus	61-67
8519419-8	1995	The 4-NQO-induced rat oral carcinogenesis model may provide a system for evaluation of the mechanisms of multistage oral carcinogenesis associated with Ha-ras mutation without Ki-ras, N-ras, or p53 mutation.	4-Nitroquinoline-1-oxide	4-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	176-182
7592744-7	1995	This difference cannot be explained by a lower affinity of non-isoprenylated rhoA p21 for GTP gamma S, as the rates of [35S]GTP gamma S binding were very similar for both recombinant preparations and the GTP gamma S-bound form of non-isoprenylated rhoA p21 did not induce PLD activation.	Guanosine Triphosphate	90-93	KRAS proto-oncogene, GTPase	Rattus norvegicus	82-85
7585583-8	1995	Thus, p21-ras may increase the percentage of cells that acquire mutations in response to DEN, or it may behave synergistically with other mutations to increase the replication rate of cells.	Diethylnitrosamine	89-92	KRAS proto-oncogene, GTPase	Rattus norvegicus	6-9
8991784-4	1995	Seizures induced a generalized increase in BBB permeability to AIB that was significant in 22 and 26 regions out of the 34 studied at P10 and P21, respectively.	2-aminoisobutyric acid	63-66	KRAS proto-oncogene, GTPase	Rattus norvegicus	142-145
7592744-9	1995	The synergistic activation was inhibited by C3 exoenzyme-catalyzed ADP-ribosylation of recombinant isoprenylated rhoA p21 in a NAD-dependent manner.	Adenosine Diphosphate	67-70	KRAS proto-oncogene, GTPase	Rattus norvegicus	118-121
7592744-9	1995	The synergistic activation was inhibited by C3 exoenzyme-catalyzed ADP-ribosylation of recombinant isoprenylated rhoA p21 in a NAD-dependent manner.	NAD	127-130	KRAS proto-oncogene, GTPase	Rattus norvegicus	118-121
7559638-7	1995	Recombinant alpha- and beta-PAKs exhibited an increase in kinase activity mediated by GTP-p21 induced autophosphorylation.	Guanosine Triphosphate	86-89	KRAS proto-oncogene, GTPase	Rattus norvegicus	90-93
7592744-2	1995	The partially purified preparation contained a 22-kDa substrate for Clostridium botulinum C3 exoenzyme ADP-ribosyltransferase, which strongly reacted with anti-rhoA p21 antibody, but not with anti-rac1 p21 or anti-cdc42Hs p21 antibody.	22-kda	47-53	KRAS proto-oncogene, GTPase	Rattus norvegicus	165-168
7592744-2	1995	The partially purified preparation contained a 22-kDa substrate for Clostridium botulinum C3 exoenzyme ADP-ribosyltransferase, which strongly reacted with anti-rhoA p21 antibody, but not with anti-rac1 p21 or anti-cdc42Hs p21 antibody.	22-kda	47-53	KRAS proto-oncogene, GTPase	Rattus norvegicus	202-205
7592744-2	1995	The partially purified preparation contained a 22-kDa substrate for Clostridium botulinum C3 exoenzyme ADP-ribosyltransferase, which strongly reacted with anti-rhoA p21 antibody, but not with anti-rac1 p21 or anti-cdc42Hs p21 antibody.	22-kda	47-53	KRAS proto-oncogene, GTPase	Rattus norvegicus	202-205
7592744-5	1995	Recombinant isoprenylated rhoA p21 expressed in and purified from Sf9 cells activated rat brain PLD in a concentration- and GTP gamma S (guanosine 5"-O-(3-thiotriphosphate))-dependent manner.	Guanosine 5'-O-(3-Thiotriphosphate)	124-135	KRAS proto-oncogene, GTPase	Rattus norvegicus	31-34
7592744-5	1995	Recombinant isoprenylated rhoA p21 expressed in and purified from Sf9 cells activated rat brain PLD in a concentration- and GTP gamma S (guanosine 5"-O-(3-thiotriphosphate))-dependent manner.	guanosine 5"-o-	137-152	KRAS proto-oncogene, GTPase	Rattus norvegicus	31-34
7592744-5	1995	Recombinant isoprenylated rhoA p21 expressed in and purified from Sf9 cells activated rat brain PLD in a concentration- and GTP gamma S (guanosine 5"-O-(3-thiotriphosphate))-dependent manner.	3-thiotriphosphate	153-171	KRAS proto-oncogene, GTPase	Rattus norvegicus	31-34
7552752-1	1995	The ARFs are a family of 21,000 M(r) proteins with biological roles in constitutive secretion and activation of phospholipase D. The structure of ARF-1 complexed to GDP determined from two crystal forms reveals a topology that is similar to that of the protein p21 ras with two differences: an additional amino-terminal helix and an extra beta-strand.	Guanosine Diphosphate	165-168	KRAS proto-oncogene, GTPase	Rattus norvegicus	261-264
7585451-0	1995	Frequent mutations of Ki-ras codon 12 in N-bis (2-hydroxypropyl)-nitrosamine-initiated thyroid, kidney and lung tumors in Wistar rats.	diisopropanolnitrosamine	41-76	KRAS proto-oncogene, GTPase	Rattus norvegicus	22-28
8522067-8	1995	Additionally, trophic hormone treatment increased steroid production in Ki-GLOM cells and this increase was partially reversed by lovastatin, a pharmacological inhibitor of ras p21 function.	Lovastatin	130-140	KRAS proto-oncogene, GTPase	Rattus norvegicus	177-180
8903758-10	1995	Indeed, the effects of the dye are quite discrete during moderate hyperbilirubinemia at P21 when no bilirubin is detectable in the brain while they are massive during severe hyperbilirubinemia at P21 and at both levels of intoxication at P10 when bilirubin has entered the brain in measurable amounts.	Bilirubin	71-80	KRAS proto-oncogene, GTPase	Rattus norvegicus	88-91
8903758-10	1995	Indeed, the effects of the dye are quite discrete during moderate hyperbilirubinemia at P21 when no bilirubin is detectable in the brain while they are massive during severe hyperbilirubinemia at P21 and at both levels of intoxication at P10 when bilirubin has entered the brain in measurable amounts.	Bilirubin	100-109	KRAS proto-oncogene, GTPase	Rattus norvegicus	88-91
7675178-2	1995	Seizures were induced by repetitive intraperitoneal injections of subconvulsive doses of pentylenetetrazol either in 10- (P10) or in 21- (P21) day-old rats.	Pentylenetetrazole	89-106	KRAS proto-oncogene, GTPase	Rattus norvegicus	138-141
7616247-5	1995	In contrast, after P21, PKC activity and alpha-, beta-, epsilon-, and gamma-PKC immunoreactivities were decreased by baclofen in the membrane fraction and increased in the cytosol.	Baclofen	117-125	KRAS proto-oncogene, GTPase	Rattus norvegicus	19-22
7675178-8	1995	In the animals exposed to seizures at P21, metabolic activity was also reduced at P60 in additional sensory and cortical regions, as well as in limbic, thalamic and hypothalamic nuclei, also considered as highly sensitive to short-term pentylenetetrazol-induced seizures [Pereira de Vasconcelos A. et.	Pentylenetetrazole	236-253	KRAS proto-oncogene, GTPase	Rattus norvegicus	38-41
7727039-5	1995	The approximately 11% frequency of mutation in IQ-induced ACF is within the range of previous ACF studies of azoxymethane, which reported a 7-37% incidence of Ki-ras mutation.	Azoxymethane	109-121	KRAS proto-oncogene, GTPase	Rattus norvegicus	159-165
7494090-4	1995	The FTase is assayed as the transfer of [3H]farnesyl group from [3H]FPP to the ras p21 at pH 7.4 and 37 degrees C in the presence of rat brain cytosol followed by the binding of radioactive farnesylated ras p21 to the phosphocellulose paper.	Tritium	41-43	KRAS proto-oncogene, GTPase	Rattus norvegicus	83-86
7537694-0	1995	cAMP inhibits IGF-I-induced mitogenesis in fetal rat brown adipocytes: role of p21 ras.	Cyclic AMP	0-4	KRAS proto-oncogene, GTPase	Rattus norvegicus	79-82
7766307-0	1995	Ki-ras mutations with frequent normal allele loss versus absence of p53 mutations in rat prostate and seminal vesicle carcinomas induced with 3,2"-dimethyl-4-aminobiphenyl.	2',3-dimethyl-4-aminobiphenyl	142-171	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-6
7766307-7	1995	These results indicate that mutational activation of the Ki-ras gene, but not of the Ha-ras or p53 genes may play a mechanistic role in prostate and seminal vesicle carcinogenesis by DMAB and that a loss of the normal allele of the Ki-ras gene may also be involved in the process.	2',3-dimethyl-4-aminobiphenyl	183-187	KRAS proto-oncogene, GTPase	Rattus norvegicus	57-63
7781173-5	1995	When rats were exposed to high levels of mercury vapour during early embryonic development there was a significant (62%) increase in hippocampal NGF levels at P21 accompanied by a 50% decrease of NGF in the basal forebrain.	Mercury	41-48	KRAS proto-oncogene, GTPase	Rattus norvegicus	159-162
21556557-1	1995	A highly sensitive mutation detection method was applied to reveal tarry K-ras alterations in exfoliated intestinal epithelium of Fischer-344 rats during the course of 1,2-dimethylhydrazine (DMH)-induced carcinogenesis.	1,2-Dimethylhydrazine	168-189	KRAS proto-oncogene, GTPase	Rattus norvegicus	73-78
7860661-1	1995	The quantitative autoradiographic [14C]-iodoantipyrine technique was applied to measure the effects of a 30-min period of pentylenetetrazol (PTZ)-induced status epilepticus (SE) on local cerebral blood flow (LCBF) in rats 10 (P10), 14 (P14), 17 (P17), and 21 (P21) days after birth.	Pentylenetetrazole	141-144	KRAS proto-oncogene, GTPase	Rattus norvegicus	260-263
21556557-1	1995	A highly sensitive mutation detection method was applied to reveal tarry K-ras alterations in exfoliated intestinal epithelium of Fischer-344 rats during the course of 1,2-dimethylhydrazine (DMH)-induced carcinogenesis.	1,2-Dimethylhydrazine	191-194	KRAS proto-oncogene, GTPase	Rattus norvegicus	73-78
21556557-3	1995	Analysis of DNA extracted from fresh fecal samples obtained individually showed that proportion of codon 12 K-ras oncogene mutant alleles (G-->A transition at the second position of codon 12) was increased in some rats at 4 weeks and clearly in all rats at 8 weeks after initial DMH injection, i.e. much earlier than the first tumors appeared (14 weeks).	1,2-Dimethylhydrazine	282-285	KRAS proto-oncogene, GTPase	Rattus norvegicus	108-113
7537485-12	1995	p21 c-Ha-ras expression and location along the colon crypt axis showed a different pattern when compared to p62 c-myc and phosphotyrosine.	Phosphotyrosine	122-137	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-3
7537485-13	1995	The p21 c-Ha-ras protein was prominently expressed in surface epithelium of normal and DMH-treated rats.	Dimenhydrinate	87-90	KRAS proto-oncogene, GTPase	Rattus norvegicus	4-7
7895812-5	1995	Likewise, DZP induced marked decreases (19-45%) in LCMRglcs in most structures studied at P10, P14, and P21.	Diazepam	10-13	KRAS proto-oncogene, GTPase	Rattus norvegicus	104-107
7718489-0	1995	Ki-ras oncogene interferes with the expression of cyclic AMP-dependent promoters.	Cyclic AMP	50-60	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-6
7961691-6	1994	These data raise the possibility that untransformed cells contain a form of Ras (K-Ras or N-Ras) whose prenylation is not inhibited by BZA-5B, thus allowing them to resist the effects of BZA-5B.	BZA 5B	187-193	KRAS proto-oncogene, GTPase	Rattus norvegicus	81-86
8562320-2	1995	Oligonucleotide probes were generated to distinguish these two homologous subtypes by in situ histochemical analysis in E14, E16, E19, P0, P8, P14, P21, and adult animals.	Oligonucleotides	0-15	KRAS proto-oncogene, GTPase	Rattus norvegicus	148-151
18475668-5	1995	Signal transduction analysis reveals that IL-6-induced MHC class II expression is specifically mediated by the G-protein system (activation of p21(ras) by IL-6) since mevalonic acid lactone (a Gprotein inhibitor) abolishes the action of IL-6.	mevalonolactone	167-189	KRAS proto-oncogene, GTPase	Rattus norvegicus	143-146
21559673-9	1994	AOM-induced G to A transitions were observed at the second nucleotide of 12th codon of K-ras substituting amino acid asp with wild-type gly.	Aspartic Acid	117-120	KRAS proto-oncogene, GTPase	Rattus norvegicus	87-92
21559673-9	1994	AOM-induced G to A transitions were observed at the second nucleotide of 12th codon of K-ras substituting amino acid asp with wild-type gly.	Glycine	136-139	KRAS proto-oncogene, GTPase	Rattus norvegicus	87-92
21559673-10	1994	Sulindac not only suppressed the selective amplification of initiated cells possessing AOM-induced mutated K-ras codon 12, but significantly inhibited the AOM-induced expression of total and mutant ras-p21.	Sulindac	0-8	KRAS proto-oncogene, GTPase	Rattus norvegicus	107-112
21559673-10	1994	Sulindac not only suppressed the selective amplification of initiated cells possessing AOM-induced mutated K-ras codon 12, but significantly inhibited the AOM-induced expression of total and mutant ras-p21.	Sulindac	0-8	KRAS proto-oncogene, GTPase	Rattus norvegicus	202-205
8062217-0	1994	Ki-ras oncogene activation in transplantable rat thyroid carcinoma induced by N-bis(2-hydroxypropyl)nitrosamine.	diisopropanolnitrosamine	78-111	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-6
8058308-1	1994	Previously we reported the detection of transforming K-ras sequences in methyl(methoxymethyl)nitrosamine (DMN-OMe)-induced rat renal mesenchymal tumors by NIH3T3 transfection assays.	Methoxymethyl-methylnitrosamine	72-104	KRAS proto-oncogene, GTPase	Rattus norvegicus	53-58
8058308-1	1994	Previously we reported the detection of transforming K-ras sequences in methyl(methoxymethyl)nitrosamine (DMN-OMe)-induced rat renal mesenchymal tumors by NIH3T3 transfection assays.	dmn-ome	106-113	KRAS proto-oncogene, GTPase	Rattus norvegicus	53-58
8058308-2	1994	Subsequent analysis by selective oligonucleotide hybridization revealed a variety of activating point mutations in codon 12 of K-ras in most of these tumors and in their NIH3T3 transformants, but in some, point mutations could not be detected by this technique.	Oligonucleotides	33-48	KRAS proto-oncogene, GTPase	Rattus norvegicus	127-132
8048943-3	1994	alpha-Difluoromethylornithine, a specific inhibitor of ODC, prevented the transcription of c-myc in cells grown at 37 degrees C. Putrescine, at physiological concentrations, triggered the transcription of c-myc and c-fos in cells grown at 42 degrees C, when Ki-ras was not expressed.	Eflornithine	0-29	KRAS proto-oncogene, GTPase	Rattus norvegicus	258-264
7962709-2	1994	To understand the role for GABA in development, we investigated the expression of transcripts encoding two forms of the GABA-synthesizing enzyme glutamate decarboxylase (GAD65 and GAD67) in the cervical enlargement of the rat spinal cord at successive postnatal days--P0, P7, P14, P21, and P90 (adult)--by using in situ hybridization histochemistry.	gamma-Aminobutyric Acid	120-124	KRAS proto-oncogene, GTPase	Rattus norvegicus	281-284
8048943-3	1994	alpha-Difluoromethylornithine, a specific inhibitor of ODC, prevented the transcription of c-myc in cells grown at 37 degrees C. Putrescine, at physiological concentrations, triggered the transcription of c-myc and c-fos in cells grown at 42 degrees C, when Ki-ras was not expressed.	Putrescine	129-139	KRAS proto-oncogene, GTPase	Rattus norvegicus	258-264
8033306-1	1994	In our previous study, we demonstrated that azoxymethane (AOM) treatment significantly enhanced the expression of ras p21, the protein product of ras genes, and that the dietary administration of chemopreventive agents such as D,L-alpha-difluoromethylornithine (DFMO), a irreversible inhibitor of ornithine decarboxylase, and piroxicam, a non-steroidal anti-inflammatory drug (NSAID), exerted a significant inhibitory effect on AOM-induced ras p21 expression.	Azoxymethane	44-56	KRAS proto-oncogene, GTPase	Rattus norvegicus	118-121
8033306-1	1994	In our previous study, we demonstrated that azoxymethane (AOM) treatment significantly enhanced the expression of ras p21, the protein product of ras genes, and that the dietary administration of chemopreventive agents such as D,L-alpha-difluoromethylornithine (DFMO), a irreversible inhibitor of ornithine decarboxylase, and piroxicam, a non-steroidal anti-inflammatory drug (NSAID), exerted a significant inhibitory effect on AOM-induced ras p21 expression.	Azoxymethane	44-56	KRAS proto-oncogene, GTPase	Rattus norvegicus	444-447
8012978-1	1994	Monoterpenes, including limonene and its in vivo rat plasma metabolites, have been shown to be inhibitors of protein isoprenylation of small G proteins, including p21 ras.	Monoterpenes	0-12	KRAS proto-oncogene, GTPase	Rattus norvegicus	163-166
8012978-1	1994	Monoterpenes, including limonene and its in vivo rat plasma metabolites, have been shown to be inhibitors of protein isoprenylation of small G proteins, including p21 ras.	Limonene	24-32	KRAS proto-oncogene, GTPase	Rattus norvegicus	163-166
8012978-3	1994	On the basis of these observations, it was hypothesized that a possible mechanism by which limonene exerts its effects on the chemoprevention and regression of mammary tumors involves the inhibition of protein isoprenylation of the small G protein p21.	Limonene	91-99	KRAS proto-oncogene, GTPase	Rattus norvegicus	248-251
8033306-1	1994	In our previous study, we demonstrated that azoxymethane (AOM) treatment significantly enhanced the expression of ras p21, the protein product of ras genes, and that the dietary administration of chemopreventive agents such as D,L-alpha-difluoromethylornithine (DFMO), a irreversible inhibitor of ornithine decarboxylase, and piroxicam, a non-steroidal anti-inflammatory drug (NSAID), exerted a significant inhibitory effect on AOM-induced ras p21 expression.	Azoxymethane	58-61	KRAS proto-oncogene, GTPase	Rattus norvegicus	118-121
8033306-1	1994	In our previous study, we demonstrated that azoxymethane (AOM) treatment significantly enhanced the expression of ras p21, the protein product of ras genes, and that the dietary administration of chemopreventive agents such as D,L-alpha-difluoromethylornithine (DFMO), a irreversible inhibitor of ornithine decarboxylase, and piroxicam, a non-steroidal anti-inflammatory drug (NSAID), exerted a significant inhibitory effect on AOM-induced ras p21 expression.	Azoxymethane	58-61	KRAS proto-oncogene, GTPase	Rattus norvegicus	444-447
7910516-0	1994	Correlation between S-adenosyl-L-methionine content and production of c-myc, c-Ha-ras, and c-Ki-ras mRNA transcripts in the early stages of rat liver carcinogenesis.	S-Adenosylmethionine	20-43	KRAS proto-oncogene, GTPase	Rattus norvegicus	91-99
8185829-5	1994	On the other hand, Ki-ras codon 12 mutations were found at low frequency in HCCs, hyperplastic foci, and cholangiofibroses induced by 3"-Me-DAB and by AFB1 but not in the lesions induced by the Solt and Farber regimen.	Methyldimethylaminoazobenzene	134-143	KRAS proto-oncogene, GTPase	Rattus norvegicus	19-25
7817118-6	1994	The protooncogene product ras p21 protein was present in the majority of PB- and TCDD-promoted AHF, hepatocellular adenomas, and hepatocellular carcinomas.	Polychlorinated Dibenzodioxins	81-85	KRAS proto-oncogene, GTPase	Rattus norvegicus	30-33
8190274-4	1994	A similar growth of dopamine fibers took place in the substantia nigra after lesions made at P6, P9 and P12, but was less pronounced after lesion at P15 and absent after lesion at P21 or later.	Dopamine	20-28	KRAS proto-oncogene, GTPase	Rattus norvegicus	180-183
8149495-0	1994	Sequential analysis of K-ras mutations in aberrant crypt foci and colonic tumors induced by azoxymethane in Fischer-344 rats on high-risk diet.	Azoxymethane	92-104	KRAS proto-oncogene, GTPase	Rattus norvegicus	23-28
8168525-3	1994	The levels of this lysolipid increased by 2-3-fold in ras-transformed cells (KiKi cells and Ts cells at the permissive temperature of 33 degrees C) as compared to differentiated cells (FRTL5) or to Ts cells maintained at 39 degrees C, i.e. at the temperature where ras-p21, the product of the ras oncogene, is inactive.	lysolipid	19-28	KRAS proto-oncogene, GTPase	Rattus norvegicus	269-272
7545909-0	1994	Analysis of K-ras, p53 and c-raf-1 mutations in beryllium-induced rat lung tumors.	Beryllium	48-57	KRAS proto-oncogene, GTPase	Rattus norvegicus	12-17
7508916-5	1994	These results show that elevation of intracellular cAMP levels abrogates the p21ras MAP kinase pathway at a step downstream of p21ras activation.	Cyclic AMP	51-55	KRAS proto-oncogene, GTPase	Rattus norvegicus	77-80
7545909-9	1994	These results suggest that activation of the K-ras protooncogene is both a rare and late event, possibly stemming from genomic instability during the progression of some Be-induced rat adenocarcinomas of the lung.	Beryllium	170-172	KRAS proto-oncogene, GTPase	Rattus norvegicus	45-50
8226727-3	1993	When expressed in Rat-1 cells, stimulation of the alpha 2A receptor, which couples to Gi2 and Gi3, causes rapid, transient activation of the protooncogene product p21ras as measured by an increase in the amount of bound GTP.	Guanosine Triphosphate	220-223	KRAS proto-oncogene, GTPase	Rattus norvegicus	163-166
8149586-8	1993	These changes in LCBF are in quite good correlation with our previous data on the effects of acute hypoxia exposure on cerebral glucose utilization but the decrease in LCBF is of higher amplitude than the one in cerebral glucose utilization translating into a relative hypoperfusion at a constant metabolic level at P14 and P21.	Glucose	221-228	KRAS proto-oncogene, GTPase	Rattus norvegicus	324-327
8226805-7	1993	The dissociation constant of p100GAPras toward ras p21 estimated by competitive inhibition using ras p21 in complex with nonhydrolyzable analog of GTP was two times higher than that of neurofibromin and was lower than that of GAP by 2 orders of magnitude.	Guanosine Triphosphate	147-150	KRAS proto-oncogene, GTPase	Rattus norvegicus	51-54
8226805-7	1993	The dissociation constant of p100GAPras toward ras p21 estimated by competitive inhibition using ras p21 in complex with nonhydrolyzable analog of GTP was two times higher than that of neurofibromin and was lower than that of GAP by 2 orders of magnitude.	Guanosine Triphosphate	147-150	KRAS proto-oncogene, GTPase	Rattus norvegicus	101-104
8403199-0	1993	K-ras mutations in aberrant crypt foci, adenomas and adenocarcinomas during azoxymethane-induced colon carcinogenesis.	Azoxymethane	76-88	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-5
8403199-10	1993	These data suggest that K-ras mutations play a role during the stages of carcinogenesis in azoxymethane-induced rat colon cancer.	Azoxymethane	91-103	KRAS proto-oncogene, GTPase	Rattus norvegicus	24-29
8478903-4	1993	The X-ray crystallographic data for [99TcO(8)]AsPh4 (space group P2(1)/n: Z = 4, a = 9.342(3) A; b = 18.594(5) A; c = 18.417(7) A; beta, deg = 90.61(3); V, A3 = 3199.1(20)) show that the Tc is bound to both thiolate sulfur atoms and to two deprotonated amide nitrogen atoms.	[99tco(	36-43	KRAS proto-oncogene, GTPase	Rattus norvegicus	65-70
8508505-1	1993	Prior studies from our laboratory have demonstrated that K-ras G to A mutations were detectable in a high percentage of carcinomas which developed in the colons of animals treated with the known colonic procarcinogen, 1,2-dimethyl-hydrazine (DMH).	1,2-Dimethylhydrazine	218-240	KRAS proto-oncogene, GTPase	Rattus norvegicus	57-62
8508505-1	1993	Prior studies from our laboratory have demonstrated that K-ras G to A mutations were detectable in a high percentage of carcinomas which developed in the colons of animals treated with the known colonic procarcinogen, 1,2-dimethyl-hydrazine (DMH).	1,2-Dimethylhydrazine	242-245	KRAS proto-oncogene, GTPase	Rattus norvegicus	57-62
8446626-0	1993	Activation of the c-Ki-ras oncogene in aflatoxin B1-induced hepatocellular carcinoma and adenoma in the rat: detection by denaturing gradient gel electrophoresis.	Aflatoxin B1	39-51	KRAS proto-oncogene, GTPase	Rattus norvegicus	18-26
8462284-6	1993	Injection of insulin in alloxan-induced diabetic rats is able to restore almost completely the level of c-Ki-ras transcript found in insulin-induced normal rats.	Alloxan	24-31	KRAS proto-oncogene, GTPase	Rattus norvegicus	104-112
8441421-0	1993	Epidermal growth factor regulates the exchange rate of guanine nucleotides on p21ras in fibroblasts.	Guanine Nucleotides	55-74	KRAS proto-oncogene, GTPase	Rattus norvegicus	78-81
8352890-0	1993	Rare frequency of activation of the Ki-ras gene in rat colon tumors induced by heterocyclic amines: possible alternative mechanisms of human colon carcinogenesis.	heterocyclic amines	79-98	KRAS proto-oncogene, GTPase	Rattus norvegicus	36-42
8429245-0	1993	[Mutational activation of H-ras and K-ras (Codon 12,61) genes in 7,12 dimethylbenz(a)anthracene induced rat ovarian tumors].	anthracene	85-95	KRAS proto-oncogene, GTPase	Rattus norvegicus	36-41
8429245-1	1993	We had studied the histogenesis and p21 expression in ovarian tumor induced by 7,12-dimethylbenz(a)anthracene (DMBA).	7,12-dimethylbenz	79-96	KRAS proto-oncogene, GTPase	Rattus norvegicus	36-39
8429245-1	1993	We had studied the histogenesis and p21 expression in ovarian tumor induced by 7,12-dimethylbenz(a)anthracene (DMBA).	anthracene	99-109	KRAS proto-oncogene, GTPase	Rattus norvegicus	36-39
8429245-1	1993	We had studied the histogenesis and p21 expression in ovarian tumor induced by 7,12-dimethylbenz(a)anthracene (DMBA).	9,10-Dimethyl-1,2-benzanthracene	111-115	KRAS proto-oncogene, GTPase	Rattus norvegicus	36-39
8435109-2	1993	Farnesyl synthesis and p21 ras farnesylation are inhibited by hydroxymethylglutaryl-CoA reductase inhibitors such as lovastatin.	Lovastatin	117-127	KRAS proto-oncogene, GTPase	Rattus norvegicus	23-26
8435109-5	1993	Membrane association of p21 ras in these cells was inhibited after in vitro treatment with lovastatin (0.1-0.5 microM) for 48 h. Concomitantly, the cells displayed a more normal morphology, decreased growth in soft agar, and enhanced GJIC.	Lovastatin	91-101	KRAS proto-oncogene, GTPase	Rattus norvegicus	24-27
8435109-5	1993	Membrane association of p21 ras in these cells was inhibited after in vitro treatment with lovastatin (0.1-0.5 microM) for 48 h. Concomitantly, the cells displayed a more normal morphology, decreased growth in soft agar, and enhanced GJIC.	Agar	215-219	KRAS proto-oncogene, GTPase	Rattus norvegicus	24-27
8435109-10	1993	These results suggest that lovastatin reversed the transformed phenotype of WB-ras cells by inhibiting p21 ras plasma membrane association.	Lovastatin	27-37	KRAS proto-oncogene, GTPase	Rattus norvegicus	103-106
8352890-3	1993	A Ki-ras gene mutation (G-->T at the second position in codon 12) was found in one Glu-P-1-induced colon adenocarcinoma.	Glutamic Acid	86-89	KRAS proto-oncogene, GTPase	Rattus norvegicus	2-8
8352890-3	1993	A Ki-ras gene mutation (G-->T at the second position in codon 12) was found in one Glu-P-1-induced colon adenocarcinoma.	Phosphorus	90-91	KRAS proto-oncogene, GTPase	Rattus norvegicus	2-8
1480166-0	1992	Transcription induction of c-Ki-ras with the tumour promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) in normal and transformed liver cells.	Tetradecanoylphorbol Acetate	61-97	KRAS proto-oncogene, GTPase	Rattus norvegicus	27-35
1480166-0	1992	Transcription induction of c-Ki-ras with the tumour promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) in normal and transformed liver cells.	Tetradecanoylphorbol Acetate	99-102	KRAS proto-oncogene, GTPase	Rattus norvegicus	27-35
1480166-1	1992	Results from nuclear run-off assays show that exposure of hepatocytes and Reuber H35B hepatoma cells to the tumour promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), leads to enhanced transcription of c-Ki-ras gene.	Tetradecanoylphorbol Acetate	125-161	KRAS proto-oncogene, GTPase	Rattus norvegicus	204-212
1424100-3	1992	The quantitative autoradiographic [14C]2-deoxyglucose technique (2DG) was applied to measure the effects of pentylenetetrazol (PTZ)-induced status epilepticus (SE) on local cerebral metabolic rates for glucose (LCMRglc) in 10 (P10)-, 14 (P14)-, 17 (P17)- and 21 (P21)-day-old rats.	Pentylenetetrazole	127-130	KRAS proto-oncogene, GTPase	Rattus norvegicus	263-266
1424100-8	1992	In a few cerebral regions, such as hippocampus, dentate gyrus and mammillary body, LCMRglc did not increase at P10 and P14 and decreased at P17 and P21 in PTZ- vs. saline-treated rats.	Pentylenetetrazole	155-158	KRAS proto-oncogene, GTPase	Rattus norvegicus	148-151
1512271-0	1992	K-ras transformation greatly increases the toxin-dependent ADP-ribosylation of GTP binding proteins in thyroid cells.	Adenosine Diphosphate	59-62	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-5
1511440-0	1992	GGT to GTT transversions in codon 12 of the K-ras oncogene in rat renal sarcomas induced with nickel subsulfide or nickel subsulfide/iron are consistent with oxidative damage to DNA.	nickel subsulfide	94-111	KRAS proto-oncogene, GTPase	Rattus norvegicus	44-49
1511440-0	1992	GGT to GTT transversions in codon 12 of the K-ras oncogene in rat renal sarcomas induced with nickel subsulfide or nickel subsulfide/iron are consistent with oxidative damage to DNA.	nickel subsulfide	115-132	KRAS proto-oncogene, GTPase	Rattus norvegicus	44-49
1511440-0	1992	GGT to GTT transversions in codon 12 of the K-ras oncogene in rat renal sarcomas induced with nickel subsulfide or nickel subsulfide/iron are consistent with oxidative damage to DNA.	Iron	133-137	KRAS proto-oncogene, GTPase	Rattus norvegicus	44-49
1511440-4	1992	Selective oligonucleotide hybridization analysis of K-ras gene sequences amplified by polymerase chain reaction revealed that 1 of 12 primary tumors induced with Ni3S2 and 7 of 9 primary tumors induced with Ni3S2/iron contained exclusively GGT to GTT activating mutations in codon 12.	Oligonucleotides	10-25	KRAS proto-oncogene, GTPase	Rattus norvegicus	52-57
1511440-4	1992	Selective oligonucleotide hybridization analysis of K-ras gene sequences amplified by polymerase chain reaction revealed that 1 of 12 primary tumors induced with Ni3S2 and 7 of 9 primary tumors induced with Ni3S2/iron contained exclusively GGT to GTT activating mutations in codon 12.	ni3s2	162-167	KRAS proto-oncogene, GTPase	Rattus norvegicus	52-57
1511440-4	1992	Selective oligonucleotide hybridization analysis of K-ras gene sequences amplified by polymerase chain reaction revealed that 1 of 12 primary tumors induced with Ni3S2 and 7 of 9 primary tumors induced with Ni3S2/iron contained exclusively GGT to GTT activating mutations in codon 12.	Iron	213-217	KRAS proto-oncogene, GTPase	Rattus norvegicus	52-57
1512271-0	1992	K-ras transformation greatly increases the toxin-dependent ADP-ribosylation of GTP binding proteins in thyroid cells.	Guanosine Triphosphate	79-82	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-5
1512271-9	1992	Rather, the enhanced ADP-ribosylation in K-ras-transformed cells appears to be due to the loss of an inhibitory factor present in the normal cells.	Adenosine Diphosphate	21-24	KRAS proto-oncogene, GTPase	Rattus norvegicus	41-46
1733572-0	1992	K-ras oncogene mutations in rat colon tumors induced by N-methyl-N-nitrosourea.	Methylnitrosourea	56-78	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-5
1549349-2	1992	p21 is a GTP-binding protein, and its activity is regulated by the bound GDP/GTP ratio.	Guanosine Triphosphate	9-12	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-3
1549349-2	1992	p21 is a GTP-binding protein, and its activity is regulated by the bound GDP/GTP ratio.	Guanosine Diphosphate	73-76	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-3
1549349-2	1992	p21 is a GTP-binding protein, and its activity is regulated by the bound GDP/GTP ratio.	Guanosine Triphosphate	77-80	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-3
1549349-4	1992	Nerve growth factors (NGF) rapidly increased the relative amount of active p21-GTP complex to as much as 20% of the total amount of p21 within 2 min.	Guanosine Triphosphate	79-82	KRAS proto-oncogene, GTPase	Rattus norvegicus	75-78
1549349-4	1992	Nerve growth factors (NGF) rapidly increased the relative amount of active p21-GTP complex to as much as 20% of the total amount of p21 within 2 min.	Guanosine Triphosphate	79-82	KRAS proto-oncogene, GTPase	Rattus norvegicus	132-135
1549349-8	1992	Interestingly, the protein kinase inhibitor K-252a specifically suppressed the NGF-induced accumulation of p21-GTP, but did not suppress the EGF-induced response.	staurosporine aglycone	44-50	KRAS proto-oncogene, GTPase	Rattus norvegicus	107-110
1644791-1	1992	The p21ras superfamily, involved in diverse processes including cell growth and intracellular trafficking, possesses intrinsic GTPase activity and cycles between GTP-bound active and GDP-bound quiescent states.	Guanosine Triphosphate	127-130	KRAS proto-oncogene, GTPase	Rattus norvegicus	4-7
1644791-1	1992	The p21ras superfamily, involved in diverse processes including cell growth and intracellular trafficking, possesses intrinsic GTPase activity and cycles between GTP-bound active and GDP-bound quiescent states.	Guanosine Diphosphate	183-186	KRAS proto-oncogene, GTPase	Rattus norvegicus	4-7
1644791-11	1992	This diversity, versatility, and tissue specificity of GAPs may be required for fine control of the down-regulation of GTP-bound p21s and the suggested specific downstream effects of individual GAPs, which could involve "cross-talk" between GAPs and p21s.	Guanosine Triphosphate	119-122	KRAS proto-oncogene, GTPase	Rattus norvegicus	129-132
1320413-3	1992	Herbimycin and genistein blocked NGF-dependent activation of ras p21 whose essential function in neuronal differentiation has been reported.	herbimycin	0-10	KRAS proto-oncogene, GTPase	Rattus norvegicus	65-68
1320413-3	1992	Herbimycin and genistein blocked NGF-dependent activation of ras p21 whose essential function in neuronal differentiation has been reported.	Genistein	15-24	KRAS proto-oncogene, GTPase	Rattus norvegicus	65-68
1544143-12	1992	In hepatomas induced by prolonged dietary methyl deficiency, methylation patterns of c-Ki-ras and c-Ha-ras were abnormal.	methyl radical	42-48	KRAS proto-oncogene, GTPase	Rattus norvegicus	85-93
1733572-3	1992	To detect potential activating point mutations in the H-ras and K-ras oncogenes in MNU-induced rat colon tumors, DNA samples from 40 adenomas, nine carcinomas, and 14 histologically normal tissue samples from 14 rats--as well as from 16 foci induced on NIH3T3 cells by tumor DNAs--were amplified by the polymerase chain reaction and hybridized with allele-specific oligonucleotide probes.	Methylnitrosourea	83-86	KRAS proto-oncogene, GTPase	Rattus norvegicus	64-69
1554412-1	1992	Renal mesenchymal tumors induced in F344 rats with methyl(methoxymethyl)nitrosamine (DMN-OMe) have previously been shown by our laboratory to contain transforming Ki-ras sequences, activated most commonly by a variety of codon 12 mutations.	Methoxymethyl-methylnitrosamine	51-83	KRAS proto-oncogene, GTPase	Rattus norvegicus	163-169
1485917-1	1992	The occurrence of Ha-ras and Ki-ras oncogenes was investigated in mammary tumors produced by treating genetically resistant Copenhagen (Cop) rats with N-methyl-N-nitrosourea.	Methylnitrosourea	151-173	KRAS proto-oncogene, GTPase	Rattus norvegicus	29-35
1554412-1	1992	Renal mesenchymal tumors induced in F344 rats with methyl(methoxymethyl)nitrosamine (DMN-OMe) have previously been shown by our laboratory to contain transforming Ki-ras sequences, activated most commonly by a variety of codon 12 mutations.	dmn-ome	85-92	KRAS proto-oncogene, GTPase	Rattus norvegicus	163-169
1554412-2	1992	Further sequence analysis of the one DMN-OMe-induced tumor with transforming Ki-ras sequences detected by NIH 3T3 transfection assay but with no mutation in codon 12 detected by selective oligonucleotide hybridization has now revealed an activating point mutation in codon 63.	dmn-ome	37-44	KRAS proto-oncogene, GTPase	Rattus norvegicus	77-83
1554412-3	1992	The observed GAG----AAG transition in codon 63, which replaces glutamic acid with lysine, was the only detectable mutation in exon 1 and 2 hotspot regions of Ki-ras in this tumor.	Glutamic Acid	63-76	KRAS proto-oncogene, GTPase	Rattus norvegicus	158-164
1554412-3	1992	The observed GAG----AAG transition in codon 63, which replaces glutamic acid with lysine, was the only detectable mutation in exon 1 and 2 hotspot regions of Ki-ras in this tumor.	Lysine	82-88	KRAS proto-oncogene, GTPase	Rattus norvegicus	158-164
1747941-6	1991	This mutation codes for glutamate instead of glycine as the 12th amino acid of the ras p21 protein.	Glutamic Acid	24-33	KRAS proto-oncogene, GTPase	Rattus norvegicus	87-90
1747941-6	1991	This mutation codes for glutamate instead of glycine as the 12th amino acid of the ras p21 protein.	Glycine	45-52	KRAS proto-oncogene, GTPase	Rattus norvegicus	87-90
1860169-6	1991	This indicates that the activation of c-K-ras is a frequent event in the multistep process of pancreatic carcinogenesis induced by the alkylating carcinogen N-nitrosobis(2-oxopropyl)amine (BOP).	nitrosobis(2-oxopropyl)amine	157-187	KRAS proto-oncogene, GTPase	Rattus norvegicus	38-45
1798057-4	1991	In a second procedure, ras p21s isolated from rat or bovine brain membranes by cholate extraction and purified by gel-permeation and hydrophobic interaction were shown to act also as potent CPIs, inhibiting rat brain cathepsin L, papain, or rat brain cathepsin B with Ki values of 3, 11, and 167 nM, respectively.	Cholates	79-86	KRAS proto-oncogene, GTPase	Rattus norvegicus	27-30
1798057-4	1991	In a second procedure, ras p21s isolated from rat or bovine brain membranes by cholate extraction and purified by gel-permeation and hydrophobic interaction were shown to act also as potent CPIs, inhibiting rat brain cathepsin L, papain, or rat brain cathepsin B with Ki values of 3, 11, and 167 nM, respectively.	cyclopropapyrroloindole	190-194	KRAS proto-oncogene, GTPase	Rattus norvegicus	27-30
1764245-0	1991	NGF and EGF rapidly activate p21ras in PC12 cells by distinct, convergent pathways involving tyrosine phosphorylation.	Tyrosine	93-101	KRAS proto-oncogene, GTPase	Rattus norvegicus	29-32
1894650-9	1991	This shows that p21 (F28L) is converted to the GDP bound form by GAP but is transforming because the high dissociation rate for nucleotides leads to a protein predominantly in the active GTP bound form.	Guanosine Diphosphate	47-50	KRAS proto-oncogene, GTPase	Rattus norvegicus	16-19
1894650-9	1991	This shows that p21 (F28L) is converted to the GDP bound form by GAP but is transforming because the high dissociation rate for nucleotides leads to a protein predominantly in the active GTP bound form.	Guanosine Triphosphate	187-190	KRAS proto-oncogene, GTPase	Rattus norvegicus	16-19
1919181-0	1991	[Immunohistochemical studies of ras oncogene product p21 in 7,12 dimethylbenz (a) anthracene-induced rat ovarian tumors].	7,12 dimethylbenz	60-77	KRAS proto-oncogene, GTPase	Rattus norvegicus	53-56
1919181-0	1991	[Immunohistochemical studies of ras oncogene product p21 in 7,12 dimethylbenz (a) anthracene-induced rat ovarian tumors].	anthracene	82-92	KRAS proto-oncogene, GTPase	Rattus norvegicus	53-56
1919181-1	1991	In the present study, ras oncogene product p21 was analyzed immunohistochemically in rat ovarian tumors induced by 7,12 dimethylbenz (a) anthracene (DMBA).	7,12 dimethylbenz	115-132	KRAS proto-oncogene, GTPase	Rattus norvegicus	43-46
1919181-1	1991	In the present study, ras oncogene product p21 was analyzed immunohistochemically in rat ovarian tumors induced by 7,12 dimethylbenz (a) anthracene (DMBA).	anthracene	137-147	KRAS proto-oncogene, GTPase	Rattus norvegicus	43-46
1919181-1	1991	In the present study, ras oncogene product p21 was analyzed immunohistochemically in rat ovarian tumors induced by 7,12 dimethylbenz (a) anthracene (DMBA).	6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene	149-153	KRAS proto-oncogene, GTPase	Rattus norvegicus	43-46
1868452-0	1991	K-ras mutations in 1,2-dimethylhydrazine-induced colonic tumors: effects of supplemental dietary calcium and vitamin D deficiency.	1,2-Dimethylhydrazine	19-40	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-5
1868452-0	1991	K-ras mutations in 1,2-dimethylhydrazine-induced colonic tumors: effects of supplemental dietary calcium and vitamin D deficiency.	Vitamin D	109-118	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-5
1868452-8	1991	These findings suggest that alterations in K-ras mutations may be one possible mechanism by which calcium and vitamin D status influence colonic carcinogenesis in this experimental model.	Calcium	98-105	KRAS proto-oncogene, GTPase	Rattus norvegicus	43-48
1868452-8	1991	These findings suggest that alterations in K-ras mutations may be one possible mechanism by which calcium and vitamin D status influence colonic carcinogenesis in this experimental model.	Vitamin D	110-119	KRAS proto-oncogene, GTPase	Rattus norvegicus	43-48
1884376-0	1991	Enhanced immunoreactivity of ras oncogene p21 protein in urinary bladder epithelium of rats treated with N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide.	FANFT	105-149	KRAS proto-oncogene, GTPase	Rattus norvegicus	42-45
1884376-2	1991	Seventy-one to 100% of transitional cell carcinomas showed strong reactivity to the antibody to ras p21 depending on treatment with long-term administration of FANFT or by 6 weeks administration of FANFT followed by sodium saccharin or DL-tryptophan.	DL-Tryptophan	236-249	KRAS proto-oncogene, GTPase	Rattus norvegicus	100-103
1884376-3	1991	Focal reactivity to the ras p21 antibody was frequently observed in the hyperplastic (57-96%) or normal appearing urinary bladder epithelium (50-100%) in rats treated with FANFT (FANFT alone or in combination with sodium saccharin or tryptophan) but not in hyperplasia or normal epithelium in rats given sodium saccharin or tryptophan alone, without pretreatment with FANFT or in untreated controls.	Saccharin	214-230	KRAS proto-oncogene, GTPase	Rattus norvegicus	28-31
1884376-3	1991	Focal reactivity to the ras p21 antibody was frequently observed in the hyperplastic (57-96%) or normal appearing urinary bladder epithelium (50-100%) in rats treated with FANFT (FANFT alone or in combination with sodium saccharin or tryptophan) but not in hyperplasia or normal epithelium in rats given sodium saccharin or tryptophan alone, without pretreatment with FANFT or in untreated controls.	Tryptophan	234-244	KRAS proto-oncogene, GTPase	Rattus norvegicus	28-31
1773788-1	1991	A poly(ADP-ribose) polymerase inhibitor, benzamide (BA), was found to induce flat revertants of NIH 3T3 cells that had been transformed by human Ha-ras, rat Ki-ras, rat c-raf, and human ret-II.	benzamide	41-50	KRAS proto-oncogene, GTPase	Rattus norvegicus	157-163
1884376-3	1991	Focal reactivity to the ras p21 antibody was frequently observed in the hyperplastic (57-96%) or normal appearing urinary bladder epithelium (50-100%) in rats treated with FANFT (FANFT alone or in combination with sodium saccharin or tryptophan) but not in hyperplasia or normal epithelium in rats given sodium saccharin or tryptophan alone, without pretreatment with FANFT or in untreated controls.	Saccharin	304-320	KRAS proto-oncogene, GTPase	Rattus norvegicus	28-31
1884376-3	1991	Focal reactivity to the ras p21 antibody was frequently observed in the hyperplastic (57-96%) or normal appearing urinary bladder epithelium (50-100%) in rats treated with FANFT (FANFT alone or in combination with sodium saccharin or tryptophan) but not in hyperplasia or normal epithelium in rats given sodium saccharin or tryptophan alone, without pretreatment with FANFT or in untreated controls.	Tryptophan	324-334	KRAS proto-oncogene, GTPase	Rattus norvegicus	28-31
1773788-1	1991	A poly(ADP-ribose) polymerase inhibitor, benzamide (BA), was found to induce flat revertants of NIH 3T3 cells that had been transformed by human Ha-ras, rat Ki-ras, rat c-raf, and human ret-II.	benzamide	52-54	KRAS proto-oncogene, GTPase	Rattus norvegicus	157-163
2032737-5	1991	These G----A mutations result in the replacement of the normal glycine in the 12th position of the ras p21 protein by a glutamic acid residue.	Glycine	63-70	KRAS proto-oncogene, GTPase	Rattus norvegicus	103-106
1991846-0	1991	Mutations in the K-ras oncogene induced by 1,2-dimethylhydrazine in preneoplastic and neoplastic rat colonic mucosa.	1,2-Dimethylhydrazine	43-64	KRAS proto-oncogene, GTPase	Rattus norvegicus	17-22
1991846-1	1991	These experiments were conducted to determine whether point mutations activating K-ras or H-ras oncogenes, induced by the procarcinogen 1,2-dimethylhydrazine (DMH), were detectable in preneoplastic or neoplastic rat colonic mucosa.	1,2-Dimethylhydrazine	136-157	KRAS proto-oncogene, GTPase	Rattus norvegicus	81-86
1991846-1	1991	These experiments were conducted to determine whether point mutations activating K-ras or H-ras oncogenes, induced by the procarcinogen 1,2-dimethylhydrazine (DMH), were detectable in preneoplastic or neoplastic rat colonic mucosa.	1,2-Dimethylhydrazine	159-162	KRAS proto-oncogene, GTPase	Rattus norvegicus	81-86
1991846-5	1991	While no H-ras mutations were detectable in any group, K-ras (G to A) mutations were found in 66% of DMH-induced colon carcinomas.	1,2-Dimethylhydrazine	101-104	KRAS proto-oncogene, GTPase	Rattus norvegicus	55-60
2032737-5	1991	These G----A mutations result in the replacement of the normal glycine in the 12th position of the ras p21 protein by a glutamic acid residue.	Glutamic Acid	120-133	KRAS proto-oncogene, GTPase	Rattus norvegicus	103-106
1899198-0	1991	Purification and characterization from rat liver cytosol of a GDP dissociation inhibitor (GDI) for liver 24K G, a ras p21-like GTP-binding protein, with properties similar to those of smg p25A GDI.	Guanosine Diphosphate	62-65	KRAS proto-oncogene, GTPase	Rattus norvegicus	118-121
2032737-6	1991	In this study, we report the generation of monoclonal antibodies (Mab) reactive with oncogenic ras p21 proteins containing glutamic acid at position 12 (p21 Glu-12).	Glutamic Acid	123-136	KRAS proto-oncogene, GTPase	Rattus norvegicus	99-102
2032737-6	1991	In this study, we report the generation of monoclonal antibodies (Mab) reactive with oncogenic ras p21 proteins containing glutamic acid at position 12 (p21 Glu-12).	Glutamic Acid	123-136	KRAS proto-oncogene, GTPase	Rattus norvegicus	153-156
2032737-6	1991	In this study, we report the generation of monoclonal antibodies (Mab) reactive with oncogenic ras p21 proteins containing glutamic acid at position 12 (p21 Glu-12).	Glutamic Acid	157-160	KRAS proto-oncogene, GTPase	Rattus norvegicus	99-102
2032737-6	1991	In this study, we report the generation of monoclonal antibodies (Mab) reactive with oncogenic ras p21 proteins containing glutamic acid at position 12 (p21 Glu-12).	Glutamic Acid	157-160	KRAS proto-oncogene, GTPase	Rattus norvegicus	153-156
2009134-0	1991	The molecular progression of plutonium-239-induced rat lung carcinogenesis: Ki-ras expression and activation.	Plutonium-239	29-42	KRAS proto-oncogene, GTPase	Rattus norvegicus	76-82
1657098-0	1991	Transformation by the k-ras oncogene correlates with increases in phospholipase A2 activity, glycerophosphoinositol production and phosphoinositide synthesis in thyroid cells.	glycerylphosphoinositol	93-115	KRAS proto-oncogene, GTPase	Rattus norvegicus	22-27
1657098-0	1991	Transformation by the k-ras oncogene correlates with increases in phospholipase A2 activity, glycerophosphoinositol production and phosphoinositide synthesis in thyroid cells.	Phosphatidylinositols	131-147	KRAS proto-oncogene, GTPase	Rattus norvegicus	22-27
1657098-2	1991	In k-ras transformed cells two phosphoinositide derivatives, glycerophosphoinositol and inositol monophosphate, were markedly increased, whereas inositol bisphosphate and trisphosphate maintained the same level as in normal cells.	Phosphatidylinositols	31-47	KRAS proto-oncogene, GTPase	Rattus norvegicus	3-8
1657098-2	1991	In k-ras transformed cells two phosphoinositide derivatives, glycerophosphoinositol and inositol monophosphate, were markedly increased, whereas inositol bisphosphate and trisphosphate maintained the same level as in normal cells.	glycerylphosphoinositol	61-83	KRAS proto-oncogene, GTPase	Rattus norvegicus	3-8
1657098-2	1991	In k-ras transformed cells two phosphoinositide derivatives, glycerophosphoinositol and inositol monophosphate, were markedly increased, whereas inositol bisphosphate and trisphosphate maintained the same level as in normal cells.	Inositol Phosphates	88-110	KRAS proto-oncogene, GTPase	Rattus norvegicus	3-8
1781304-5	1991	Cerebral uptake of beta-hydroxybutyrate was unchanged at P10 and increased by two-fold at P14 and by threefold at P21 by phenobarbital.	3-Hydroxybutyric Acid	19-39	KRAS proto-oncogene, GTPase	Rattus norvegicus	114-117
1781304-5	1991	Cerebral uptake of beta-hydroxybutyrate was unchanged at P10 and increased by two-fold at P14 and by threefold at P21 by phenobarbital.	Phenobarbital	121-134	KRAS proto-oncogene, GTPase	Rattus norvegicus	114-117
1781304-7	1991	At P14 and P21, the calculated amount of oxygen used by the brain for the oxidation of ketone bodies was twice as high in barbiturate- as in saline-treated rats and reached values of 47 and 16% respectively in phenobarbital-exposed animals.	Oxygen	41-47	KRAS proto-oncogene, GTPase	Rattus norvegicus	11-14
1781304-7	1991	At P14 and P21, the calculated amount of oxygen used by the brain for the oxidation of ketone bodies was twice as high in barbiturate- as in saline-treated rats and reached values of 47 and 16% respectively in phenobarbital-exposed animals.	Ketones	87-93	KRAS proto-oncogene, GTPase	Rattus norvegicus	11-14
1793484-1	1991	A high frequency of point mutations at codon 12 of the Ki-ras gene has previously been reported for rat kidney mesenchymal tumors induced by methylating N-nitroso compounds.	n-nitroso compounds	153-172	KRAS proto-oncogene, GTPase	Rattus norvegicus	55-61
1680340-0	1991	Frequent activation of the Ki-ras oncogene at codon 12 in N-methyl-N-nitrosourea-induced rat prostate adenocarcinomas and neurogenic sarcomas.	Methylnitrosourea	58-80	KRAS proto-oncogene, GTPase	Rattus norvegicus	27-33
1680340-4	1991	Activating mutations in codon 12 of the Ki-ras gene were found in 7 of 10 carcinomas and 4 of 5 sarcomas, using selective oligonucleotide hybridization analysis of DNA amplified by the polymerase chain reaction (PCR).	Oligonucleotides	122-137	KRAS proto-oncogene, GTPase	Rattus norvegicus	40-46
1793484-5	1991	Amplification of Ki-ras sequences from formalin-fixed, paraffin-embedded tissue by the polymerase chain reaction was followed by direct DNA sequencing.	Formaldehyde	39-47	KRAS proto-oncogene, GTPase	Rattus norvegicus	17-23
1680340-7	1991	Production of O6-methylguanine adducts in the Ki-ras codon 12 followed by base mispairing during replicative DNA synthesis is thus the likely molecular mechanism of initiation of prostatic carcinogenesis by MNU in the rat.	O-(6)-methylguanine	14-30	KRAS proto-oncogene, GTPase	Rattus norvegicus	46-52
2009134-2	1991	Our objective were to evaluate the molecular and genetic alterations of Ki-ras in preneoplastic foci and neoplasms in the lungs of rats that inhaled 239PuO2 aerosols.	plutonium dioxide	149-156	KRAS proto-oncogene, GTPase	Rattus norvegicus	72-78
1680340-7	1991	Production of O6-methylguanine adducts in the Ki-ras codon 12 followed by base mispairing during replicative DNA synthesis is thus the likely molecular mechanism of initiation of prostatic carcinogenesis by MNU in the rat.	Methylnitrosourea	207-210	KRAS proto-oncogene, GTPase	Rattus norvegicus	46-52
1793484-5	1991	Amplification of Ki-ras sequences from formalin-fixed, paraffin-embedded tissue by the polymerase chain reaction was followed by direct DNA sequencing.	Paraffin	55-63	KRAS proto-oncogene, GTPase	Rattus norvegicus	17-23
1793484-6	1991	GGT----GAT point mutations at codon 12 of the Ki-ras gene were found in 9 of 12 (75%) renal mesenchymal tumors and in 9 of 12 (75%) cortical epithelial tumors induced by NDMA.	Dimethylnitrosamine	170-174	KRAS proto-oncogene, GTPase	Rattus norvegicus	46-52
2015062-0	1991	The antisense c-Ha-ras oligodeoxynucleotides inhibit the proliferation of the gastrocarcinoma-DNA-transformed rat 3-3 cells and reduce the p21 expression of the cells.	c-ha-ras oligodeoxynucleotides	14-44	KRAS proto-oncogene, GTPase	Rattus norvegicus	139-142
1844236-7	1991	In the present studies low incidences of mutations were detected in p53 or K-ras genes in noninvasive and invasive rat prostate carcinomas induced by DMAB.	2',3-dimethyl-4-aminobiphenyl	150-154	KRAS proto-oncogene, GTPase	Rattus norvegicus	75-80
2062444-5	1991	Between P17 and P21, regional 14C concentrations were again reduced by about twofold in all areas studied and decreased further by about 50% after weaning reaching quite low levels by P35.	Carbon-14	30-33	KRAS proto-oncogene, GTPase	Rattus norvegicus	16-19
1981788-5	1990	Compared to naive PC12 cells, K-ras infected PC12 cells had (a) higher activities of acetylcholinesterase and choline acetyltransferase, two enzymes involved in acetylcholine metabolism; (b) enhanced activity of tyrosine hydroxylase, the rate-limiting enzyme in catecholamine biosynthesis; (c) a higher, evoked norepinephrine release; and (d) similar levels of sodium-dependent uptake of both choline and norepinephrine.	Acetylcholine	85-98	KRAS proto-oncogene, GTPase	Rattus norvegicus	30-35
2265474-0	1990	H-ras activation and ras p21 expression in bladder tumors induced in F344/NCr rats by N-butyl-N-(4-hydroxybutyl)nitrosamine.	Butylhydroxybutylnitrosamine	86-123	KRAS proto-oncogene, GTPase	Rattus norvegicus	25-28
2265474-4	1990	Increased expression of ras p21 was detected by avidin-biotin immunohistochemistry in 18/21 (85%) of the neoplastic bladder lesions.	avidin-biotin	48-61	KRAS proto-oncogene, GTPase	Rattus norvegicus	28-31
2174364-1	1990	Glucagon at a low concentration has a stimulatory effect on Ki-ras expression, whereas, at high concentrations the hormone suppresses the level of the Ki-ras transcripts.	Glucagon	0-8	KRAS proto-oncogene, GTPase	Rattus norvegicus	60-66
2174364-2	1990	Incubation of the hepatoma cells with 10 microM dibutyryl cyclic AMP results in suppression of Ki-ras expression but the phorbol ester, 21-O-tetradecanoylphorbol 13-acetate (TPA) causes an increase.	Bucladesine	48-68	KRAS proto-oncogene, GTPase	Rattus norvegicus	95-101
2174364-3	1990	Down regulation of protein kinase C by prolonged exposure of hepatoma cells to TPA causes a dramatic decrease in the glucagon-stimulated effect on Ki-ras expression.	Tetradecanoylphorbol Acetate	79-82	KRAS proto-oncogene, GTPase	Rattus norvegicus	147-153
2174364-3	1990	Down regulation of protein kinase C by prolonged exposure of hepatoma cells to TPA causes a dramatic decrease in the glucagon-stimulated effect on Ki-ras expression.	Glucagon	117-125	KRAS proto-oncogene, GTPase	Rattus norvegicus	147-153
2174364-4	1990	The presence of diacylglycerol for 2 h in the culture medium results in a significant increase in Ki-ras expression, while treatment of the cells with 1-(5-isoquinolinylsulphonyl)-2-methylpiperazine, a potent inhibitor of protein kinase C, leads to a dramatic reduction.	Diglycerides	16-30	KRAS proto-oncogene, GTPase	Rattus norvegicus	98-104
2174364-5	1990	The calcium ionophore, A23187 is able to stimulate Ki-ras expression, whereas, addition of verapamil or EGTA results in its suppression.	Calcium	4-11	KRAS proto-oncogene, GTPase	Rattus norvegicus	51-57
2174364-5	1990	The calcium ionophore, A23187 is able to stimulate Ki-ras expression, whereas, addition of verapamil or EGTA results in its suppression.	Calcimycin	23-29	KRAS proto-oncogene, GTPase	Rattus norvegicus	51-57
2174364-6	1990	The present findings suggest that the inductive effect of glucagon on Ki-ras expression at low concentrations is via the activation of protein kinase C which causes phosphorylation of some regulatory proteins that may eventually affect the level of Ki-ras mRNA.	Glucagon	58-66	KRAS proto-oncogene, GTPase	Rattus norvegicus	70-76
2174364-6	1990	The present findings suggest that the inductive effect of glucagon on Ki-ras expression at low concentrations is via the activation of protein kinase C which causes phosphorylation of some regulatory proteins that may eventually affect the level of Ki-ras mRNA.	Glucagon	58-66	KRAS proto-oncogene, GTPase	Rattus norvegicus	249-255
1981788-5	1990	Compared to naive PC12 cells, K-ras infected PC12 cells had (a) higher activities of acetylcholinesterase and choline acetyltransferase, two enzymes involved in acetylcholine metabolism; (b) enhanced activity of tyrosine hydroxylase, the rate-limiting enzyme in catecholamine biosynthesis; (c) a higher, evoked norepinephrine release; and (d) similar levels of sodium-dependent uptake of both choline and norepinephrine.	Catecholamines	262-275	KRAS proto-oncogene, GTPase	Rattus norvegicus	30-35
1981788-5	1990	Compared to naive PC12 cells, K-ras infected PC12 cells had (a) higher activities of acetylcholinesterase and choline acetyltransferase, two enzymes involved in acetylcholine metabolism; (b) enhanced activity of tyrosine hydroxylase, the rate-limiting enzyme in catecholamine biosynthesis; (c) a higher, evoked norepinephrine release; and (d) similar levels of sodium-dependent uptake of both choline and norepinephrine.	Norepinephrine	311-325	KRAS proto-oncogene, GTPase	Rattus norvegicus	30-35
1981788-5	1990	Compared to naive PC12 cells, K-ras infected PC12 cells had (a) higher activities of acetylcholinesterase and choline acetyltransferase, two enzymes involved in acetylcholine metabolism; (b) enhanced activity of tyrosine hydroxylase, the rate-limiting enzyme in catecholamine biosynthesis; (c) a higher, evoked norepinephrine release; and (d) similar levels of sodium-dependent uptake of both choline and norepinephrine.	Sodium	361-367	KRAS proto-oncogene, GTPase	Rattus norvegicus	30-35
1981788-5	1990	Compared to naive PC12 cells, K-ras infected PC12 cells had (a) higher activities of acetylcholinesterase and choline acetyltransferase, two enzymes involved in acetylcholine metabolism; (b) enhanced activity of tyrosine hydroxylase, the rate-limiting enzyme in catecholamine biosynthesis; (c) a higher, evoked norepinephrine release; and (d) similar levels of sodium-dependent uptake of both choline and norepinephrine.	Choline	91-98	KRAS proto-oncogene, GTPase	Rattus norvegicus	30-35
1981788-5	1990	Compared to naive PC12 cells, K-ras infected PC12 cells had (a) higher activities of acetylcholinesterase and choline acetyltransferase, two enzymes involved in acetylcholine metabolism; (b) enhanced activity of tyrosine hydroxylase, the rate-limiting enzyme in catecholamine biosynthesis; (c) a higher, evoked norepinephrine release; and (d) similar levels of sodium-dependent uptake of both choline and norepinephrine.	Norepinephrine	405-419	KRAS proto-oncogene, GTPase	Rattus norvegicus	30-35
1981788-6	1990	Although the total content of catecholamines in K-ras-differentiated PC12 cells was less than that of naive cells, both norepinephrine and dopamine were present in substantial amounts and norepinephrine was released after stimulation.	Catecholamines	30-44	KRAS proto-oncogene, GTPase	Rattus norvegicus	48-53
2108319-8	1990	Dexamethasone-induced expression of activated N-ras p21 results in blocking of c-fos RNA induction by NGF or bFGF in a time-dependent manner.	Dexamethasone	0-13	KRAS proto-oncogene, GTPase	Rattus norvegicus	52-55
2118994-1	1990	A dominant inhibitory mutation of Ha-ras which changes Ser-17 to Asn-17 in the gene product p21 [p21 (Asn-17)Ha-ras] has been used to investigate the role of ras in neuronal differentiation of PC12 cells.	Asparagine	65-68	KRAS proto-oncogene, GTPase	Rattus norvegicus	92-95
2202952-5	1990	In contrast, morphologic transformation develops more slowly and does not appear until 72-96 h after Zn++ stimulation in cells with very low basal levels of activated p21 (MR4 cells) and 24-48 h in cells with higher basal levels (MR5 cells).	Zinc	101-105	KRAS proto-oncogene, GTPase	Rattus norvegicus	167-170
2111441-1	1990	We have made a specific antiserum recognizing both smg p21A (the rap1A/Krev-1 protein) and -B (the rap1B protein), ras p21-like GTP-binding proteins having the same putative effector domain as ras p21s and have used this antiserum to study the tissue and subcellular distributions of smg p21s by immunoblot and immunocytochemical analyses.	Guanosine Triphosphate	128-131	KRAS proto-oncogene, GTPase	Rattus norvegicus	119-122
2116389-0	1990	Mutational activation of H-ras and K-ras genes is absent in N-nitroso-N-methylurea-induced liver tumors in rats.	Methylnitrosourea	60-82	KRAS proto-oncogene, GTPase	Rattus norvegicus	35-40
2116389-1	1990	We examined mutational activation of H- and K-ras genes in hyperplastic nodules and hepatocellular carcinomas induced by N-nitroso-N-methylurea or diethylnitrosamine using the polymerase chain reaction, followed by dot-blot hybridization.	Methylnitrosourea	121-143	KRAS proto-oncogene, GTPase	Rattus norvegicus	44-49
2116389-1	1990	We examined mutational activation of H- and K-ras genes in hyperplastic nodules and hepatocellular carcinomas induced by N-nitroso-N-methylurea or diethylnitrosamine using the polymerase chain reaction, followed by dot-blot hybridization.	Diethylnitrosamine	147-165	KRAS proto-oncogene, GTPase	Rattus norvegicus	44-49
2188105-6	1990	Using ras-inducible cell lines, we observed that expression of the oncogenic N-ras p21 protein interferes with the ability of phorbol esters to induce downregulation of protein kinase C. This effect was associated with the appearance of immunologically detectable protein kinase C as well as the activity of the enzyme as analyzed either by binding of [3H]phorbol-12,13-dibutyrate in intact cells or by in vitro kinase activity.	Phorbol Esters	126-140	KRAS proto-oncogene, GTPase	Rattus norvegicus	83-86
2188105-6	1990	Using ras-inducible cell lines, we observed that expression of the oncogenic N-ras p21 protein interferes with the ability of phorbol esters to induce downregulation of protein kinase C. This effect was associated with the appearance of immunologically detectable protein kinase C as well as the activity of the enzyme as analyzed either by binding of [3H]phorbol-12,13-dibutyrate in intact cells or by in vitro kinase activity.	3h]phorbol-12,13-dibutyrate	353-380	KRAS proto-oncogene, GTPase	Rattus norvegicus	83-86
2105496-0	1990	Characterization of c-Ki-ras and N-ras oncogenes in aflatoxin B1-induced rat liver tumors.	Aflatoxin B1	52-64	KRAS proto-oncogene, GTPase	Rattus norvegicus	20-28
2105496-1	1990	c-Ki-ras and N-ras oncogenes have been characterized in aflatoxin B1-induced hepatocellular carcinomas.	Aflatoxin B1	56-68	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-8
2105496-5	1990	Distributions of c-Ki-ras sequences in tumors and normal liver DNA indicated that the observed nucleotide changes were consistent with those expected to result from direct mutagenesis of the germ-line protooncogene by aflatoxin B1.	Aflatoxin B1	218-230	KRAS proto-oncogene, GTPase	Rattus norvegicus	17-25
7835279-1	1995	In the present studies, insulin was found to stimulate in a rat hepatoma cell line (called FAO cells) the tyrosine phosphorylation of the 60-kilodalton p21ras GTPase-activating protein (GAP)-associated protein called p60.	Tyrosine	106-114	KRAS proto-oncogene, GTPase	Rattus norvegicus	152-155
2400819-1	1990	We have studied the effects of 2 hepatic promoters: an exogenous one:phenobarbital, and an endogenous one biliverdin (a bile pigment) on the expression of 3 oncogenes c-Ki-ras, c-fos and c-myc involved in growth process, differentiation and tumorigenesis for the liver.	Biliverdine	106-116	KRAS proto-oncogene, GTPase	Rattus norvegicus	167-175
33237045-7	2020	These effects were accompanied by attenuation of the H2O2-induced strengthening of the G2/M-phase inhibitory system, including increased mRNA and protein levels of cyclin-dependent kinase 1 (CDK1) and decreased p21 mRNA levels.	Hydrogen Peroxide	53-57	KRAS proto-oncogene, GTPase	Rattus norvegicus	211-214
17056180-6	2007	At P21, capsaicin induced intense phosphoERK expression in the superficial dorsal horn throughout several lumbar segments, consistent with the spread of secondary hyperalgesia.	Capsaicin	8-17	KRAS proto-oncogene, GTPase	Rattus norvegicus	3-6
17056180-7	2007	Intrathecal administration of the MEK (ERK kinase) inhibitor PD98059 prevented mustard oil and capsaicin-induced secondary hyperalgesia at P21, but had no effect on primary hyperalgesia at P3 or P21.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	61-68	KRAS proto-oncogene, GTPase	Rattus norvegicus	139-142
17056180-7	2007	Intrathecal administration of the MEK (ERK kinase) inhibitor PD98059 prevented mustard oil and capsaicin-induced secondary hyperalgesia at P21, but had no effect on primary hyperalgesia at P3 or P21.	Capsaicin	95-104	KRAS proto-oncogene, GTPase	Rattus norvegicus	139-142
2125516-2	1990	Characterization of these sublines has shown that long-term culture in methionine-deprived medium significantly decreases their ability to grow in vitro, their tumorigenicity in new-born syngeneic animals and their level of transcription of 3 oncogenes (c-Ki-ras, c-Ha-ras, c-myc) involved in hepatic growth.	Methionine	71-81	KRAS proto-oncogene, GTPase	Rattus norvegicus	254-262
2125516-4	1990	A shift in methionine-supplemented medium for several cell generations of the various sublines grown in methionine deprived medium, has revealed that under these conditions, the cells maintain a diminished in vitro growth and tumorigenic capacity, despite an increased transcription of c-Ki-ras, c-Ha-ras and c-myc.	Methionine	11-21	KRAS proto-oncogene, GTPase	Rattus norvegicus	286-294
2278633-0	1990	Expression of c-myc, c-raf-1, and c-Ki-ras in azaserine-induced pancreatic carcinomas and growing pancreas in rats.	Azaserine	46-55	KRAS proto-oncogene, GTPase	Rattus norvegicus	34-42
2278633-2	1990	The levels of c-myc, c-raf-1, and c-Ki-ras mRNAs were increased in regenerating pancreata following surgical partial pancreatectomy and following administration of camostat.	camostat	164-172	KRAS proto-oncogene, GTPase	Rattus norvegicus	34-42
2278633-6	1990	We observed increased expression of c-myc, c-raf-1, and c-Ki-ras in azaserine-induced adenomas and carcinomas.	Azaserine	68-77	KRAS proto-oncogene, GTPase	Rattus norvegicus	56-64
33801246-2	2021	Hepassocin (HPS/FGL1) is involved in regulating lipid metabolism and the progression of several cancer types; however, the underlying mechanism of HPS/FGL1 in the KRAS mutant PDAC cells undergoing eicosapentaenoic acid (EPA) treatment remains unclear.	Eicosapentaenoic Acid	197-218	KRAS proto-oncogene, GTPase	Rattus norvegicus	163-167
34763226-7	2022	RESULTS: The number of senescence-positive cells in rat liver tissues was increased as well as the level of IL-8 and the expression levels of p16, p21 and IKBKG in fluoride exposure to rat depending on the fluoride concentration.	Fluorides	164-172	KRAS proto-oncogene, GTPase	Rattus norvegicus	147-150
34763226-7	2022	RESULTS: The number of senescence-positive cells in rat liver tissues was increased as well as the level of IL-8 and the expression levels of p16, p21 and IKBKG in fluoride exposure to rat depending on the fluoride concentration.	Fluorides	206-214	KRAS proto-oncogene, GTPase	Rattus norvegicus	147-150
34903582-1	2022	On May 28, 2021, the U.S. Food and Drug Administration (FDA) granted accelerated approval to sotorasib (Lumakras, Amgen) for the treatment of adults with advanced non-small cell lung cancer (NSCLC) with a Kirsten rat sarcoma proto-oncogene (KRAS) G12C mutation who have received at least one prior systemic therapy.	AMG-510	93-102	KRAS proto-oncogene, GTPase	Rattus norvegicus	241-245
34628167-16	2021	In addition, MTX significantly increased p21-positive cell numbers and MDA levels.	Methotrexate	13-16	KRAS proto-oncogene, GTPase	Rattus norvegicus	41-44
34224586-9	2021	In Doxorubicin-treated H9C2 cardiomyocytes, cell senescence marker p21 and reactive oxygen species were significantly reduced after cultured with MR409.	Doxorubicin	3-14	KRAS proto-oncogene, GTPase	Rattus norvegicus	67-70
34224586-9	2021	In Doxorubicin-treated H9C2 cardiomyocytes, cell senescence marker p21 and reactive oxygen species were significantly reduced after cultured with MR409.	Oxygen	84-90	KRAS proto-oncogene, GTPase	Rattus norvegicus	67-70
34224586-9	2021	In Doxorubicin-treated H9C2 cardiomyocytes, cell senescence marker p21 and reactive oxygen species were significantly reduced after cultured with MR409.	(N-acetyl-tyr1,D-arg2)fragment 1-29 amide	146-151	KRAS proto-oncogene, GTPase	Rattus norvegicus	67-70
34804374-5	2021	Results: The VPA-treated rats showed a significant increase in malondialdehyde (MDA) levels in the hippocampus and p21-positive cells in the subgranular zone (SGZ) of the dentate gyrus (DG) but decreased superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) activities.	Valproic Acid	13-16	KRAS proto-oncogene, GTPase	Rattus norvegicus	115-118
34776511-6	2021	Excitingly, AMG510 was the first drug-targeting KRAS (G12C) to be approved for clinical use this year.	AMG-510	12-18	KRAS proto-oncogene, GTPase	Rattus norvegicus	48-52
34748962-6	2022	Using high-throughput optimization and a series of evaluations, a stable water-dispersible 150-200nm nano-encapsulated drug (named P-4) conjugated with hepatic targeting moiety was synthesized and characterized (named P-21).	Water	73-78	KRAS proto-oncogene, GTPase	Rattus norvegicus	218-222
34188208-11	2021	Moreover, PGQYD significantly decreased vascular aging in SHRs, as indicated by reduced SA-beta-Gal staining, NADPH oxidase activity, and p53 and p21 expression, and increased anti-superoxide anion and SOD content.	pgqyd	10-15	KRAS proto-oncogene, GTPase	Rattus norvegicus	146-149
34382399-10	2021	OMG ameliorated the acetylation of p53 at lysine 382 (K382) and subsequent activation of p21 via inhibition of PAI-1.	2-(2,5-difluorophenyl)-5-(2-(methylsulfonyl)-2,6-dihydropyrrolo(3,4-c)pyrazol-5(4H)-yl)tetrahydro-2H-pyran-3-amine	0-3	KRAS proto-oncogene, GTPase	Rattus norvegicus	89-92
34382399-10	2021	OMG ameliorated the acetylation of p53 at lysine 382 (K382) and subsequent activation of p21 via inhibition of PAI-1.	Lysine	42-48	KRAS proto-oncogene, GTPase	Rattus norvegicus	89-92
34137282-0	2021	Nonclinical Safety Profile of Sotorasib, a KRASG12C-Specific Covalent Inhibitor for the Treatment of KRAS p.G12C-Mutated Cancer.	AMG-510	30-39	KRAS proto-oncogene, GTPase	Rattus norvegicus	101-105
34137282-1	2021	Sotorasib is a first-in-class KRASG12C covalent inhibitor in clinical development for the treatment of tumors with the KRAS p.G12C mutation.	AMG-510	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	119-123
34563044-9	2021	Additionally, the senescence markers (p53, p16 and p21) which were also reported to play a role in the pathogenesis of vascular calcification, were reduced upon treatment with resveratrol and estrogen.	Resveratrol	176-187	KRAS proto-oncogene, GTPase	Rattus norvegicus	51-54
34145930-6	2021	Experiments involving KRAS knockdown in resistant cells and KRAS-G12V overexpression in parental cells revealed the involvement of KRAS-G12V in osimertinib resistance.	osimertinib	144-155	KRAS proto-oncogene, GTPase	Rattus norvegicus	22-26
34145930-6	2021	Experiments involving KRAS knockdown in resistant cells and KRAS-G12V overexpression in parental cells revealed the involvement of KRAS-G12V in osimertinib resistance.	osimertinib	144-155	KRAS proto-oncogene, GTPase	Rattus norvegicus	60-64
34145930-6	2021	Experiments involving KRAS knockdown in resistant cells and KRAS-G12V overexpression in parental cells revealed the involvement of KRAS-G12V in osimertinib resistance.	osimertinib	144-155	KRAS proto-oncogene, GTPase	Rattus norvegicus	131-135
35107747-4	2022	In this study, we extracted RAECs from 2-month-old male Wistar rats by the tissue explant method and found that APS ameliorated the high-glucose-induced increase in the frequency of SA-beta-Gal positivity and the levels of the senescence-related proteins p16, p21, and p53.	aps	112-115	KRAS proto-oncogene, GTPase	Rattus norvegicus	260-263
34175838-6	2021	Acacetin decreased p21 and p53 expression, up-regulated PINK1/Parkin, LC3II/LC3I ratio, pLKB1, pAMPK and Sirt6, and reversed the depolarized mitochondrial membrane potential in aging cardiac cells.	acacetin	0-8	KRAS proto-oncogene, GTPase	Rattus norvegicus	19-22
34427862-11	2021	Daphnetin-treated rats showed an increased level of proteins p21 and p53 and reduced level of cyclins D1 and E.	daphnetin	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	61-64
34347973-5	2021	Conophylline induced flat morphology and inhibited cellular invasion in K-Ras-transformed normal rat kidney (K-Ras-NRK) cells.	conophylline	0-12	KRAS proto-oncogene, GTPase	Rattus norvegicus	72-77
35623405-0	2022	Harmine prevents 3-nitropropionic acid-induced neurotoxicity in rats via enhancing NRF2-mediated signaling: Involvement of p21 and AMPK.	Harmine	0-7	KRAS proto-oncogene, GTPase	Rattus norvegicus	123-126
35623405-5	2022	Harmine successfully increased the protein levels of NRF2, AMPK and p21 and the gene expression of Ho-1, Nqo-1 and p62, restored redox homeostasis, and reduced CASPASE-3 level.	Harmine	0-7	KRAS proto-oncogene, GTPase	Rattus norvegicus	68-71
35623405-7	2022	This study draws attention to the protective role of harmine against 3-NP-induced motor and cognitive dysfunction that could be mediated via enhancing NRF2-mediated signaling with subsequent amelioration of oxidative stress injury via NRF2 activators, p21 and AMPK, in the striatum, prefrontal cortex, and hippocampus which could offer a promising therapeutic tool to slow the progression of HD.	Harmine	53-60	KRAS proto-oncogene, GTPase	Rattus norvegicus	252-255
35107747-4	2022	In this study, we extracted RAECs from 2-month-old male Wistar rats by the tissue explant method and found that APS ameliorated the high-glucose-induced increase in the frequency of SA-beta-Gal positivity and the levels of the senescence-related proteins p16, p21, and p53.	Glucose	137-144	KRAS proto-oncogene, GTPase	Rattus norvegicus	260-263
35592435-2	2022	PMBA (1.7-29 muM) exhibited potent proliferation inhibition on the cell lines and showed sensitivity in microsatellite instability and microsatellite stable (GSE39582 and GSE92921) subsets of KRAS gene (Kirsten rat sarcoma viral oncogene homolog)-mutated colon cell lines, as revealed via flow cytometry analysis.	PMBA	0-4	KRAS proto-oncogene, GTPase	Rattus norvegicus	192-196
35593021-7	2022	In addition, the results demonstrated that exercise and supplementation of UA impeded the interactions among p53/ATF4/p21.	ursolic acid	75-77	KRAS proto-oncogene, GTPase	Rattus norvegicus	118-121
35593021-8	2022	Moreover, ET and ursolic acid had a synergetic effect on the signaling pathway of p53/ATF4/p21 and probably could inhibit the aging process and modulate the p53/ATF4/p21 molecular pathway.	ursolic acid	17-29	KRAS proto-oncogene, GTPase	Rattus norvegicus	91-94
35593021-8	2022	Moreover, ET and ursolic acid had a synergetic effect on the signaling pathway of p53/ATF4/p21 and probably could inhibit the aging process and modulate the p53/ATF4/p21 molecular pathway.	ursolic acid	17-29	KRAS proto-oncogene, GTPase	Rattus norvegicus	166-169
35593021-9	2022	The interaction between UA and endurance exercise significantly modified the activity of the p53/ATF4/p21 signaling pathway.	ursolic acid	24-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	102-105
35560535-0	2022	Evaluation of p21 expression and related autism-like behavior in Bisphenol-A exposed offspring of Wistar albino rats.	bis(4-hydroxyphenyl)sulfone	65-74	KRAS proto-oncogene, GTPase	Rattus norvegicus	14-17
35560535-2	2022	A possible role of altered expression of p21 in autistic-like behavior in rat offspring was examined with prenatal and postnatal BPA exposure.	bisphenol A	129-132	KRAS proto-oncogene, GTPase	Rattus norvegicus	41-44
35560535-9	2022	Over expression of p21 was also detected in BPA-exposed offspring.	bisphenol A	44-47	KRAS proto-oncogene, GTPase	Rattus norvegicus	19-22
35543250-4	2022	The advancement of AMG510 and MRTX849 as inhibitors of cysteine mutated KRAS (KRASG12C) to phase-III clinical trials informed the biased selection of AMG510 and MRTX849 for this study.	AMG-510	19-25	KRAS proto-oncogene, GTPase	Rattus norvegicus	72-76
35543250-4	2022	The advancement of AMG510 and MRTX849 as inhibitors of cysteine mutated KRAS (KRASG12C) to phase-III clinical trials informed the biased selection of AMG510 and MRTX849 for this study.	AMG-510	19-25	KRAS proto-oncogene, GTPase	Rattus norvegicus	78-86
35543250-4	2022	The advancement of AMG510 and MRTX849 as inhibitors of cysteine mutated KRAS (KRASG12C) to phase-III clinical trials informed the biased selection of AMG510 and MRTX849 for this study.	Cysteine	55-63	KRAS proto-oncogene, GTPase	Rattus norvegicus	72-76
35543250-4	2022	The advancement of AMG510 and MRTX849 as inhibitors of cysteine mutated KRAS (KRASG12C) to phase-III clinical trials informed the biased selection of AMG510 and MRTX849 for this study.	Cysteine	55-63	KRAS proto-oncogene, GTPase	Rattus norvegicus	78-86
35543250-4	2022	The advancement of AMG510 and MRTX849 as inhibitors of cysteine mutated KRAS (KRASG12C) to phase-III clinical trials informed the biased selection of AMG510 and MRTX849 for this study.	AMG-510	150-156	KRAS proto-oncogene, GTPase	Rattus norvegicus	72-76
35543250-4	2022	The advancement of AMG510 and MRTX849 as inhibitors of cysteine mutated KRAS (KRASG12C) to phase-III clinical trials informed the biased selection of AMG510 and MRTX849 for this study.	AMG-510	150-156	KRAS proto-oncogene, GTPase	Rattus norvegicus	78-86
35543250-6	2022	In this study, we employed computational tools to unravel the atomistic interactions and subsequent conformational effects of AMG510 and MRTX849 on the mutant KRASG12C.	AMG-510	126-132	KRAS proto-oncogene, GTPase	Rattus norvegicus	159-167
35592435-4	2022	PMBA was further found to target KRAS at its guanosine diphosphate site.	PMBA	0-4	KRAS proto-oncogene, GTPase	Rattus norvegicus	33-37
35592435-4	2022	PMBA was further found to target KRAS at its guanosine diphosphate site.	Guanosine Diphosphate	45-66	KRAS proto-oncogene, GTPase	Rattus norvegicus	33-37
35449573-1	2022	Sotorasib is a novel targeted inhibitor of Kirsten rat sarcoma (KRAS) (G12C) that has shown exciting tumor-suppressing effects not only for single targeted agents but also for combination with immune checkpoint inhibitors.	AMG-510	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	64-68
35412531-1	2022	Sotorasib, a direct inhibitor of the enzyme Kirsten rat sarcoma viral oncogene (KRAS) with the G12C mutation, was approved by the U.S. Food and Drug Administration (FDA), as a second-line treatment for locally advanced or metastatic non-small cell lung cancer (NSCLC) containing the KRAS G12C mutation, on the basis of results of a phase II clinical trial (Code- BreaK100).	AMG-510	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	80-84
35412531-1	2022	Sotorasib, a direct inhibitor of the enzyme Kirsten rat sarcoma viral oncogene (KRAS) with the G12C mutation, was approved by the U.S. Food and Drug Administration (FDA), as a second-line treatment for locally advanced or metastatic non-small cell lung cancer (NSCLC) containing the KRAS G12C mutation, on the basis of results of a phase II clinical trial (Code- BreaK100).	AMG-510	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	283-287
35412531-2	2022	In this article, we review the mechanism of action of KRAS G12C inhibitors and the latest clinical trials with sotorasib to provide a comprehensive understanding of its efficacy and toxicity.	AMG-510	111-120	KRAS proto-oncogene, GTPase	Rattus norvegicus	54-58
35147202-0	2022	Metformin inhibits pulmonary artery smooth muscle cell proliferation by upregulating p21 via NONRATT015587.2.	Metformin	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	85-88
34993844-10	2022	Resveratrol, in turn, presented anti-inflammatory effects in aged astrocyte cultures, which were associated with downregulation of p21 and pro-inflammatory cytokines, Toll-like receptors (TLRs), and nuclear factor kappaB (NFkappaB).	Resveratrol	0-11	KRAS proto-oncogene, GTPase	Rattus norvegicus	131-134
35163234-7	2022	Molecular docking results highlighted a higher affinity of four hit compounds towards KRAS G12D in comparison to the reference inhibitor, BI-2852.	BI-2852	138-145	KRAS proto-oncogene, GTPase	Rattus norvegicus	86-90
35280376-7	2022	The MSI ratio (%) had no linear correlation with TMB, and a significant difference of TMB between Kirsten rat sarcoma viral oncogene homologue (KRAS) other alterations and p.G12 alteration was identified.	1,2,4,5-tetramethoxybenzene	86-89	KRAS proto-oncogene, GTPase	Rattus norvegicus	144-148
35280376-11	2022	TMB among KRAS p.G12A, p.G12C, p.G12D, p.G12R, p.G12S, p.G12V, and other KRAS alterations were observed in tissue samples.	1,2,4,5-tetramethoxybenzene	0-3	KRAS proto-oncogene, GTPase	Rattus norvegicus	10-14
35280376-12	2022	Conclusions: In conclusion, analysis of age, tumor types, and KRAS mutations may provide a relative effectivity for estimating TMB.	1,2,4,5-tetramethoxybenzene	127-130	KRAS proto-oncogene, GTPase	Rattus norvegicus	62-66
35099637-0	2022	LINC01354/microRNA-216b/KRAS Axis Promotes the Occurrence and Metastasis of Endometrial Cancer.	linc01354	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	24-28
35099637-11	2022	LINC01354 counteracted with miR-216b to target KRAS.	linc01354	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	47-51
35083149-4	2021	Recently, the discovery of a new pocket under the effector binding switch II region of KRAS G12C has allowed the development of direct KRAS inhibitors such as sotorasib, the first FDA-approved drug targeting KRAS G12C, or adagrasib, initiating a new exciting era.	AMG-510	159-168	KRAS proto-oncogene, GTPase	Rattus norvegicus	87-91
35083149-4	2021	Recently, the discovery of a new pocket under the effector binding switch II region of KRAS G12C has allowed the development of direct KRAS inhibitors such as sotorasib, the first FDA-approved drug targeting KRAS G12C, or adagrasib, initiating a new exciting era.	AMG-510	159-168	KRAS proto-oncogene, GTPase	Rattus norvegicus	135-139
35156189-16	2022	CONCLUSIONS: IGF-1 can inhibit the apoptosis of rat GSMCs under high glucose conditions, its mechanism may be related to the regulation of expression and activity of p53, PI3K, TSC-2, Akt, mTOR, 4E-BP1, p70S6K, p21, CaMKII, and PLC-beta3 in rat GSMCs acting through AMPK pathway.	gsmcs	52-57	KRAS proto-oncogene, GTPase	Rattus norvegicus	211-214
34387588-2	2022	Trametinib, a selective allosteric inhibitor of the MEK1/2, demonstrated debatable clinical activity in KRAS-mutant NSCLC.	trametinib	0-10	KRAS proto-oncogene, GTPase	Rattus norvegicus	104-108
34387588-3	2022	In this case, we present a recurrent advanced NSCLC with KRAS G12C mutation successfully treated with single-agent trametinib therapy.	trametinib	115-125	KRAS proto-oncogene, GTPase	Rattus norvegicus	57-61
34387588-8	2022	This case advocates for routine screening of KRAS point mutations in the utility of precision medicine and suggests that treatment with trametinib in advanced NSCLC cases with KRAS G12C mutation is well tolerated and effective, especially for those very elderly or unsuitable for more aggressive chemotherapy.	trametinib	136-146	KRAS proto-oncogene, GTPase	Rattus norvegicus	45-49
34387588-8	2022	This case advocates for routine screening of KRAS point mutations in the utility of precision medicine and suggests that treatment with trametinib in advanced NSCLC cases with KRAS G12C mutation is well tolerated and effective, especially for those very elderly or unsuitable for more aggressive chemotherapy.	trametinib	136-146	KRAS proto-oncogene, GTPase	Rattus norvegicus	176-180
35110505-0	2022	Fenbendazole Suppresses Growth and Induces Apoptosis of Actively Growing H4IIE Hepatocellular Carcinoma Cells via p21-Mediated Cell-Cycle Arrest.	Fenbendazole	0-12	KRAS proto-oncogene, GTPase	Rattus norvegicus	114-117
35110505-8	2022	FZ up-regulated p21 (an inhibitor of cyclin-CDK) but suppressed the expression of cell cycle-promoting proteins (cyclin D1 and cyclin B1).	Fenbendazole	0-2	KRAS proto-oncogene, GTPase	Rattus norvegicus	16-19
35110505-12	2022	Taken together, FZ selectively suppressed the growth of cells via p21-mediated cell cycle arrest at G1/S and G2/M, and resulted in apoptosis only in actively growing cells but not in quiescent cells.	Fenbendazole	16-18	KRAS proto-oncogene, GTPase	Rattus norvegicus	66-69
35410520-0	2022	Bisphenol-A/Radiation mediated inflammatory response activates EGFR/KRAS/ERK1/2 signaling pathway leads to lung carcinogenesis incidence.	bisphenol A	0-11	KRAS proto-oncogene, GTPase	Rattus norvegicus	68-72
2545731-5	1989	This uncoupling of phosphoinositide turnover from binding was preceded by a drop in hepatic membrane ras p21 content, as assayed by liquid competition radioimmunoassay.	Phosphatidylinositols	19-35	KRAS proto-oncogene, GTPase	Rattus norvegicus	105-108
35145347-4	2022	Additionally, Diac, 5-FU and their combination suppressed colonic content/gene expression of IL-6, its downstream oncogene, Kirsten rat sarcoma viral oncogene homolog (K-Ras), and consequently Notch intracellular domain and nuclear factor-kappa B (NF-kappaB) p65.	Fluorouracil	20-24	KRAS proto-oncogene, GTPase	Rattus norvegicus	168-173
2472229-4	1989	A low SAM/SAH ratio was coupled, in nodules, with a high labeling index (LI), 2-fold fall in 5mC DNA content, increase in c-myc, c-Ha-ras and c-Ki-ras expression and hypomethylation of CCGG sequences in the DNA hybridizing with the three protooncogenes.	S-Adenosylhomocysteine	10-13	KRAS proto-oncogene, GTPase	Rattus norvegicus	142-150
2510583-13	1989	Whether these changes in eicosanoids can explain differences in ras p21 levels as judged by cross-linking to a-32 P-GTP remains to be investigated in greater detail.	Eicosanoids	25-36	KRAS proto-oncogene, GTPase	Rattus norvegicus	68-71
2645046-0	1989	Infrequent activation of K-ras, H-ras, and other oncogenes in hepatocellular neoplasms initiated by methyl(acetoxymethyl)nitrosamine, a methylating agent, and promoted by phenobarbital in F344 rats.	methyl(acetoxymethyl)nitrosamine	100-132	KRAS proto-oncogene, GTPase	Rattus norvegicus	25-30
2540743-3	1989	Hepatic expression of the c-k-ras protooncogene was 3-fold higher in THC exposed animals.	Dronabinol	69-72	KRAS proto-oncogene, GTPase	Rattus norvegicus	26-33
2645046-0	1989	Infrequent activation of K-ras, H-ras, and other oncogenes in hepatocellular neoplasms initiated by methyl(acetoxymethyl)nitrosamine, a methylating agent, and promoted by phenobarbital in F344 rats.	Phenobarbital	171-184	KRAS proto-oncogene, GTPase	Rattus norvegicus	25-30
2645046-10	1989	Selective oligonucleotide analysis revealed that a G----A transition in the second base of codon 12 of K-ras was present in the 9 K-ras-positive transformants and also in DNAs prepared from the original tumors.	Oligonucleotides	10-25	KRAS proto-oncogene, GTPase	Rattus norvegicus	103-108
2645046-10	1989	Selective oligonucleotide analysis revealed that a G----A transition in the second base of codon 12 of K-ras was present in the 9 K-ras-positive transformants and also in DNAs prepared from the original tumors.	Oligonucleotides	10-25	KRAS proto-oncogene, GTPase	Rattus norvegicus	130-135
2645046-11	1989	In contrast, oligonucleotide hybridization experiments with DNAs from 35 hepatocellular tumors that were negative in transfection assays revealed the presence of mutant K-ras in 1 of 15 HCCs; no mutation could be detected in 20 transfection-negative adenomas.	Oligonucleotides	13-28	KRAS proto-oncogene, GTPase	Rattus norvegicus	169-174
2647284-0	1989	Over expression of proto-oncogenes: ki-ras, fos and myc in rat liver cells treated in vitro by two liver tumor promoters: phenobarbital and biliverdin.	Biliverdine	140-150	KRAS proto-oncogene, GTPase	Rattus norvegicus	36-42
2536620-0	1989	Site-selective 8-chloroadenosine 3",5"-cyclic monophosphate inhibits transformation and transforming growth factor alpha production in Ki-ras-transformed rat fibroblasts.	8-chloro-cyclic adenosine monophosphate	15-59	KRAS proto-oncogene, GTPase	Rattus norvegicus	135-141
2495774-0	1989	[ras p21-like small MW GTP-binding proteins in transmembrane signaling].	Guanosine Triphosphate	23-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	5-8
2643467-0	1989	Induction by the guanosine analogue oxanosine of reversion toward the normal phenotype of K-ras-transformed rat kidney cells.	Guanosine	17-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	90-95
2643467-0	1989	Induction by the guanosine analogue oxanosine of reversion toward the normal phenotype of K-ras-transformed rat kidney cells.	oxanosine	36-45	KRAS proto-oncogene, GTPase	Rattus norvegicus	90-95
2643467-1	1989	Oxanosine, a guanosine analogue antibiotic, altered the "transformed" morphology of rat kidney cells integrating a temperature-sensitive K-ras gene into "normal" morphology at 34 degrees C, a permissive temperature.	oxanosine	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	137-142
2643467-4	1989	These changes in p21 were the same as those which occurred to p21 in the cells cultured in the absence of oxanosine at 39.5 degrees C, a nonpermissive temperature.	oxanosine	106-115	KRAS proto-oncogene, GTPase	Rattus norvegicus	17-20
2536620-1	1989	A site-selective cAMP analog, 8-chloroadenosine 3",5"-cyclic monophosphate (8-Cl-cAMP), was demonstrated to be a potent inhibitor of both the monolayer and soft agar growth of normal rat kidney (NRK) fibroblasts that had been transformed with the v-Ki-ras oncogene or treated with transforming growth factor alpha (TGF alpha).	8-chloro-cyclic adenosine monophosphate	30-74	KRAS proto-oncogene, GTPase	Rattus norvegicus	249-255
2536620-1	1989	A site-selective cAMP analog, 8-chloroadenosine 3",5"-cyclic monophosphate (8-Cl-cAMP), was demonstrated to be a potent inhibitor of both the monolayer and soft agar growth of normal rat kidney (NRK) fibroblasts that had been transformed with the v-Ki-ras oncogene or treated with transforming growth factor alpha (TGF alpha).	8-chloro-cyclic adenosine monophosphate	17-21	KRAS proto-oncogene, GTPase	Rattus norvegicus	249-255
2536620-1	1989	A site-selective cAMP analog, 8-chloroadenosine 3",5"-cyclic monophosphate (8-Cl-cAMP), was demonstrated to be a potent inhibitor of both the monolayer and soft agar growth of normal rat kidney (NRK) fibroblasts that had been transformed with the v-Ki-ras oncogene or treated with transforming growth factor alpha (TGF alpha).	8-chloro-cyclic adenosine monophosphate	76-85	KRAS proto-oncogene, GTPase	Rattus norvegicus	249-255
2833347-4	1988	In addition, rat embryo fibroblasts (CREF) and normal rat kidney fibroblasts (NRK) after transformation with a Ki-ras oncogene exhibit a similar increase in their sensitivity to CHP-induced growth inhibition.	chp	178-181	KRAS proto-oncogene, GTPase	Rattus norvegicus	111-117
2536620-3	1989	These effects of 8-Cl-cAMP were linked to the cAMP analog"s selective modulation of the type I and type II cAMP-dependent protein kinase regulatory subunits, RI and RII, present in Ki-ras-transformed and TGF alpha-treated NRK cells.	8-chloro-cyclic adenosine monophosphate	17-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	181-187
2536620-3	1989	These effects of 8-Cl-cAMP were linked to the cAMP analog"s selective modulation of the type I and type II cAMP-dependent protein kinase regulatory subunits, RI and RII, present in Ki-ras-transformed and TGF alpha-treated NRK cells.	8-chloro-cyclic adenosine monophosphate	22-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	181-187
2536620-3	1989	These effects of 8-Cl-cAMP were linked to the cAMP analog"s selective modulation of the type I and type II cAMP-dependent protein kinase regulatory subunits, RI and RII, present in Ki-ras-transformed and TGF alpha-treated NRK cells.	8-chloro-cyclic adenosine monophosphate	46-50	KRAS proto-oncogene, GTPase	Rattus norvegicus	181-187
2842801-5	1988	Similar increases in agonist displacement of [3H]naloxone binding (33-fold) and its abolition by guanosine 5"-[gamma-thio]triphosphate were observed with Go, the G protein of unknown function, but not with the v-Ki-ras protein p21.	Naloxone	45-57	KRAS proto-oncogene, GTPase	Rattus norvegicus	227-230
3042464-1	1988	The ras gene product (p21) specifically binds GDP or GTP.	Guanosine Diphosphate	46-49	KRAS proto-oncogene, GTPase	Rattus norvegicus	22-25
3042464-1	1988	The ras gene product (p21) specifically binds GDP or GTP.	Guanosine Triphosphate	53-56	KRAS proto-oncogene, GTPase	Rattus norvegicus	22-25
3042464-3	1988	Previously, we reported that not only oncogenic p21(Val-12) but also proto-oncogenic p21(Gly-12) could induce morphological differentiation in rat pheochromocytoma PC12 cells when microinjected in the complexed form with GTP gamma S [(1987) Mol.	val-12	52-58	KRAS proto-oncogene, GTPase	Rattus norvegicus	48-51
3042464-3	1988	Previously, we reported that not only oncogenic p21(Val-12) but also proto-oncogenic p21(Gly-12) could induce morphological differentiation in rat pheochromocytoma PC12 cells when microinjected in the complexed form with GTP gamma S [(1987) Mol.	gly-12	89-95	KRAS proto-oncogene, GTPase	Rattus norvegicus	85-88
3042464-3	1988	Previously, we reported that not only oncogenic p21(Val-12) but also proto-oncogenic p21(Gly-12) could induce morphological differentiation in rat pheochromocytoma PC12 cells when microinjected in the complexed form with GTP gamma S [(1987) Mol.	Guanosine 5'-O-(3-Thiotriphosphate)	221-232	KRAS proto-oncogene, GTPase	Rattus norvegicus	48-51
3042464-3	1988	Previously, we reported that not only oncogenic p21(Val-12) but also proto-oncogenic p21(Gly-12) could induce morphological differentiation in rat pheochromocytoma PC12 cells when microinjected in the complexed form with GTP gamma S [(1987) Mol.	Guanosine 5'-O-(3-Thiotriphosphate)	221-232	KRAS proto-oncogene, GTPase	Rattus norvegicus	85-88
3042464-9	1988	Then we analyzed the guanine nucleotide bound to p21 in the intact PC12 cells.	Guanine Nucleotides	21-39	KRAS proto-oncogene, GTPase	Rattus norvegicus	49-52
3042464-10	1988	It was found that conditionally induced p21(Val-12) was mostly present in the GTP-bound form, whereas the endogenous p21(Gly-12) was in the GDP-bound form.	val-12	44-50	KRAS proto-oncogene, GTPase	Rattus norvegicus	40-43
3042464-10	1988	It was found that conditionally induced p21(Val-12) was mostly present in the GTP-bound form, whereas the endogenous p21(Gly-12) was in the GDP-bound form.	Guanosine Triphosphate	78-81	KRAS proto-oncogene, GTPase	Rattus norvegicus	40-43
3042464-10	1988	It was found that conditionally induced p21(Val-12) was mostly present in the GTP-bound form, whereas the endogenous p21(Gly-12) was in the GDP-bound form.	gly-12	121-127	KRAS proto-oncogene, GTPase	Rattus norvegicus	117-120
3042464-10	1988	It was found that conditionally induced p21(Val-12) was mostly present in the GTP-bound form, whereas the endogenous p21(Gly-12) was in the GDP-bound form.	Guanosine Diphosphate	140-143	KRAS proto-oncogene, GTPase	Rattus norvegicus	117-120
3042464-11	1988	These results indicate again that p21.GTP induces the morphological differentiation of PC12 cells.	Guanosine Triphosphate	38-41	KRAS proto-oncogene, GTPase	Rattus norvegicus	34-37
3287372-8	1988	The activated Ki-ras oncogene was further characterized by use of synthetic oligonucleotide probes and was shown to contain a G----A transition at the second nucleotide in codon 12.	Oligonucleotides	76-91	KRAS proto-oncogene, GTPase	Rattus norvegicus	14-20
3276902-4	1988	In contrast to mutational activation of ras genes, enhanced expression of p21 was observed in all tumors examined by immunohistochemical techniques with the use of Formalin-fixed paraffin-embedded tissue sections and an anti-ras p21 antibody, RAP-5.	Formaldehyde	164-172	KRAS proto-oncogene, GTPase	Rattus norvegicus	74-77
3276902-4	1988	In contrast to mutational activation of ras genes, enhanced expression of p21 was observed in all tumors examined by immunohistochemical techniques with the use of Formalin-fixed paraffin-embedded tissue sections and an anti-ras p21 antibody, RAP-5.	Paraffin	179-187	KRAS proto-oncogene, GTPase	Rattus norvegicus	74-77
3276902-5	1988	Further histochemical analysis of bladder tissues at various stages of the BBN-induced carcinogenic process indicated that the enhanced expression of p21 appeared early; the reactivity with RAP-5 was observed in diffuse hyperplastic epithelia after 5 weeks of exposure to BBN.	Butylhydroxybutylnitrosamine	75-78	KRAS proto-oncogene, GTPase	Rattus norvegicus	150-153
3276902-5	1988	Further histochemical analysis of bladder tissues at various stages of the BBN-induced carcinogenic process indicated that the enhanced expression of p21 appeared early; the reactivity with RAP-5 was observed in diffuse hyperplastic epithelia after 5 weeks of exposure to BBN.	Butylhydroxybutylnitrosamine	272-275	KRAS proto-oncogene, GTPase	Rattus norvegicus	150-153
3345576-0	1988	c-H-ras and c-K-ras gene hypomethylation in the livers and hepatomas of rats fed methyl-deficient, amino acid-defined diets.	methyl radical	29-35	KRAS proto-oncogene, GTPase	Rattus norvegicus	12-19
3288862-8	1988	We found that cells expressing elevated levels of the normal p21(H-ras) could be fully transformed by the activated (Val-12) form and that such cells continued to overexpress p21(H-ras) (Gly-12), arguing against a role for normal ras genes in suppression of the oncogenic potential of their mutationally activated counterparts.	val-12	117-123	KRAS proto-oncogene, GTPase	Rattus norvegicus	61-64
3288862-8	1988	We found that cells expressing elevated levels of the normal p21(H-ras) could be fully transformed by the activated (Val-12) form and that such cells continued to overexpress p21(H-ras) (Gly-12), arguing against a role for normal ras genes in suppression of the oncogenic potential of their mutationally activated counterparts.	Glycine	187-190	KRAS proto-oncogene, GTPase	Rattus norvegicus	175-178
3345576-3	1988	The results indicated that both c-H-ras and c-K-ras oncogenes were hypomethylated in all DNA samples derived from both neoplastic and preneoplastic livers of rats fed any of the methyl-deficient diets used, regardless of whether or not the rats had received an initiating dose of DEN.	Diethylnitrosamine	280-283	KRAS proto-oncogene, GTPase	Rattus norvegicus	44-51
3130359-0	1988	Activated K-ras in tumorigenic and non-tumorigenic cell variants from a rat colon adenocarcinoma, induced by dimethylhydrazine.	Dimethylhydrazines	109-126	KRAS proto-oncogene, GTPase	Rattus norvegicus	10-15
3321305-3	1986	We found that normal rat kidney cells transformed with ras and sis contained elevated levels of DAG, and cells transformed with temperature-sensitive K-ras had elevated DAG levels at the permissive but not the restrictive temperature.	dag	169-172	KRAS proto-oncogene, GTPase	Rattus norvegicus	150-155
3325827-6	1987	These results indicate that the binary p21-GTP complex, but not the p21-GDP complex, is effective in inducing differentiation in PC12 cells, irrespective of the oncogenic or the proto-oncogenic protein.	Guanosine Triphosphate	43-46	KRAS proto-oncogene, GTPase	Rattus norvegicus	39-42
3329719-4	1987	In contrast, in v-ras-transformed rat thyroid cells, which express very high levels of p21, treatment with either TSH, forskolin or TPA does not induce c-fos gene expression, while c-myc expression was constitutive.	Thyrotropin	114-117	KRAS proto-oncogene, GTPase	Rattus norvegicus	87-90
3329719-4	1987	In contrast, in v-ras-transformed rat thyroid cells, which express very high levels of p21, treatment with either TSH, forskolin or TPA does not induce c-fos gene expression, while c-myc expression was constitutive.	Colforsin	119-128	KRAS proto-oncogene, GTPase	Rattus norvegicus	87-90
3329719-4	1987	In contrast, in v-ras-transformed rat thyroid cells, which express very high levels of p21, treatment with either TSH, forskolin or TPA does not induce c-fos gene expression, while c-myc expression was constitutive.	Tetradecanoylphorbol Acetate	132-135	KRAS proto-oncogene, GTPase	Rattus norvegicus	87-90
3581065-0	1987	Activation of the K-ras protooncogene in lung tumors from rats and mice chronically exposed to tetranitromethane.	Tetranitromethane	95-112	KRAS proto-oncogene, GTPase	Rattus norvegicus	18-23
3581065-15	1987	Tetranitromethane may exert its carcinogenic action by both activation of the K-ras oncogene and stimulation of cell proliferation by its irritant properties.	Tetranitromethane	0-17	KRAS proto-oncogene, GTPase	Rattus norvegicus	78-83
3099282-0	1986	Identification of an activated c-Ki-ras oncogene in rat liver tumors induced by aflatoxin B1.	Aflatoxin B1	80-92	KRAS proto-oncogene, GTPase	Rattus norvegicus	31-39
3785207-0	1986	Activated K-ras and N-ras oncogenes in primary renal mesenchymal tumors induced in F344 rats by methyl(methoxymethyl)nitrosamine.	Methoxymethyl-methylnitrosamine	96-128	KRAS proto-oncogene, GTPase	Rattus norvegicus	10-15
3023888-6	1986	In contrast to serum, p21 did not stimulate total RNA or protein synthesis, but some RNA and protein synthesis must have been needed for the p21-driven G1 transit because it could be stopped by actinomycin D or cycloheximide.	Dactinomycin	194-207	KRAS proto-oncogene, GTPase	Rattus norvegicus	141-144
3023888-6	1986	In contrast to serum, p21 did not stimulate total RNA or protein synthesis, but some RNA and protein synthesis must have been needed for the p21-driven G1 transit because it could be stopped by actinomycin D or cycloheximide.	Cycloheximide	211-224	KRAS proto-oncogene, GTPase	Rattus norvegicus	141-144
3023884-0	1986	Structure of the c-Ki-ras gene in a rat fibrosarcoma induced by 1,8-dinitropyrene.	1,8-dinitropyrene	64-81	KRAS proto-oncogene, GTPase	Rattus norvegicus	17-25
3023884-1	1986	Restriction enzyme maps were made of the region around exons 1 and 2 of activated c-Ki-ras of a fibrosarcoma (1,8-DNP2) induced in a rat by 1,8-dinitropyrene.	1,8-dnp2	110-118	KRAS proto-oncogene, GTPase	Rattus norvegicus	82-90
3023884-1	1986	Restriction enzyme maps were made of the region around exons 1 and 2 of activated c-Ki-ras of a fibrosarcoma (1,8-DNP2) induced in a rat by 1,8-dinitropyrene.	1,8-dinitropyrene	140-157	KRAS proto-oncogene, GTPase	Rattus norvegicus	82-90
3023884-2	1986	Nucleotide sequence analysis revealed that activated c-Ki-ras shows a G----T transversion in codon 12 and consequently encodes cysteine instead of glycine in normal rat c-Ki-ras.	Cysteine	127-135	KRAS proto-oncogene, GTPase	Rattus norvegicus	53-61
3023884-2	1986	Nucleotide sequence analysis revealed that activated c-Ki-ras shows a G----T transversion in codon 12 and consequently encodes cysteine instead of glycine in normal rat c-Ki-ras.	Glycine	147-154	KRAS proto-oncogene, GTPase	Rattus norvegicus	53-61
24254822-11	1987	At P21, Pb concentrations were 2-4 times higher in blood, brain, bone, and liver of pups that had access to Pb-contaminated feces than in pups that were exposed to Pb primarily through the mother"s milk.	Lead	8-10	KRAS proto-oncogene, GTPase	Rattus norvegicus	3-6
3501927-2	1987	In Western blotting, high levels of c-Ha-ras p 21 were found in serially transplantable rat duodenal carcinomas induced by MNNG and rat colon carcinomas induced by DMH.	1,2-Dimethylhydrazine	164-167	KRAS proto-oncogene, GTPase	Rattus norvegicus	45-49
3501927-6	1987	These findings suggest that c-Ha-ras p 21 expression plays an important role in tumor proliferation, invasion and metastasis of DMH-induced colon carcinoma.	1,2-Dimethylhydrazine	128-131	KRAS proto-oncogene, GTPase	Rattus norvegicus	37-41
3553214-3	1987	The Ki-RAS protein increased the sensitivity of adenylate cyclase to guanyl nucleotides by a mechanism that seemed to involve inactivation of the enzyme"s inhibitory G1 regulatory protein.	guanyl nucleotides	69-87	KRAS proto-oncogene, GTPase	Rattus norvegicus	4-10
3013856-6	1986	In K-ras-transformed NRK cells grown at 34 or 38 degrees C, DAG levels were elevated 168 or 138%, respectively.	dag	60-63	KRAS proto-oncogene, GTPase	Rattus norvegicus	3-8
3013856-7	1986	When a temperature-sensitive K-ras NRK cell line was investigated, the amount of DAG present was elevated at the permissive but not at the restrictive temperature.	dag	81-84	KRAS proto-oncogene, GTPase	Rattus norvegicus	29-34
3013856-8	1986	These data are consistent with the K-ras protein functioning in transmembrane signalling by activating phospholipase C. Protein kinase C (Ca2+/phospholipid-dependent enzyme) activation by DAG may play an important role in cellular transformation.	Phospholipids	143-155	KRAS proto-oncogene, GTPase	Rattus norvegicus	35-40
3013856-8	1986	These data are consistent with the K-ras protein functioning in transmembrane signalling by activating phospholipase C. Protein kinase C (Ca2+/phospholipid-dependent enzyme) activation by DAG may play an important role in cellular transformation.	dag	188-191	KRAS proto-oncogene, GTPase	Rattus norvegicus	35-40
6092966-5	1984	Analysis of rat fibroblasts transfected with these altered genes demonstrates that all amino acids except glycine (which is encoded by normal cellular ras genes) and proline at position 12 activate p21, suggesting a requirement for an alpha-helical structure in this region of the polypeptide.	Proline	166-173	KRAS proto-oncogene, GTPase	Rattus norvegicus	198-201
4075282-0	1985	Activation of K-ras and oncogenes other than ras family in rat fibrosarcomas induced by 1,8-dinitropyrene.	1,8-dinitropyrene	88-105	KRAS proto-oncogene, GTPase	Rattus norvegicus	14-19
4075282-3	1985	A transformant, 1,8-DNP2-2, induced by DNA of a fibrosarcoma, 1,8-DNP2, and 7 secondary transformants derived from it contained rat K-ras sequences.	1,8-dnp2	16-24	KRAS proto-oncogene, GTPase	Rattus norvegicus	132-137
6089789-3	1984	The amount of p21-translated protein sharply decreased in the translation products of the regressing tumors within 6 hours post ovariectomy or dibutyryl cyclic AMP treatment.	Cyclic AMP	153-163	KRAS proto-oncogene, GTPase	Rattus norvegicus	14-17
34004237-1	2021	Sotorasib is a first-in class KRASG12C covalent inhibitor in clinical development for the treatment of tumors with the KRAS p.G12C mutation.	AMG-510	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	30-34
33774143-6	2021	Next, the up-regulation of lncRNA p21 and miR-181b was used as a reversal experiment, and the results suggested that the up-regulation of miR-181b attenuated the promoting effect of lncRNA p21 and Tnfaip1 on apoptosis and inflammatory response, which may be related to the activation of AKT/cAMP response element binding protein (CREB) axis.	Cyclic AMP	291-295	KRAS proto-oncogene, GTPase	Rattus norvegicus	189-192
34019861-12	2021	The protein levels of the electron transport chain complexes, LONP1, UCP2, and P21 showed significant differences after lenvatinib treatment.	lenvatinib	120-130	KRAS proto-oncogene, GTPase	Rattus norvegicus	79-82
228288-3	1979	We report herein that when extracts from cells transformed by Kirsten or Harvey sarcoma virus are incubated with [(3)H]GDP or [alpha-(32)P]GTP, picomole quantities of guanine nucleotide can be immunoprecipitated with antisera that contain antibodies to the p21.	Guanosine Diphosphate	119-122	KRAS proto-oncogene, GTPase	Rattus norvegicus	257-260
228288-3	1979	We report herein that when extracts from cells transformed by Kirsten or Harvey sarcoma virus are incubated with [(3)H]GDP or [alpha-(32)P]GTP, picomole quantities of guanine nucleotide can be immunoprecipitated with antisera that contain antibodies to the p21.	alpha-(32)p	127-138	KRAS proto-oncogene, GTPase	Rattus norvegicus	257-260
228288-3	1979	We report herein that when extracts from cells transformed by Kirsten or Harvey sarcoma virus are incubated with [(3)H]GDP or [alpha-(32)P]GTP, picomole quantities of guanine nucleotide can be immunoprecipitated with antisera that contain antibodies to the p21.	Guanine Nucleotides	167-185	KRAS proto-oncogene, GTPase	Rattus norvegicus	257-260
228288-4	1979	Previously we have shown that the immunoprecipitability of [(35)S]methionine-labeled p21 of the temperature-sensitive mutant of Kirsten sarcoma virus is thermolabile.	Sulfur	63-65	KRAS proto-oncogene, GTPase	Rattus norvegicus	85-88
228288-4	1979	Previously we have shown that the immunoprecipitability of [(35)S]methionine-labeled p21 of the temperature-sensitive mutant of Kirsten sarcoma virus is thermolabile.	Methionine	66-76	KRAS proto-oncogene, GTPase	Rattus norvegicus	85-88
228288-6	1979	However, the immunoprecipitability of the [(35)S]methionine-labeled p21 in such extracts of the temperature-sensitive mutant can be preserved if the extracts containing labeled p21 are incubated with added GDP or GTP prior to heating.	Methionine	49-59	KRAS proto-oncogene, GTPase	Rattus norvegicus	68-71
228288-6	1979	However, the immunoprecipitability of the [(35)S]methionine-labeled p21 in such extracts of the temperature-sensitive mutant can be preserved if the extracts containing labeled p21 are incubated with added GDP or GTP prior to heating.	Methionine	49-59	KRAS proto-oncogene, GTPase	Rattus norvegicus	177-180
228288-6	1979	However, the immunoprecipitability of the [(35)S]methionine-labeled p21 in such extracts of the temperature-sensitive mutant can be preserved if the extracts containing labeled p21 are incubated with added GDP or GTP prior to heating.	Guanosine Diphosphate	206-209	KRAS proto-oncogene, GTPase	Rattus norvegicus	68-71
228288-6	1979	However, the immunoprecipitability of the [(35)S]methionine-labeled p21 in such extracts of the temperature-sensitive mutant can be preserved if the extracts containing labeled p21 are incubated with added GDP or GTP prior to heating.	Guanosine Triphosphate	213-216	KRAS proto-oncogene, GTPase	Rattus norvegicus	68-71
228288-7	1979	The results suggest an interaction between p21 and certain guanine nucleotides, and the possible roles of guanine nucleotides and p21 in the maintenance of transformation are discussed.	Guanine Nucleotides	59-78	KRAS proto-oncogene, GTPase	Rattus norvegicus	43-46
33737050-6	2021	We found that MPP+ induced cell senescence with increased beta-galactosidase activity and the expression of p53, p21 and p16 activation in cells.	mangion-purified polysaccharide (Candida albicans)	14-18	KRAS proto-oncogene, GTPase	Rattus norvegicus	113-116
34012925-4	2021	The latest published clinical trial data on new small-molecule KRAS G12C inhibitors, AMG510 and MRTX849, indicate that these molecules may potentially help treat KRAS-mutant NSCLC.	AMG-510	85-91	KRAS proto-oncogene, GTPase	Rattus norvegicus	63-67
34012925-4	2021	The latest published clinical trial data on new small-molecule KRAS G12C inhibitors, AMG510 and MRTX849, indicate that these molecules may potentially help treat KRAS-mutant NSCLC.	AMG-510	85-91	KRAS proto-oncogene, GTPase	Rattus norvegicus	162-166
33393722-0	2021	Linseed ameliorates renal apoptosis in rat fetuses induced by single or combined exposure to diesel nanoparticles or fenitrothion by inhibiting transcriptional activation of p21/p53 and caspase-3/9 through pro-oxidant stimulus.	Fenitrothion	117-129	KRAS proto-oncogene, GTPase	Rattus norvegicus	174-177
33936050-7	2021	Furthermore, LXA4 inhibited NF-kappaB-mediated inflammatory response and the p53/p21 senescence pathway in vivo and in vitro.	lipoxin A4	13-17	KRAS proto-oncogene, GTPase	Rattus norvegicus	81-84
33923672-12	2021	The results showed that melatonin reduced the number of p21-positive cells in the SGZ of the dentate gyrus and increased Nrf2, DCX and BDNF protein expression in rats treated with 5-FU.	Melatonin	24-33	KRAS proto-oncogene, GTPase	Rattus norvegicus	56-59
33888646-9	2021	Besides, the expression of anti-aging protein SIRT1 was upregulated significantly, while p53 and p21 were downregulated significantly after LMV treatment.	lmv	140-143	KRAS proto-oncogene, GTPase	Rattus norvegicus	97-100
33325046-8	2021	In vitro, under the stimulation of homocysteine (500 mumol/L, 24 hours), the rat vascular smooth muscle cells (VSMCs) presented senescence, which was characterized by the increased expression of ageing-related markers, such as p16, p21 and p53 as well as increased senescence-associated beta-galactosidase (SA-beta-gal) activity.	Homocysteine	35-47	KRAS proto-oncogene, GTPase	Rattus norvegicus	232-235
33414460-4	2021	Furthermore, oncogenic K-Ras altered SL metabolism, with an increase of long-chain (LC) C18, C20 ceramides (Cer), and very-long-chain (VLC) C22:1, C24 Cer, and an increase of sphingosine kinase 1 (SK1) expression.	Ceramides	97-106	KRAS proto-oncogene, GTPase	Rattus norvegicus	23-28
33791811-9	2021	Also, sorafenib significantly decreased the levels of P21, CyclinD1, CDK4 and proliferating cell nuclear antigen, as well as up-regulated P53 expression in adjuvant arthritis fibroblast-like synoviocytes.	Sorafenib	6-15	KRAS proto-oncogene, GTPase	Rattus norvegicus	54-57
33620658-4	2021	CpG loci in H-Ras and K-Ras were observed to be more hypomethylated in MIBC, whereas more hypomethylation in N-Ras was noted in NMIBC.	4-METHYL-2-PENTANOL	71-75	KRAS proto-oncogene, GTPase	Rattus norvegicus	22-27
33785097-3	2021	As a new therapeutic strategy, the C19 molecule ((2S)-N-(2,5-dichlorophenyl)-2-[(3,4-dimethoxyphenyl)-methylamine]propanamide) blocks the KRAS-membrane association in cancer cells.	(2s)-n-(2,5-dichlorophenyl)-2-[(3,4-dimethoxyphenyl)-methylamine]propanamide	49-125	KRAS proto-oncogene, GTPase	Rattus norvegicus	138-142
33246030-7	2021	p21 and p27 were shown to be involved in the miR-137- and AZD9291-mediated effects on GH3 cells.	osimertinib	58-65	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-3
33409483-4	2021	Following 7 days of oral exposure to EGME, activities of GPx and SOD were significantly increased, as well as levels of K-Ras, c-Myc, p53, caspase-3, TNF-alpha and, IL-6, while NO level and GST activity were significantly reduced compared with control.	methyl cellosolve	37-41	KRAS proto-oncogene, GTPase	Rattus norvegicus	120-125
33409483-6	2021	After 21 days of EGME administration, levels of Bcl-2, IL-10, GSH and NO as well as GST activity were significantly decreased, while levels of K-Ras, c-Myc, p53, Bax, caspase-3, IL-6, IL-1beta, TNF-alpha, as well as GPx, CAT, and SOD activities were significantly elevated compared with control.	methyl cellosolve	17-21	KRAS proto-oncogene, GTPase	Rattus norvegicus	143-148
33354317-13	2020	Monocrotaline treatment increased p-AKT/AKT and decreased P21 expression and caused pulmonary vascular remodeling in the model rats.	Monocrotaline	0-13	KRAS proto-oncogene, GTPase	Rattus norvegicus	58-61
33603790-4	2021	We first showed that after treatment with bleomycin in vitro, rat patellar TSCs (PTSCs) underwent senescence, characterized by morphological alterations, induction of senescence-associated beta-galactosidase (SA-beta-gal) activity, and an increase in p53, p21, and p62 protein expression.	Bleomycin	42-51	KRAS proto-oncogene, GTPase	Rattus norvegicus	256-259
33438560-8	2021	Docking studies of the active THIQs were also performed in our laboratory, targeting the active sites of KRas and VEGF receptors.	1,2,3,4-tetrahydroisoquinoline	30-35	KRAS proto-oncogene, GTPase	Rattus norvegicus	105-109
33438560-9	2021	RESULTS: Compound GM-3-18 was found to possess significant activities for KRas inhibition, with IC50 values in the rage of 0.9 microM to 10.7 microM, for all colon cancer cell lines.	gm-3-18	18-25	KRAS proto-oncogene, GTPase	Rattus norvegicus	74-78
33438560-13	2021	The THIQs bearing the chloro group at the 4-postiton of the phenyl ring (GM-3-18) exhibited significant KRas inhibition against all colon cancer cell lines.	1,2,3,4-tetrahydroisoquinoline	4-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	104-108
33438560-13	2021	The THIQs bearing the chloro group at the 4-postiton of the phenyl ring (GM-3-18) exhibited significant KRas inhibition against all colon cancer cell lines.	Hydrochloric Acid	22-28	KRAS proto-oncogene, GTPase	Rattus norvegicus	104-108
33438560-13	2021	The THIQs bearing the chloro group at the 4-postiton of the phenyl ring (GM-3-18) exhibited significant KRas inhibition against all colon cancer cell lines.	gm-3-18	73-80	KRAS proto-oncogene, GTPase	Rattus norvegicus	104-108
33469262-15	2021	P21 and PAI-1 were significantly upregulated and SIRT1 was greatly downregulated by Doxorubicin, all of which were reversed by Roflumilast.	Doxorubicin	84-95	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-3
33469262-15	2021	P21 and PAI-1 were significantly upregulated and SIRT1 was greatly downregulated by Doxorubicin, all of which were reversed by Roflumilast.	Roflumilast	127-138	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-3
33414460-5	2021	Since Cer and sphingosine-1-phosphate have been shown to exert opposite effects on cellular senescence, we hypothesized that targeting SK1 could enhance oncogenic K-Ras-induced senescence.	sphingosine 1-phosphate	14-37	KRAS proto-oncogene, GTPase	Rattus norvegicus	163-168
33414460-6	2021	Indeed, SK1 downregulation or inhibition enhanced p21 expression and SA-beta-gal in cells expressing oncogenic K-Ras and impeded cell growth.	2-(2-quinolinyl)-1H-indene--1,3(2H)-dione-6'-sulfonic acid	69-80	KRAS proto-oncogene, GTPase	Rattus norvegicus	111-116
33152944-12	2020	CONCLUSION: A. senegelensis n-hexane extract demonstrates its anticancer properties by improving the liver architecture, increasing the antioxidant defense systems, downregulating the pro-inflammatory, anti-apoptotic, angiogenic, alpha-fetoprotein and farnesyl transferase mRNAs expression and hitherto up-regulate the expression of tumor suppressor (P21 and P53) mRNAs.	n-hexane	28-36	KRAS proto-oncogene, GTPase	Rattus norvegicus	351-354
33384595-6	2020	Results: ANI treatment significantly reduced the apoptosis, caspase-3 and SA-beta-gal activities, and p53 and p21 proteins expression, while promoted telomerase activity and aggrecan and collagen II synthesis in IL-1beta-induced HNPCs.	anisodamine	9-12	KRAS proto-oncogene, GTPase	Rattus norvegicus	110-113
33384595-8	2020	Additionally, the application of ANI abolished the effects of IL-6 on apoptosis, SA-beta-gal and telomerase activity, and the expression of p53, p21, aggrecan and collagen II proteins in degenerated HNPCs.	anisodamine	33-36	KRAS proto-oncogene, GTPase	Rattus norvegicus	145-148
33170712-3	2020	In this work, a G12D-mutated farnesylated GTP-bound Kirsten RAt sarcoma (KRAS) protein has been simulated at the interface of a DOPC/DOPS/cholesterol model anionic cell membrane.	Guanosine Triphosphate	42-45	KRAS proto-oncogene, GTPase	Rattus norvegicus	52-71
33170712-3	2020	In this work, a G12D-mutated farnesylated GTP-bound Kirsten RAt sarcoma (KRAS) protein has been simulated at the interface of a DOPC/DOPS/cholesterol model anionic cell membrane.	Guanosine Triphosphate	42-45	KRAS proto-oncogene, GTPase	Rattus norvegicus	73-77
33170712-3	2020	In this work, a G12D-mutated farnesylated GTP-bound Kirsten RAt sarcoma (KRAS) protein has been simulated at the interface of a DOPC/DOPS/cholesterol model anionic cell membrane.	1,2-oleoylphosphatidylcholine	128-132	KRAS proto-oncogene, GTPase	Rattus norvegicus	52-71
33170712-3	2020	In this work, a G12D-mutated farnesylated GTP-bound Kirsten RAt sarcoma (KRAS) protein has been simulated at the interface of a DOPC/DOPS/cholesterol model anionic cell membrane.	1,2-oleoylphosphatidylcholine	128-132	KRAS proto-oncogene, GTPase	Rattus norvegicus	73-77
33170712-3	2020	In this work, a G12D-mutated farnesylated GTP-bound Kirsten RAt sarcoma (KRAS) protein has been simulated at the interface of a DOPC/DOPS/cholesterol model anionic cell membrane.	Droxidopa	133-137	KRAS proto-oncogene, GTPase	Rattus norvegicus	52-71
33170712-3	2020	In this work, a G12D-mutated farnesylated GTP-bound Kirsten RAt sarcoma (KRAS) protein has been simulated at the interface of a DOPC/DOPS/cholesterol model anionic cell membrane.	Droxidopa	133-137	KRAS proto-oncogene, GTPase	Rattus norvegicus	73-77
33170712-3	2020	In this work, a G12D-mutated farnesylated GTP-bound Kirsten RAt sarcoma (KRAS) protein has been simulated at the interface of a DOPC/DOPS/cholesterol model anionic cell membrane.	Cholesterol	138-149	KRAS proto-oncogene, GTPase	Rattus norvegicus	52-71
33170712-3	2020	In this work, a G12D-mutated farnesylated GTP-bound Kirsten RAt sarcoma (KRAS) protein has been simulated at the interface of a DOPC/DOPS/cholesterol model anionic cell membrane.	Cholesterol	138-149	KRAS proto-oncogene, GTPase	Rattus norvegicus	73-77
33010296-7	2020	In the enalapril-treated group, intrarenal p16 and p21 protein expressions decreased compared to controls.	Enalapril	7-16	KRAS proto-oncogene, GTPase	Rattus norvegicus	51-54
33010296-8	2020	The expressions of both p21 and p16 were reduced throughout the renal cortex and medulla of enalapril-treated rats.	Enalapril	92-101	KRAS proto-oncogene, GTPase	Rattus norvegicus	24-27
32947833-0	2020	Bioinformatics Data Mining Repurposes the JAK2 (Janus Kinase 2) Inhibitor Fedratinib for Treating Pancreatic Ductal Adenocarcinoma by Reversing the KRAS (Kirsten Rat Sarcoma 2 Viral Oncogene Homolog)-Driven Gene Signature.	Fedratinib	74-84	KRAS proto-oncogene, GTPase	Rattus norvegicus	148-152
33066270-7	2020	Artificial senescence induced by H2O2 caused a dose-dependent increase in Ccn3 gene and CCN3 protein expression, along with enhanced expression of p21 and p53 mRNA and proteins, as well as SA-beta gal activity.	Hydrogen Peroxide	33-37	KRAS proto-oncogene, GTPase	Rattus norvegicus	147-150
32963259-4	2020	Furthermore, EECGL significantly inhibited HM-induced increased population of cells in sub G0/G1 phase, decreased Bcl2 expression and thereby loss of mitochondrial membrane potential with over expression of Bax, p53, p21, activation of caspase 3 and 9 indicated the apoptosis and suppression of cell survival.	eecgl	13-18	KRAS proto-oncogene, GTPase	Rattus norvegicus	217-220
32798748-5	2020	The comet assay and western blot analysis showed a concentration-dependent increase in DNA damage and in p53 and p21 protein levels 24 h after TEB treatment.	tebuconazole	143-146	KRAS proto-oncogene, GTPase	Rattus norvegicus	113-116
32605718-2	2020	Recently, KRAS G12C was identified to be a potential drug target and predictor of response to the novel on AMG510 target treatment.	AMG-510	107-113	KRAS proto-oncogene, GTPase	Rattus norvegicus	10-14
32650051-7	2020	RESULTS: Rats in the vehicle plus sevoflurane group responded to sevoflurane exposure on P19, P20 or P21 with electroencephalography-detectable seizures and stress-like corticosterone secretion and had altered hippocampal dendrite morphology in adulthood.	Sevoflurane	34-45	KRAS proto-oncogene, GTPase	Rattus norvegicus	101-104
32650051-7	2020	RESULTS: Rats in the vehicle plus sevoflurane group responded to sevoflurane exposure on P19, P20 or P21 with electroencephalography-detectable seizures and stress-like corticosterone secretion and had altered hippocampal dendrite morphology in adulthood.	Sevoflurane	65-76	KRAS proto-oncogene, GTPase	Rattus norvegicus	101-104
32959498-7	2020	Metformin increased the levels of p-AMPK and PGC-1alpha, a downstream AMPK target which regulates mitochondrial biogenesis, at P4, P10, and P21 in hyperoxia pups.	Metformin	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	140-143
31810868-8	2020	Besides, treatment of 1,25(OH)2D3 at 1mug/kg, 5mug/kg or 10mug/kg reduced oxidative stress and inflammation, inhibited the p53-p21 signaling pathway and consequent cell senescence.	25-hydroxyvitamin D3-bromoacetate	22-33	KRAS proto-oncogene, GTPase	Rattus norvegicus	127-130
31810868-10	2020	CONCLUSION: Collectively, the evidences from this study demonstrated that active VD could alleviate the development of NAFLD through blocking the p53-p21 signaling pathway, which provided a novel nutritional therapeutic insight for NAFLD.	Vitamin D	81-83	KRAS proto-oncogene, GTPase	Rattus norvegicus	150-153
32553926-6	2020	KEY FINDINGS: Upon the treatment of aged pancreatic islets cells with cannabidiol and tetrahydrocannabinol, the expression of p53, p38, p21 and the activity of beta-galactosidase were reduced.	Cannabidiol	70-81	KRAS proto-oncogene, GTPase	Rattus norvegicus	136-139
32553926-6	2020	KEY FINDINGS: Upon the treatment of aged pancreatic islets cells with cannabidiol and tetrahydrocannabinol, the expression of p53, p38, p21 and the activity of beta-galactosidase were reduced.	Dronabinol	86-106	KRAS proto-oncogene, GTPase	Rattus norvegicus	136-139
32582979-7	2020	In vitro, selective antagonism of MR partially blocked H2O2-induced myocardial aging as assessed by p16, p21 and p53 expression levels and excessive reactive oxygen species (ROS) accumulation.	Hydrogen Peroxide	55-59	KRAS proto-oncogene, GTPase	Rattus norvegicus	105-108
32959498-8	2020	Lung ATP levels decreased during hyperoxia and were increased by metformin at P10 and P21.	Adenosine Triphosphate	5-8	KRAS proto-oncogene, GTPase	Rattus norvegicus	86-89
32959498-9	2020	Radial alveolar count and alveolar septal tips were decreased and mean linear intercept increased in hyperoxia-exposed pups at P10 and the changes persisted at P21; these were improved by metformin.	Metformin	188-197	KRAS proto-oncogene, GTPase	Rattus norvegicus	160-163
32194168-1	2020	In a clinically-relevant model of 4 week, low-dose cisplatin-induced AKI, mice were injected subcutaneously with non small cell lung cancer (NSCLC) cells that harbor an activating Kirsten rat sarcoma viral oncogene homolog (KRAS)G12V mutation.	Cisplatin	51-60	KRAS proto-oncogene, GTPase	Rattus norvegicus	224-228
32913901-4	2020	Following 7 days of administration of 2-ME, there was a significant increase in the level of Bax, c-Myc, K-Ras, TNF-alpha, IL-1beta, IL-6, MDA and GPx activity, while the levels of Bcl-2, NO and GSH were significantly reduced compared with control.	methyl cellosolve	38-42	KRAS proto-oncogene, GTPase	Rattus norvegicus	105-110
32522593-6	2020	After treatment with MTX, p21-positive cells had increased significantly and doublecortin (DCX) expression in the hippocampus had decreased significantly.	Methotrexate	21-24	KRAS proto-oncogene, GTPase	Rattus norvegicus	26-29
32200462-11	2020	STZ-induced DN showed a p21/p53-dependent induction of premature senescence and RUP administration decreased the expression of p21 and p53 levels in injured renal tissue.	Streptozocin	0-3	KRAS proto-oncogene, GTPase	Rattus norvegicus	24-27
32200462-11	2020	STZ-induced DN showed a p21/p53-dependent induction of premature senescence and RUP administration decreased the expression of p21 and p53 levels in injured renal tissue.	Streptozocin	0-3	KRAS proto-oncogene, GTPase	Rattus norvegicus	127-130
32542591-8	2020	Importantly, ammonia exposure in mature astrocytes potentiated the expression of the senescence marker p21, inflammatory response, activation of p38 MAPK/NFkappaB pathways, and the decrease of cytoprotective pathways.	Ammonia	13-20	KRAS proto-oncogene, GTPase	Rattus norvegicus	103-106
32802465-1	2020	In advanced stage non-small cell lung cancer (NSCLC) patients, Kirsten Rat Sarcoma Viral Oncogene Homolog (KRAS) testing may soon acquire a predictive significance to select patients for AMG510 treatment.	AMG-510	187-193	KRAS proto-oncogene, GTPase	Rattus norvegicus	107-111
32626908-7	2020	Microglia in the group receiving 72 h of PMA stimulation displayed the highest percentage of cells arrested in G0/G1, the highest amount of senescence-associated expression of p53 and p21, and the most prominent secretion of TNF-alpha and IL-1beta.	Tetradecanoylphorbol Acetate	41-44	KRAS proto-oncogene, GTPase	Rattus norvegicus	184-187
32597268-0	2022	25I-NBOMe, a phenethylamine derivative, induces adverse cardiovascular effects in rodents: possible involvement of p21 (CDC42/RAC)-activated kinase 1.	2-(4-iodo-2,5-dimethoxyphenyl)-N-(2-methoxybenzyl)ethanamine	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	115-118
32597268-5	2022	Thus, in this study, we investigated the adverse cardiovascular effects of 25I-NBOMe, related to p21 (CDC42/RAC)-activated kinase 1 (PAK1).	2-(4-iodo-2,5-dimethoxyphenyl)-N-(2-methoxybenzyl)ethanamine	75-84	KRAS proto-oncogene, GTPase	Rattus norvegicus	97-100
32388065-7	2020	Among these eight patients, acquired molecular events potentially responsible for resistance were detected in three who progressed on dabrafenib-trametinib combination, that is, MEK1 K57N, RAS viral (v-ras) oncogene homolog (NRAS) Q61R and rat sarcoma viral oncogene homolog (KRAS) Q61R mutations.	dabrafenib	134-144	KRAS proto-oncogene, GTPase	Rattus norvegicus	276-280
32642444-4	2020	Following 7 days of administration of MC, there was a significant increase in the levels of K-Ras, c-Myc, TNF-alpha, IL-6 and NO, while GSH level and SOD activity were significantly reduced compared with control.	methyl cellosolve	38-40	KRAS proto-oncogene, GTPase	Rattus norvegicus	92-97
32642444-6	2020	After 21 days of MC administration, RKW, GSH, NO, IL-10 and Bcl-2 levels were significantly decreased, while levels of K-Ras, c-Myc, p53, Bax, caspase-3, TNF-alpha, IL-1beta, IL-6, MDA and GST activity were significantly increased compared with control.	methyl cellosolve	17-19	KRAS proto-oncogene, GTPase	Rattus norvegicus	119-124
32105957-7	2020	In addition, Nano-Al2O3 decreased the expression of cyclin D1, bcl-2, Mdm2, and phospho-Rb and increased the expression of p53, p21, Bax, and Rb.	Aluminum Oxide	18-23	KRAS proto-oncogene, GTPase	Rattus norvegicus	128-131
32014824-0	2020	KRAS G12C Game of Thrones, which direct KRAS inhibitor will claim the iron throne?	Iron	70-81	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-4
32014824-0	2020	KRAS G12C Game of Thrones, which direct KRAS inhibitor will claim the iron throne?	Iron	70-81	KRAS proto-oncogene, GTPase	Rattus norvegicus	40-44
32014824-2	2020	The lack of an ideal small molecule binding pocket in the KRAS protein and its high affinity towards the abundance of cellular guanosine triphosphate (GTP) renders the design of specific small molecule drugs challenging.	Guanosine Triphosphate	127-149	KRAS proto-oncogene, GTPase	Rattus norvegicus	58-62
32014824-2	2020	The lack of an ideal small molecule binding pocket in the KRAS protein and its high affinity towards the abundance of cellular guanosine triphosphate (GTP) renders the design of specific small molecule drugs challenging.	Guanosine Triphosphate	151-154	KRAS proto-oncogene, GTPase	Rattus norvegicus	58-62
32014824-6	2020	Both AMG 510 from Amgen and MRTX849 from Mirati Therapeutics covalently binds to KRASG12C at the cysteine at residue 12, keeping KRASG12C in its inactive GDP-bound state and inhibiting KRAS-dependent signaling.	AMG 3	5-8	KRAS proto-oncogene, GTPase	Rattus norvegicus	81-85
32014824-6	2020	Both AMG 510 from Amgen and MRTX849 from Mirati Therapeutics covalently binds to KRASG12C at the cysteine at residue 12, keeping KRASG12C in its inactive GDP-bound state and inhibiting KRAS-dependent signaling.	Cysteine	97-105	KRAS proto-oncogene, GTPase	Rattus norvegicus	81-85
32014824-6	2020	Both AMG 510 from Amgen and MRTX849 from Mirati Therapeutics covalently binds to KRASG12C at the cysteine at residue 12, keeping KRASG12C in its inactive GDP-bound state and inhibiting KRAS-dependent signaling.	Guanosine Diphosphate	154-157	KRAS proto-oncogene, GTPase	Rattus norvegicus	81-85
32014824-8	2020	In addition, two novel KRAS G12C inhibitors JNJ-74699157 and LY3499446 will have entered phase 1 studies by the end of 2019.	7-(3-(2-amino-1-fluoroethylidene)-1-piperidinyl)-1-cyclopropyl-6-fluoro-1,4-dihydro-8-methoxy-4-oxo-3-quinolinecarboxylic acid	44-56	KRAS proto-oncogene, GTPase	Rattus norvegicus	23-27
32405345-9	2020	Conclusion: The lowered frequency of K-ras mutations correlated with decreased formation of hydroxyl radicals, O5-meG and 8-OH-dG levels in phytate-supplemented animals with lowered tumor burden.	Hydroxyl Radical	92-109	KRAS proto-oncogene, GTPase	Rattus norvegicus	37-42
31730896-10	2020	Treatment with cryptotanshinone, a specific inhibitor of STAT3, could inhibit the phosphorylation of STAT3 and its downstream proteins p53 and p21 expression and decrease the activity of SA-beta-Gal in activated HSCs induced by IL-10.	cryptotanshinone	15-31	KRAS proto-oncogene, GTPase	Rattus norvegicus	143-146
31810114-8	2020	We further demonstrated that treatment with osthole significantly induced cell cycle arrest at the G0/G1 phase in PASMCs, which was supported by the finding that osthole significantly decreased cyclin D1/CDK4 and cyclin E1/CDK2 protein levels and increased p53, p27 and p21 protein levels.	osthol	44-51	KRAS proto-oncogene, GTPase	Rattus norvegicus	270-273
31810114-8	2020	We further demonstrated that treatment with osthole significantly induced cell cycle arrest at the G0/G1 phase in PASMCs, which was supported by the finding that osthole significantly decreased cyclin D1/CDK4 and cyclin E1/CDK2 protein levels and increased p53, p27 and p21 protein levels.	osthol	162-169	KRAS proto-oncogene, GTPase	Rattus norvegicus	270-273
32405345-0	2020	Dietary phytate lowers K-ras mutational frequency, decreases DNA-adduct and hydroxyl radical formation in azoxymethane-induced colon cancer.	Phytic Acid	8-15	KRAS proto-oncogene, GTPase	Rattus norvegicus	23-28
32405345-9	2020	Conclusion: The lowered frequency of K-ras mutations correlated with decreased formation of hydroxyl radicals, O5-meG and 8-OH-dG levels in phytate-supplemented animals with lowered tumor burden.	o5-meg	111-117	KRAS proto-oncogene, GTPase	Rattus norvegicus	37-42
32405345-9	2020	Conclusion: The lowered frequency of K-ras mutations correlated with decreased formation of hydroxyl radicals, O5-meG and 8-OH-dG levels in phytate-supplemented animals with lowered tumor burden.	8-ohdg	122-129	KRAS proto-oncogene, GTPase	Rattus norvegicus	37-42
32405345-9	2020	Conclusion: The lowered frequency of K-ras mutations correlated with decreased formation of hydroxyl radicals, O5-meG and 8-OH-dG levels in phytate-supplemented animals with lowered tumor burden.	Phytic Acid	140-147	KRAS proto-oncogene, GTPase	Rattus norvegicus	37-42
29886761-4	2020	METHODS: Paeonol (50, 100, and 150 mg/kg body weight/day) was given orally to separate groups of neonatal rats from postnatal day 3 (P3) to P21 and were exposed to isoflurane (0.75%; 6 h) on P7.	paeonol	9-16	KRAS proto-oncogene, GTPase	Rattus norvegicus	140-143
31710386-7	2020	The UtSMC cell cycle was arrested by melatonin treatment through up-regulation of p21, p27, and PTEN protein expression, but melatonin did not further promote apoptosis program activation.	Melatonin	37-46	KRAS proto-oncogene, GTPase	Rattus norvegicus	82-85
31152635-7	2019	In line with this, levels of serine20-phosphorylated p53 and of its target gene p21 were elevated by GCDC in a TUDC-sensitive way.	ursodoxicoltaurine	111-115	KRAS proto-oncogene, GTPase	Rattus norvegicus	80-83
31152635-7	2019	In line with this, levels of serine20-phosphorylated p53 and of its target gene p21 were elevated by GCDC in a TUDC-sensitive way.	Glycochenodeoxycholic Acid	101-105	KRAS proto-oncogene, GTPase	Rattus norvegicus	80-83
31308624-9	2019	Results: Our results showed that DEX dose-dependently restored impaired proliferation of PC12 cells induced by lidocaine,as reflected by the increased cell viability and EdU positive cells, which were consistent with the decreased expression of tumor suppressor protein p21 and increased expression of cell cycle-related cyclin D1 and CDK1.	Dexmedetomidine	33-36	KRAS proto-oncogene, GTPase	Rattus norvegicus	270-273
30827793-8	2019	In contrast, when amikacin was administered from P7 to P15, microglia maintained large cell bodies with relatively shorter processes at both P15 and P21.	Amikacin	18-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	149-152
31655619-17	2019	Additionally, when the upstream activator KRAS was knocked down by siRNA, the protective effect of artemisinin was also blocked.	Artemisinins	99-110	KRAS proto-oncogene, GTPase	Rattus norvegicus	42-46
31461438-0	2019	Targeting oxidative pentose phosphate pathway prevents recurrence in mutant Kras colorectal carcinomas.	Pentosephosphates	20-37	KRAS proto-oncogene, GTPase	Rattus norvegicus	76-80
30802826-12	2019	Furthermore, luteolin alleviated H2O2-induced inactivation of PI3K/AKT pathway and activation of PDCD4/p21 pathway in PC-12 cells by up-regulating miR-21.	Hydrogen Peroxide	33-37	KRAS proto-oncogene, GTPase	Rattus norvegicus	103-106
31047895-5	2019	KEY FINDINGS: Our results demonstrated that simultaneous treatment with either TQ or Ger and CP significantly abrogated oxidative stress and downregulated the apoptotic markers p38 mitogen-activated protein kinase (MAPK), STAT-1, p53, p21 and MMP9; FMO3, however, was insignificantly decreased.	thymoquinone	79-81	KRAS proto-oncogene, GTPase	Rattus norvegicus	235-238
31047895-5	2019	KEY FINDINGS: Our results demonstrated that simultaneous treatment with either TQ or Ger and CP significantly abrogated oxidative stress and downregulated the apoptotic markers p38 mitogen-activated protein kinase (MAPK), STAT-1, p53, p21 and MMP9; FMO3, however, was insignificantly decreased.	geraniol	85-88	KRAS proto-oncogene, GTPase	Rattus norvegicus	235-238
31171766-7	2019	In vitro, H2O2 caused abnormal accumulation of progerin in nuclear and activation of nuclear p53-progerin interaction to trigger primary rat hepatocyte premature senescence through the p21-independent pathway; while these effects were rescued by prolonged exogenous IGF-1 or the IGF-1 adenovirus vector.	Hydrogen Peroxide	10-14	KRAS proto-oncogene, GTPase	Rattus norvegicus	185-188
30603881-1	2019	OBJECTIVE: The purpose of the current study was to investigate the diagnostic performance of F-18 fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) for the prediction of v-Ki-ras-2 Kirsten rat sarcoma viral oncogene homolog (KRAS) mutation in colorectal cancer (CRC) patients through a systematic review and meta-analysis.	Fluorodeoxyglucose F18	93-116	KRAS proto-oncogene, GTPase	Rattus norvegicus	258-262
30603881-1	2019	OBJECTIVE: The purpose of the current study was to investigate the diagnostic performance of F-18 fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) for the prediction of v-Ki-ras-2 Kirsten rat sarcoma viral oncogene homolog (KRAS) mutation in colorectal cancer (CRC) patients through a systematic review and meta-analysis.	Fluorodeoxyglucose F18	118-121	KRAS proto-oncogene, GTPase	Rattus norvegicus	258-262
30649504-7	2019	5-Aza also decreased methylation at the rat p21 promoter about 250 bp upstream of the p21 TSS.	Decitabine	0-5	KRAS proto-oncogene, GTPase	Rattus norvegicus	44-47
30143816-1	2019	PURPOSE: To investigate the association between metabolic parameters of dual time point 18F-FDG PET/CT imaging and Kirsten rat sarcoma (KRAS) mutation status in colorectal liver metastases (CRLM).	Fluorodeoxyglucose F18	88-95	KRAS proto-oncogene, GTPase	Rattus norvegicus	136-140
30388256-13	2019	Regular use of NSAIDs and aspirin may be more strongly associated with risk reduction of MSI-high CRC without KRAS or BRAF mutation.	Aspirin	26-33	KRAS proto-oncogene, GTPase	Rattus norvegicus	110-114
30511343-8	2019	The overexpression of CPT1 in PASMCs also promoted proliferation and ATP production and subsequently inhibited the phosphorylation of AMPK, p53, as well as p21 in PASMCs.	pasmcs	30-36	KRAS proto-oncogene, GTPase	Rattus norvegicus	156-159
30511343-8	2019	The overexpression of CPT1 in PASMCs also promoted proliferation and ATP production and subsequently inhibited the phosphorylation of AMPK, p53, as well as p21 in PASMCs.	pasmcs	163-169	KRAS proto-oncogene, GTPase	Rattus norvegicus	156-159
30511343-9	2019	Furthermore, AMPK was activated by ETO, which increased the expression of p53 and p21, and the proportion of cells in the cell cycle G2/M phase in response to PDGF-BB stimulation in PASMCs.	etomoxir	35-38	KRAS proto-oncogene, GTPase	Rattus norvegicus	82-85
30802826-15	2019	Luteolin protected PC-12 cells from H2O2-induced oxidative injury by up-regulating miR-21, activating PI3K/AKT pathway and inactivating PDCD4/p21 pathway.	Hydrogen Peroxide	36-40	KRAS proto-oncogene, GTPase	Rattus norvegicus	142-145
30668434-9	2019	Our results also supported the involvement of p53-p21 axis in the anticancer effects of curcumin and PTX.	Curcumin	88-96	KRAS proto-oncogene, GTPase	Rattus norvegicus	50-53
30668434-9	2019	Our results also supported the involvement of p53-p21 axis in the anticancer effects of curcumin and PTX.	Paclitaxel	101-104	KRAS proto-oncogene, GTPase	Rattus norvegicus	50-53
29933685-5	2018	As compared with the model group, alisol A 24-acetate inhibited the proliferation of VSMCs in rats induced by ox-LDL and inhibited the protein expression of VSMCs PCNA, cyclinD1, cyclinE and enhanced the protein and mRNA p21 and p27 expression levels (P<0.05).	alisol A 24-acetate	34-53	KRAS proto-oncogene, GTPase	Rattus norvegicus	221-224
31030716-11	2019	P16 and P21 proteins had high expression in AngII, H2O2 and PA groups, most obviously in H2O2 group.	Hydrogen Peroxide	51-55	KRAS proto-oncogene, GTPase	Rattus norvegicus	8-11
31030716-11	2019	P16 and P21 proteins had high expression in AngII, H2O2 and PA groups, most obviously in H2O2 group.	Palmitic Acid	60-62	KRAS proto-oncogene, GTPase	Rattus norvegicus	8-11
31030716-11	2019	P16 and P21 proteins had high expression in AngII, H2O2 and PA groups, most obviously in H2O2 group.	Hydrogen Peroxide	89-93	KRAS proto-oncogene, GTPase	Rattus norvegicus	8-11
30119179-0	2018	Hydrogen alleviates cellular senescence via regulation of ROS/p53/p21 pathway in bone marrow-derived mesenchymal stem cells in vivo.	Hydrogen	0-8	KRAS proto-oncogene, GTPase	Rattus norvegicus	66-69
30119179-0	2018	Hydrogen alleviates cellular senescence via regulation of ROS/p53/p21 pathway in bone marrow-derived mesenchymal stem cells in vivo.	Reactive Oxygen Species	58-61	KRAS proto-oncogene, GTPase	Rattus norvegicus	66-69
30119179-10	2018	And the underlying mechanism of antisenescence effects of hydrogen in BMSCs was via the ROS/p53/p21 signaling pathway.	Hydrogen	58-66	KRAS proto-oncogene, GTPase	Rattus norvegicus	96-99
30119179-10	2018	And the underlying mechanism of antisenescence effects of hydrogen in BMSCs was via the ROS/p53/p21 signaling pathway.	Reactive Oxygen Species	88-91	KRAS proto-oncogene, GTPase	Rattus norvegicus	96-99
30096914-10	2018	In addition, 5-FU significantly increased p21 positive cell number in the subgranular zone (SGZ) and malondialdehyde (MDA) levels in the hippocampus.	Fluorouracil	13-17	KRAS proto-oncogene, GTPase	Rattus norvegicus	42-45
29758348-11	2018	PS led to an increase in total score of seizure at the P14 and P21.	ps	0-2	KRAS proto-oncogene, GTPase	Rattus norvegicus	63-66
30677774-5	2019	In type 2 diabetic rats, cinnamyl-3,4-dihydroxy-alpha-cynanocinnamate (inhibitor of 12-LO) attenuated the increases in glomerular p21 and p27 protein expression, while in normal rats, 12(S)-HETE injection increased glomerular p21 and p27 expression.	cinnamyl-3,4-dihydroxy-alpha-cynanocinnamate	25-69	KRAS proto-oncogene, GTPase	Rattus norvegicus	130-133
30677774-5	2019	In type 2 diabetic rats, cinnamyl-3,4-dihydroxy-alpha-cynanocinnamate (inhibitor of 12-LO) attenuated the increases in glomerular p21 and p27 protein expression, while in normal rats, 12(S)-HETE injection increased glomerular p21 and p27 expression.	cinnamyl-3,4-dihydroxy-alpha-cynanocinnamate	25-69	KRAS proto-oncogene, GTPase	Rattus norvegicus	226-229
30048695-8	2018	The increased caspase-3, caspase-7, p21 immunoreactivity and reduced Cdk4 immunoreactivity in ethanol treated rats confirmed that ethanol increases the apoptosis in testis and a reduced expression in the rats treated with PCA in addition to ethanol indicates a protective role of PCA.	Ethanol	130-137	KRAS proto-oncogene, GTPase	Rattus norvegicus	36-39
30048695-8	2018	The increased caspase-3, caspase-7, p21 immunoreactivity and reduced Cdk4 immunoreactivity in ethanol treated rats confirmed that ethanol increases the apoptosis in testis and a reduced expression in the rats treated with PCA in addition to ethanol indicates a protective role of PCA.	Ethanol	130-137	KRAS proto-oncogene, GTPase	Rattus norvegicus	36-39
29275358-13	2018	Sorafenib-resistant HCC cells showed elevated KRAS expression, and KRAS inhibition resensitised sorafenib-resistant cells to suppression of proliferation and induction of apoptosis.	Sorafenib	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	46-50
29275358-13	2018	Sorafenib-resistant HCC cells showed elevated KRAS expression, and KRAS inhibition resensitised sorafenib-resistant cells to suppression of proliferation and induction of apoptosis.	Sorafenib	96-105	KRAS proto-oncogene, GTPase	Rattus norvegicus	67-71
29275358-14	2018	CONCLUSIONS: KRAS is dysregulated in HCC by loss of tumour-suppressive microRNA-622, contributing to tumour progression, sorafenib sensitivity and resistance.	Sorafenib	121-130	KRAS proto-oncogene, GTPase	Rattus norvegicus	13-17
29369427-0	2018	Pioglitazone/metformin adduct regulates insulin secretion and inhibits high glucose-induced apoptosis via p21-p53-MDM2 signaling in INS-1 cells.	Pioglitazone	0-12	KRAS proto-oncogene, GTPase	Rattus norvegicus	106-109
29369427-0	2018	Pioglitazone/metformin adduct regulates insulin secretion and inhibits high glucose-induced apoptosis via p21-p53-MDM2 signaling in INS-1 cells.	Metformin	13-22	KRAS proto-oncogene, GTPase	Rattus norvegicus	106-109
29369427-0	2018	Pioglitazone/metformin adduct regulates insulin secretion and inhibits high glucose-induced apoptosis via p21-p53-MDM2 signaling in INS-1 cells.	Glucose	76-83	KRAS proto-oncogene, GTPase	Rattus norvegicus	106-109
29933685-7	2018	These data indicate that alisol A 24-acetate can inhibit the proliferation of VSMCs induced by ox-LDL and the mechanism may be associated with inhibiting expression of cyclin protein, including cyclinD1, cyclinE, p21, p27 and so on.	alisol A 24-acetate	25-44	KRAS proto-oncogene, GTPase	Rattus norvegicus	213-216
29695641-5	2018	H2O2 mediated oxidative stress in 2G11 cells, a rat MPC clone previously established in our laboratory, successfully induced senescence, as shown by the upregulation of p21 and SASP factors, including IL-6.	Hydrogen Peroxide	0-4	KRAS proto-oncogene, GTPase	Rattus norvegicus	169-172
29765446-0	2018	Inhibitory effect of PDGF-BB and serum-stimulated responses in vascular smooth muscle cell proliferation by hinokitiol via up-regulation of p21 and p53.	beta-thujaplicin	108-118	KRAS proto-oncogene, GTPase	Rattus norvegicus	140-143
29427224-10	2018	Further, DMH treatment revealed alterations in the protein expressions of various genes involved in the p53-mediated apoptotic pathway such as p53, p21, Bcl-2, Bax, caspase-9 and caspase-3, which, however, were shifted towards normal control levels upon simultaneous supplementation with probiotics.	1,2-Dimethylhydrazine	9-12	KRAS proto-oncogene, GTPase	Rattus norvegicus	148-151
29353801-5	2018	Shortened telomeres, telomere-associated DNA damage, reduced telomerase activity, and TERT expression were also observed in BPDE-treated cells, accompanied with the activation of DNA damage response pathway (ATM/Chk1/p53/p21).	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	124-128	KRAS proto-oncogene, GTPase	Rattus norvegicus	221-224
29187496-5	2017	Mutations of Kirsten rat sarcoma viral oncogene homolog (KRAS) were more frequent in the r-MCN group (83%) (p-MCN; 11%, p<0.05).	r-mcn	89-94	KRAS proto-oncogene, GTPase	Rattus norvegicus	57-61
28255652-5	2018	RESULTS: Glycerol treatment reduced the volume of preneoplastic lesions by decreasing the proliferative status of liver foci, increasing the expression of p53 and p21 proteins and reducing the expression of cyclin D1 and cyclin-dependent kinase 1.	Glycerol	9-17	KRAS proto-oncogene, GTPase	Rattus norvegicus	163-166
29378551-7	2018	Further, the mechanism of ICA-induced cell proliferation of neural stem cells was investigated by analyzing the gene and protein expression of cell cycle related genes cyclin D1 and p21.	icariin	26-29	KRAS proto-oncogene, GTPase	Rattus norvegicus	182-185
29378551-10	2018	In addition, it was found that icariin-induced effect on neural stem cells is associated with increased mRNA and protein expression of cell cycle genes cyclin D1 and p21.	icariin	31-38	KRAS proto-oncogene, GTPase	Rattus norvegicus	166-169
29441600-0	2018	Berberine inhibits experimental varicocele-induced cell cycle arrest via regulating cyclin D1, cdk4 and p21 proteins expression in rat testicles.	Berberine	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	104-107
29196166-10	2018	The overall pulmonary hypertension and hypoxia-induced proliferation and migration of PAECs were attenuated by administration of 1,25(OH)2D3, which was associated with the suppressed expressions of Tgfbr2, alpha-SMA, and Smad7 and induced expressions of miR-204, p21 and Smad2 both in vitro and in vivo.	25(oh)2d3	131-140	KRAS proto-oncogene, GTPase	Rattus norvegicus	263-266
29184501-5	2017	Further mechanism study showed that compound 0375-0604 can block the formation of the complex of guanosine triphosphate (GTP) and KRAS in vitro.	Guanosine Triphosphate	97-119	KRAS proto-oncogene, GTPase	Rattus norvegicus	130-134
29184501-5	2017	Further mechanism study showed that compound 0375-0604 can block the formation of the complex of guanosine triphosphate (GTP) and KRAS in vitro.	Guanosine Triphosphate	121-124	KRAS proto-oncogene, GTPase	Rattus norvegicus	130-134
28370226-10	2017	Furthermore, TFE inhibited p-P53/p21 and chk1/chk2 expression levels.	Trifluoroethanol	13-16	KRAS proto-oncogene, GTPase	Rattus norvegicus	33-36
28643448-10	2017	Metformin synchronized the apoptotic proteins such as FasL and antiapoptotic proteins such as Bcl2, Bcl-xL and p21 which can be attributed as the major mechanism of cardioprotection.	Metformin	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	111-114
30338269-9	2017	Sph and dhSph profiles show a similar trend with an initial peak at P10 and then a comparatively smaller peak at P21 maintaining a ratio of (2-2.5:1) of Sph:dhSph.	Sphingosine	0-3	KRAS proto-oncogene, GTPase	Rattus norvegicus	113-116
30338269-9	2017	Sph and dhSph profiles show a similar trend with an initial peak at P10 and then a comparatively smaller peak at P21 maintaining a ratio of (2-2.5:1) of Sph:dhSph.	safingol	8-13	KRAS proto-oncogene, GTPase	Rattus norvegicus	113-116
30338269-9	2017	Sph and dhSph profiles show a similar trend with an initial peak at P10 and then a comparatively smaller peak at P21 maintaining a ratio of (2-2.5:1) of Sph:dhSph.	Sphingosine	10-13	KRAS proto-oncogene, GTPase	Rattus norvegicus	113-116
30338269-10	2017	The profiles of all these sphingolipids, specifically at P21, clearly indicate their importance during rat brain development but somewhat unspecified roles in myelination.	Sphingolipids	26-39	KRAS proto-oncogene, GTPase	Rattus norvegicus	57-60
29187496-5	2017	Mutations of Kirsten rat sarcoma viral oncogene homolog (KRAS) were more frequent in the r-MCN group (83%) (p-MCN; 11%, p<0.05).	mcn	91-94	KRAS proto-oncogene, GTPase	Rattus norvegicus	57-61
28915719-2	2017	Due to a Kirsten rat sarcoma viral oncogene homolog (KRAS) mutation, regorafenib was given in the third line setting.	regorafenib	69-80	KRAS proto-oncogene, GTPase	Rattus norvegicus	53-57
27262357-0	2017	Cell cycle activation in p21 dependent pathway: An alternative mechanism of organophosphate induced dopaminergic neurodegeneration.	Organophosphates	76-91	KRAS proto-oncogene, GTPase	Rattus norvegicus	25-28
27262357-4	2017	Dichlorvos exposed cells exhibited an increased expression of p53, cyclin-D1, pRb and decreased expression of p21suggesting a re-entry of differentiated cells into the cell cycle.	Dichlorvos	0-10	KRAS proto-oncogene, GTPase	Rattus norvegicus	110-113
28502303-5	2017	The expressions of P21 and c-caspase-3 increased, meanwhile, the expressions of CDK4, cyclin D1, caspase-3 and Bcl-2 decreased by metformin.	Metformin	130-139	KRAS proto-oncogene, GTPase	Rattus norvegicus	19-22
28617435-4	2017	We found that DHA treatment induced the accumulation of senescent activated HSCs in rat fibrotic liver, and promoted the expression of senescence markers p53, p16, p21 and Hmga1 in cell model.	artenimol	14-17	KRAS proto-oncogene, GTPase	Rattus norvegicus	164-167
29736383-6	2018	Agarose gel electrophoresis was used to analyze the K-ras gene extracted from the pancreas tissues of experimental rats while hematoxylinand eosin staining was used for histological assay.	Sepharose	0-7	KRAS proto-oncogene, GTPase	Rattus norvegicus	52-57
29736383-10	2018	While the agarose gel electrophoresis revealed that there may be possibility of prevention of damage to k-ras gene as a result of the effect of plants extract.	Sepharose	10-17	KRAS proto-oncogene, GTPase	Rattus norvegicus	104-109
29147462-5	2017	Consequently, ROS induced by 20% O2 caused DNA damage and then activated p53-p21-Rb and p16-Rb pathways via ERK signaling to induce NP cell senescence.	ros	14-17	KRAS proto-oncogene, GTPase	Rattus norvegicus	77-80
28006059-2	2017	Objectives: To examine whether the Kirsten rat sarcoma viral oncogene homolog (KRAS)-variant, a germline mutation in a microRNA-binding site in KRAS, is a predictive biomarker of cetuximab response and altered immunity in the setting of radiotherapy and cisplatin treatment and to evaluate the interaction of the KRAS-variant with p16 status and blood-based transforming growth factor beta1 (TGF-beta1).	Cisplatin	254-263	KRAS proto-oncogene, GTPase	Rattus norvegicus	79-83
28006059-2	2017	Objectives: To examine whether the Kirsten rat sarcoma viral oncogene homolog (KRAS)-variant, a germline mutation in a microRNA-binding site in KRAS, is a predictive biomarker of cetuximab response and altered immunity in the setting of radiotherapy and cisplatin treatment and to evaluate the interaction of the KRAS-variant with p16 status and blood-based transforming growth factor beta1 (TGF-beta1).	Cisplatin	254-263	KRAS proto-oncogene, GTPase	Rattus norvegicus	144-148
28006059-2	2017	Objectives: To examine whether the Kirsten rat sarcoma viral oncogene homolog (KRAS)-variant, a germline mutation in a microRNA-binding site in KRAS, is a predictive biomarker of cetuximab response and altered immunity in the setting of radiotherapy and cisplatin treatment and to evaluate the interaction of the KRAS-variant with p16 status and blood-based transforming growth factor beta1 (TGF-beta1).	Cisplatin	254-263	KRAS proto-oncogene, GTPase	Rattus norvegicus	144-148
27677429-10	2017	Meanwhile, genistein reversed the leptin-induced expression of cyclin D1, and cyclin-dependent kinase inhibitor, p21.	Genistein	11-20	KRAS proto-oncogene, GTPase	Rattus norvegicus	113-116
29147462-5	2017	Consequently, ROS induced by 20% O2 caused DNA damage and then activated p53-p21-Rb and p16-Rb pathways via ERK signaling to induce NP cell senescence.	Oxygen	33-35	KRAS proto-oncogene, GTPase	Rattus norvegicus	77-80
27721019-3	2016	Here we show that the orally available tyrosine kinase inhibitor, BAY61-3606, enhances the sensitivity of human colon cancer cells, especially those harboring active mutations in Kirsten Rat Sarcoma Viral Oncogene Homolog (KRAS) gene, to TRAIL-induced apoptosis in vitro and in vivo.	2-(7-(3,4-dimethoxyphenyl)imidazo(1,2-c)pyrimidin-5-ylamino)nicotinamide	66-76	KRAS proto-oncogene, GTPase	Rattus norvegicus	223-227
27821908-3	2016	Immunohistochemical analysis revealed that 4-methylthio-3-butenyl isothiocyanate induced apoptosis, suppressed cell proliferation, and increased p21 expression when administered in the promotion phase.	4-(methylthio)-3-butenyl isothiocyanate	43-80	KRAS proto-oncogene, GTPase	Rattus norvegicus	145-148
27681411-6	2016	Using qRT-PCR analysis, we demonstrated that, among those genes, p21 (Cdc42/Rac)-activated kinase 1 (pak1) mRNA was downregulated by treatment with terfenadine and astemizole.	Terfenadine	148-159	KRAS proto-oncogene, GTPase	Rattus norvegicus	65-68
27681411-6	2016	Using qRT-PCR analysis, we demonstrated that, among those genes, p21 (Cdc42/Rac)-activated kinase 1 (pak1) mRNA was downregulated by treatment with terfenadine and astemizole.	Astemizole	164-174	KRAS proto-oncogene, GTPase	Rattus norvegicus	65-68
27916938-3	2016	In this study, we explored sorafenib-induced cellular effects in Kirsten rat sarcoma viral oncogene homolog olog (KRAS) wild-type and KRAS-mutated CRC cell lines (Caco-2 and HRT-18), and finally profiled expression changes of specific miRNAs within the miRNome (>1000 human miRNAs) after exposure to sorafenib.	Sorafenib	27-36	KRAS proto-oncogene, GTPase	Rattus norvegicus	114-118
27916938-3	2016	In this study, we explored sorafenib-induced cellular effects in Kirsten rat sarcoma viral oncogene homolog olog (KRAS) wild-type and KRAS-mutated CRC cell lines (Caco-2 and HRT-18), and finally profiled expression changes of specific miRNAs within the miRNome (>1000 human miRNAs) after exposure to sorafenib.	Sorafenib	27-36	KRAS proto-oncogene, GTPase	Rattus norvegicus	134-138
27257137-4	2016	Wistar rats were chronically exposed to 5 mug/kg/day BPA from day 1 of gestation to day 65 after birth (P65) and 5 mM fluoride from P21 to P65.	Fluorides	118-126	KRAS proto-oncogene, GTPase	Rattus norvegicus	132-135
26333174-0	2016	MiR-622 inhibited colorectal cancer occurrence and metastasis by suppressing K-Ras.	mir-622	0-7	KRAS proto-oncogene, GTPase	Rattus norvegicus	77-82
27600103-1	2016	The aim of the present study was to examine the impacts and mechanisms of 12-lipoxygenase (12-LO) and its metabolites on the acetylation and methylation of histone-3-lysine (H3K) in the p21 gene.	histone-3-lysine	156-172	KRAS proto-oncogene, GTPase	Rattus norvegicus	186-189
27600103-4	2016	The cells were transfected to induce the overexpression of p300 to examine changes in 12 (S)-HETE-associated p21 regulation and epigenetic modifications.	Hydroxyeicosatetraenoic Acids	89-97	KRAS proto-oncogene, GTPase	Rattus norvegicus	109-112
26333174-8	2016	More importantly, K-Ras overexpression can rescue the inhibitory effect of miR-622 on CRC development.	mir-622	75-82	KRAS proto-oncogene, GTPase	Rattus norvegicus	18-23
27602102-1	2016	The current study aimed to determine the association between protein kinase Calpha (PKCalpha) and Kirsten rat sarcoma viral oncogene homolog (KRAS) expression and the response to folinic acid, 5-fluorouracil and oxaliplatin (FOLFOX regimen) in patients with colorectal cancer (CRC).	Leucovorin	179-191	KRAS proto-oncogene, GTPase	Rattus norvegicus	142-146
27602102-1	2016	The current study aimed to determine the association between protein kinase Calpha (PKCalpha) and Kirsten rat sarcoma viral oncogene homolog (KRAS) expression and the response to folinic acid, 5-fluorouracil and oxaliplatin (FOLFOX regimen) in patients with colorectal cancer (CRC).	Fluorouracil	193-207	KRAS proto-oncogene, GTPase	Rattus norvegicus	142-146
27602102-1	2016	The current study aimed to determine the association between protein kinase Calpha (PKCalpha) and Kirsten rat sarcoma viral oncogene homolog (KRAS) expression and the response to folinic acid, 5-fluorouracil and oxaliplatin (FOLFOX regimen) in patients with colorectal cancer (CRC).	Oxaliplatin	212-223	KRAS proto-oncogene, GTPase	Rattus norvegicus	142-146
27602102-1	2016	The current study aimed to determine the association between protein kinase Calpha (PKCalpha) and Kirsten rat sarcoma viral oncogene homolog (KRAS) expression and the response to folinic acid, 5-fluorouracil and oxaliplatin (FOLFOX regimen) in patients with colorectal cancer (CRC).	Folfox protocol	225-231	KRAS proto-oncogene, GTPase	Rattus norvegicus	142-146
27236325-10	2016	Icilin also antagonized the activation of p38 and MMP-2 and the repression of p21 caused by FBS.	icilin	0-6	KRAS proto-oncogene, GTPase	Rattus norvegicus	78-81
27565756-8	2016	Immunoblot analysis showed decreased Mre11, Rad51, Rad50, and Ku86 as well as increased Bax and p21 in samples from ethanol-treated rats.	Ethanol	116-123	KRAS proto-oncogene, GTPase	Rattus norvegicus	96-99
27077805-7	2016	At the same time, curcumin induced HSC senescence by elevating the expression of senescence markers P16, P21 and Hmga1, concomitant with reduced abundance of HSC activation markers alpha-smooth muscle actin and alpha1(I)-procollagen in cultured HSCs.	Curcumin	18-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	105-108
27184741-10	2016	The number of bromodeoxyuridine (BrdU) and doublecortin (DCX) double-positive cells in the hippocampal dentate gyrus of P21 rats was significantly lower than that in controls, indicating reduced neurogenesis.	Bromodeoxyuridine	14-31	KRAS proto-oncogene, GTPase	Rattus norvegicus	120-123
27184741-10	2016	The number of bromodeoxyuridine (BrdU) and doublecortin (DCX) double-positive cells in the hippocampal dentate gyrus of P21 rats was significantly lower than that in controls, indicating reduced neurogenesis.	Bromodeoxyuridine	33-37	KRAS proto-oncogene, GTPase	Rattus norvegicus	120-123
27184741-10	2016	The number of bromodeoxyuridine (BrdU) and doublecortin (DCX) double-positive cells in the hippocampal dentate gyrus of P21 rats was significantly lower than that in controls, indicating reduced neurogenesis.	doublecortin	43-55	KRAS proto-oncogene, GTPase	Rattus norvegicus	120-123
27184741-11	2016	In the P21 rat"s brain of the formalin group, the expression of autism-related gene neurexin 1 (NRXN1), fragile X mental retardation 1 (FMR1), and oxytocin was significantly downregulated, consistent with the gene alteration in ASD.	Formaldehyde	30-38	KRAS proto-oncogene, GTPase	Rattus norvegicus	7-10
27217775-3	2016	The guanosine triphosphate-bound active K-Ras interacts with a range of effectors, resulting in the stimulation of downstream signaling pathways regulating cell proliferation, differentiation, and apoptosis.	Guanosine Triphosphate	4-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	40-45
27217775-5	2016	K-Ras transduces signals when it binds to guanosine triphosphate by directly binding to downstream effector proteins, but in case of guanosine diphosphate-bound conformation, these interactions get disrupted.	Guanosine Triphosphate	42-64	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-5
27217775-5	2016	K-Ras transduces signals when it binds to guanosine triphosphate by directly binding to downstream effector proteins, but in case of guanosine diphosphate-bound conformation, these interactions get disrupted.	Guanosine Diphosphate	133-154	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-5
27217775-9	2016	Moreover, the designed compounds" interactions are similar to guanosine diphosphate and, thus, could presumably act as a potential lead for K-Ras.	Guanosine Diphosphate	62-83	KRAS proto-oncogene, GTPase	Rattus norvegicus	140-145
26823281-10	2016	Sustained p21 and increased p27 expression in PT cells were found in the AKI group in response to UA and lead acetate.	uranyl acetate	98-100	KRAS proto-oncogene, GTPase	Rattus norvegicus	10-13
26823281-10	2016	Sustained p21 and increased p27 expression in PT cells were found in the AKI group in response to UA and lead acetate.	lead acetate	105-117	KRAS proto-oncogene, GTPase	Rattus norvegicus	10-13
27133074-5	2016	In the current study, we demonstrated that BA suppressed HG-induced MC proliferation, arrested HG-induced cell-cycle progression, reversed HG-inhibited expression of p21(Waf1/Cip1) and p27(Kip1).	betulinic acid	43-45	KRAS proto-oncogene, GTPase	Rattus norvegicus	166-169
26927081-7	2016	HI insult also resulted in brain inflammation (as indicated by microglia activation) and neuronal death (as indicated by Jade B positive staining) in the white matter, striatum, cortex, and hippocampal areas of the P21 rat.	hi	0-2	KRAS proto-oncogene, GTPase	Rattus norvegicus	215-218
26567004-5	2016	Intraluminal transduction of adenovirus encoding CaMKIIgammaC rescued expression to 35% of uninjured controls, inhibited neointima formation (>70%), inhibited VSM proliferation (>60%), and increased expression of the cell-cycle inhibitor p21 (>2-fold).	camkiigammac	49-61	KRAS proto-oncogene, GTPase	Rattus norvegicus	244-247
27461625-6	2016	RESULTS: The treatment of DMBA-exposed rats with ZOL and RT, both alone and in combination, successfully upregulates the transcriptional levels of Bax, caspase-3, caspase-9, p21, and BRCA 1 in mammary tissues, which may account for the elevated apoptotic activities observed and the eventual inhibition of tumor growth.	6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene	26-30	KRAS proto-oncogene, GTPase	Rattus norvegicus	174-177
26927081-7	2016	HI insult also resulted in brain inflammation (as indicated by microglia activation) and neuronal death (as indicated by Jade B positive staining) in the white matter, striatum, cortex, and hippocampal areas of the P21 rat.	jade b	121-127	KRAS proto-oncogene, GTPase	Rattus norvegicus	215-218
27665772-3	2016	Results showed that single exposure of propofol only induced great neuronal apoptosis and deficit at postnatal day 9(P9); while multiple exposures of propofol could induce significant neuronal apoptosis, neuronal deficit and synaptic loss at P9, P14, P21, or P35 compared with intact, and spatial learning and memory impairment from P36 to P41.	Propofol	39-47	KRAS proto-oncogene, GTPase	Rattus norvegicus	251-254
26500193-6	2016	However, on P14 and P21, density of capillaries, tortuosity index of arterioles, and diameter of veins significantly increased in KRN633-treated rats, compared to vehicle (0.5% methylcellulose)-treated animals.	N-(2-chloro-4-((6,7-dimethoxy-4-quinazolinyl)oxy)phenyl)-N'-propylurea	130-136	KRAS proto-oncogene, GTPase	Rattus norvegicus	20-23
27815471-7	2016	In comparison to the groups exposed to DEN, the ArtinM-treated rats showed diminution of preneoplastic foci, decreased expression of proliferating cell nuclear antigen (PCNA), increased number of nuclear p21 and p27 stained cells, augmented number of apoptotic cells, increased expression of p53, p42/44 MAPK and p21 proteins, reduced cyclin D1 (CCND1) protein levels and increased expression of TNFalpha and IFNgamma genes.	artinm	48-54	KRAS proto-oncogene, GTPase	Rattus norvegicus	204-207
27815471-7	2016	In comparison to the groups exposed to DEN, the ArtinM-treated rats showed diminution of preneoplastic foci, decreased expression of proliferating cell nuclear antigen (PCNA), increased number of nuclear p21 and p27 stained cells, augmented number of apoptotic cells, increased expression of p53, p42/44 MAPK and p21 proteins, reduced cyclin D1 (CCND1) protein levels and increased expression of TNFalpha and IFNgamma genes.	artinm	48-54	KRAS proto-oncogene, GTPase	Rattus norvegicus	313-316
26747726-7	2016	Metabolic memory by palmitate was found to be associated with increased FOXO1 activity as evident from increased expression of FOXO1 target genes such as PDK4, p21, G6Pc and IGFBP1.	Palmitates	20-29	KRAS proto-oncogene, GTPase	Rattus norvegicus	160-163
27247942-0	2016	Histone Lysine Methylation in TGF-beta1 Mediated p21 Gene Expression in Rat Mesangial Cells.	Lysine	8-14	KRAS proto-oncogene, GTPase	Rattus norvegicus	49-52
27652271-0	2016	Involvement of Histone Lysine Methylation in p21 Gene Expression in Rat Kidney In Vivo and Rat Mesangial Cells In Vitro under Diabetic Conditions.	Lysine	23-29	KRAS proto-oncogene, GTPase	Rattus norvegicus	45-48
27652271-4	2016	However, precise regulatory mechanism of histone lysine methylation (HKme) mediating p21 related hypertrophy associated with DN is not clear.	Lysine	49-55	KRAS proto-oncogene, GTPase	Rattus norvegicus	85-88
27652271-6	2016	p21 gene expression was upregulated in diabetic rats glomeruli; chromatin immunoprecipitation (ChIP) assays showed decreased histone H3-lysine9-dimethylation (H3K9me2) accompanied with enhanced histone H3-lysine4-methylation (H3K4me1/3) and SET7/9 occupancies at the p21 promoter.	lysine9	136-143	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-3
27652271-6	2016	p21 gene expression was upregulated in diabetic rats glomeruli; chromatin immunoprecipitation (ChIP) assays showed decreased histone H3-lysine9-dimethylation (H3K9me2) accompanied with enhanced histone H3-lysine4-methylation (H3K4me1/3) and SET7/9 occupancies at the p21 promoter.	lysine4	205-212	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-3
27665772-3	2016	Results showed that single exposure of propofol only induced great neuronal apoptosis and deficit at postnatal day 9(P9); while multiple exposures of propofol could induce significant neuronal apoptosis, neuronal deficit and synaptic loss at P9, P14, P21, or P35 compared with intact, and spatial learning and memory impairment from P36 to P41.	Propofol	150-158	KRAS proto-oncogene, GTPase	Rattus norvegicus	251-254
26647880-0	2016	Epigallocatechin-3-gallate suppresses alveolar epithelial cell apoptosis in seawater aspiration-induced acute lung injury via inhibiting STAT1-caspase-3/p21 associated pathway.	epigallocatechin gallate	0-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	153-156
26647880-5	2016	Furthermore, EGCG decreased seawater aspiration-induced apoptosis and the expression of caspase-3 and p21 in lung tissue cells.	epigallocatechin gallate	13-17	KRAS proto-oncogene, GTPase	Rattus norvegicus	102-105
26647880-8	2016	This suggests that EGCG suppresses alveolar epithelial cell apoptosis in seawater aspiration-induced ALI via inhibiting the STAT1-caspase-3/p21 associated pathway.	epigallocatechin gallate	19-23	KRAS proto-oncogene, GTPase	Rattus norvegicus	140-143
26394119-8	2015	Reverse transcription-polymerase chain reaction and Western blot analysis showed overexpression of cyclin D1 and p21(Cip1) in the NMU-induced breast tumors; however, the expression of both of them suppressed by crocin treatment.	Methylnitrosourea	130-133	KRAS proto-oncogene, GTPase	Rattus norvegicus	113-116
26282612-7	2015	Also, the ERbeta activation by its agonist DPN changed the subcellular localization of p21, inducing an increase in the p21 nuclear expression, where it acts as a tumoral suppressor.	NAD	43-46	KRAS proto-oncogene, GTPase	Rattus norvegicus	87-90
26282612-7	2015	Also, the ERbeta activation by its agonist DPN changed the subcellular localization of p21, inducing an increase in the p21 nuclear expression, where it acts as a tumoral suppressor.	NAD	43-46	KRAS proto-oncogene, GTPase	Rattus norvegicus	120-123
26492952-7	2015	Furthermore, it significantly ameliorated testosterone-induced reduction of mRNA expression Bax/Bcl-2 ratio, P21 and phosphatase and tensin homolog (PTEN) and AMPK [PT-172] activity.	Testosterone	42-54	KRAS proto-oncogene, GTPase	Rattus norvegicus	109-128
26459397-9	2015	In conclusion, repeated intra-nigrostriatal treatment with PMA induced microglial senescence with increased expression levels of beta-galactosidase and p21 in the substantia nigra of the rats.	Tetradecanoylphorbol Acetate	59-62	KRAS proto-oncogene, GTPase	Rattus norvegicus	152-155
25744732-10	2015	The anticarcinogenic effects shown after the inhibition of telomerase activity by diclofenac and curcumin may be associated with upregulation of tumor suppressor proteins p51, Rb, and p21, whose activation induces the cells cycle arrest and apoptosis.	Diclofenac	82-92	KRAS proto-oncogene, GTPase	Rattus norvegicus	184-187
26770644-7	2015	RESULTS: p27(kip1), p21(cip1) protein expression in podocytes exposed to high glucose for 72 h and in 16 weeks diabetic glomeruli significantly increased (P<0.01).	Glucose	78-85	KRAS proto-oncogene, GTPase	Rattus norvegicus	20-23
26462257-7	2015	As such, ss-lap treatment concurrent with inhibition of glutamine metabolism in mutant KRAS, NQO1 overexpressing PDA leads to massive redox imbalance, extensive DNA damage, rapid PARP-mediated NAD+ consumption, and PDA cell death-features not observed in NQO1-low, wild-type KRAS expressing cells.	Glutamine	56-65	KRAS proto-oncogene, GTPase	Rattus norvegicus	87-91
26462257-4	2015	RESULTS: Here, we report that reducing NADPH pools by genetically or pharmacologically (bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide (BPTES) or CB-839) inhibiting glutamine metabolism in mutant Kirsten rat sarcoma viral oncogene homolog (KRAS) PDA sensitizes cell lines and tumors to ss-lapachone (ss-lap, clinical form ARQ761).	NADP	39-44	KRAS proto-oncogene, GTPase	Rattus norvegicus	254-258
26462257-4	2015	RESULTS: Here, we report that reducing NADPH pools by genetically or pharmacologically (bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide (BPTES) or CB-839) inhibiting glutamine metabolism in mutant Kirsten rat sarcoma viral oncogene homolog (KRAS) PDA sensitizes cell lines and tumors to ss-lapachone (ss-lap, clinical form ARQ761).	bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl	88-134	KRAS proto-oncogene, GTPase	Rattus norvegicus	254-258
26462257-4	2015	RESULTS: Here, we report that reducing NADPH pools by genetically or pharmacologically (bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide (BPTES) or CB-839) inhibiting glutamine metabolism in mutant Kirsten rat sarcoma viral oncogene homolog (KRAS) PDA sensitizes cell lines and tumors to ss-lapachone (ss-lap, clinical form ARQ761).	diethyl sulfide	135-148	KRAS proto-oncogene, GTPase	Rattus norvegicus	254-258
26462257-4	2015	RESULTS: Here, we report that reducing NADPH pools by genetically or pharmacologically (bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide (BPTES) or CB-839) inhibiting glutamine metabolism in mutant Kirsten rat sarcoma viral oncogene homolog (KRAS) PDA sensitizes cell lines and tumors to ss-lapachone (ss-lap, clinical form ARQ761).	bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide	150-155	KRAS proto-oncogene, GTPase	Rattus norvegicus	254-258
26462257-4	2015	RESULTS: Here, we report that reducing NADPH pools by genetically or pharmacologically (bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide (BPTES) or CB-839) inhibiting glutamine metabolism in mutant Kirsten rat sarcoma viral oncogene homolog (KRAS) PDA sensitizes cell lines and tumors to ss-lapachone (ss-lap, clinical form ARQ761).	CB-839	160-166	KRAS proto-oncogene, GTPase	Rattus norvegicus	254-258
26462257-4	2015	RESULTS: Here, we report that reducing NADPH pools by genetically or pharmacologically (bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide (BPTES) or CB-839) inhibiting glutamine metabolism in mutant Kirsten rat sarcoma viral oncogene homolog (KRAS) PDA sensitizes cell lines and tumors to ss-lapachone (ss-lap, clinical form ARQ761).	Glutamine	179-188	KRAS proto-oncogene, GTPase	Rattus norvegicus	254-258
26462257-4	2015	RESULTS: Here, we report that reducing NADPH pools by genetically or pharmacologically (bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide (BPTES) or CB-839) inhibiting glutamine metabolism in mutant Kirsten rat sarcoma viral oncogene homolog (KRAS) PDA sensitizes cell lines and tumors to ss-lapachone (ss-lap, clinical form ARQ761).	ss-lapachone	300-312	KRAS proto-oncogene, GTPase	Rattus norvegicus	254-258
26617745-7	2015	The induction of A10 cells proliferation by miR-181b appeared to be involved in activation of S and G2/M checkpoint, concomitant with decreases in cell-cycle inhibitors p21 and p27, and increases in cell-cycle activators CDK4 and cyclinD1.	mir-181b	44-52	KRAS proto-oncogene, GTPase	Rattus norvegicus	169-172
25953318-4	2015	We observed significant increases in the protein expression of p27, p21, phospho-eukaryotic elongation factor 4E-binding protein 1, and phospho-p70 S6 ribosomal protein kinase, in both cultured podocytes exposed to high-glucose (HG) medium, and streptozotocin-induced diabetes mellitus (DM) rat glomeruli.	Streptozocin	245-259	KRAS proto-oncogene, GTPase	Rattus norvegicus	68-130
25744732-10	2015	The anticarcinogenic effects shown after the inhibition of telomerase activity by diclofenac and curcumin may be associated with upregulation of tumor suppressor proteins p51, Rb, and p21, whose activation induces the cells cycle arrest and apoptosis.	Curcumin	97-105	KRAS proto-oncogene, GTPase	Rattus norvegicus	184-187
25805267-8	2015	After osteogenesis, P5, P10, P15 and P21 MDSCs formed Alizarin red- and osteocalcin-positive bone nodules.	alizarin	54-66	KRAS proto-oncogene, GTPase	Rattus norvegicus	37-40
26170905-0	2015	Tripterygium glycosides induce premature ovarian failure in rats by promoting p53 phosphorylation and activating the serine/threonine kinase 11-p53-p21 signaling pathway.	Glycosides	13-23	KRAS proto-oncogene, GTPase	Rattus norvegicus	148-151
26170905-8	2015	Furthermore, reverse transcription-quantitative polymerase chain reaction (PCR) and immunohistochemistry assays indicated that the expression levels of serine/threonine kinase 11 (Stk11), p53 p21 and activated caspase-3 were elevated significantly in the TG-treated groups.	Thioguanine	255-257	KRAS proto-oncogene, GTPase	Rattus norvegicus	192-195
25738595-9	2015	The present study demonstrated that ATRA decreases the chondrogenesis of rEHBMCs by inhibiting cartilage-specific molecules, including aggrecan, Sox9 and Col2al, via regulating the expression of p53 and p21.	Tretinoin	36-40	KRAS proto-oncogene, GTPase	Rattus norvegicus	203-206
25818358-5	2015	RESULTS: BRV 100 mg/kg significantly increased the afterdischarge threshold (ADT) at all ages, whereas BRV at 10 mg/kg increased ADT in P60, P28, and P21 rats.	brivaracetam	103-106	KRAS proto-oncogene, GTPase	Rattus norvegicus	150-153
25702091-4	2015	We analysed clinical data of 67 patients with locally advanced (IIIB) or metastatic stage (IV) NSCLC harbouring Kirsten rat sarcoma viral oncogene (KRAS) mutation treated with erlotinib or gefitinib.	Erlotinib Hydrochloride	176-185	KRAS proto-oncogene, GTPase	Rattus norvegicus	148-152
26192324-7	2015	Aniline treatment resulted in significant increases in cell cycle regulatory proteins, including cyclins A, B and CDK1, particularly phosphor-CDK1, and decreases in CDK inhibitors p21 and p27, which could promote the splenocytes to go through G2/M transition.	aniline	0-7	KRAS proto-oncogene, GTPase	Rattus norvegicus	180-183
25414256-4	2015	Exposure of normal rat epithelial cells to etoposide caused cellular senescence, as manifested by enlarged cell size, a flattened cell body, reduced cell proliferation, enhanced beta-galactosidase activity, and elevated p53 and p21.	Etoposide	43-52	KRAS proto-oncogene, GTPase	Rattus norvegicus	228-231
26323151-1	2015	To study the effect of the combined administration of different doses of Glycyrrhizae Radix et Rhizoma and Atractylodis Macrocephalae Rhizoma on the proliferation of DFMO-treated intestinal epithelial cells (IEC-6) and p53, p21 mRNA and protein expressions, in order to define the molecular basis for the effect of the combined administration of different doses of Glycyrrhizae Radix et Rhizoma and Atractylodis Macrocephalae Rhizoma on the cell proliferation.	Eflornithine	166-170	KRAS proto-oncogene, GTPase	Rattus norvegicus	224-227
26323151-5	2015	Atractylodis Macrocephalae Rhizoma could increase p53, p21 mRNA and proteins expression in DFMO-treated IEC-6 cells.	Eflornithine	91-95	KRAS proto-oncogene, GTPase	Rattus norvegicus	55-58
26323151-6	2015	The combined administration of different ratios of Atractylodis Macrocephalae Rhizoma and Glycyrrhizae Radix et Rhizoma could significantly down-regulate Atractylodis Macrocephalae Rhizoma"s effect on p53, p21 mRNA and proteins expression in DFMO-treated IEC-6 cells and promote the proliferation of IEC-6 cells.	Eflornithine	242-246	KRAS proto-oncogene, GTPase	Rattus norvegicus	206-209
25901224-12	2015	However, the levels of p53 and p21 proteins were decreased in adult rat NP cells treated with both high glucose concentrations.	Glucose	104-111	KRAS proto-oncogene, GTPase	Rattus norvegicus	31-34
25667638-7	2015	To gain insight into the mechanism underlying the effect of BZD on the cell cycle progression, the mRNA and protein expression of cyclin D1, cyclin-dependent kinase 4 (CDK4), CDK6 and p21 was measured by reverse transcription-polymerase chain reaction and western blotting, respectively.	N-BENZOYL-N'-BETA-D-GLUCOPYRANOSYL UREA	60-63	KRAS proto-oncogene, GTPase	Rattus norvegicus	184-187
27308397-0	2015	KRAS-driven ROS promote malignant transformation.	Reactive Oxygen Species	12-15	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-4
27308397-3	2015	recently reported that levels of reactive oxygen species (ROS) are increased by KRAS and are responsible for KRAS-driven malignant transformation, and further identified the signaling cascade involved as KRAS/p38/PDPK1/PKCdelta/p47(phox)/NOX1.	Reactive Oxygen Species	33-56	KRAS proto-oncogene, GTPase	Rattus norvegicus	80-84
27308397-3	2015	recently reported that levels of reactive oxygen species (ROS) are increased by KRAS and are responsible for KRAS-driven malignant transformation, and further identified the signaling cascade involved as KRAS/p38/PDPK1/PKCdelta/p47(phox)/NOX1.	Reactive Oxygen Species	33-56	KRAS proto-oncogene, GTPase	Rattus norvegicus	109-113
27308397-3	2015	recently reported that levels of reactive oxygen species (ROS) are increased by KRAS and are responsible for KRAS-driven malignant transformation, and further identified the signaling cascade involved as KRAS/p38/PDPK1/PKCdelta/p47(phox)/NOX1.	Reactive Oxygen Species	33-56	KRAS proto-oncogene, GTPase	Rattus norvegicus	109-113
27308397-3	2015	recently reported that levels of reactive oxygen species (ROS) are increased by KRAS and are responsible for KRAS-driven malignant transformation, and further identified the signaling cascade involved as KRAS/p38/PDPK1/PKCdelta/p47(phox)/NOX1.	Reactive Oxygen Species	58-61	KRAS proto-oncogene, GTPase	Rattus norvegicus	80-84
27308397-3	2015	recently reported that levels of reactive oxygen species (ROS) are increased by KRAS and are responsible for KRAS-driven malignant transformation, and further identified the signaling cascade involved as KRAS/p38/PDPK1/PKCdelta/p47(phox)/NOX1.	Reactive Oxygen Species	58-61	KRAS proto-oncogene, GTPase	Rattus norvegicus	109-113
27308397-3	2015	recently reported that levels of reactive oxygen species (ROS) are increased by KRAS and are responsible for KRAS-driven malignant transformation, and further identified the signaling cascade involved as KRAS/p38/PDPK1/PKCdelta/p47(phox)/NOX1.	Reactive Oxygen Species	58-61	KRAS proto-oncogene, GTPase	Rattus norvegicus	109-113
25752339-8	2015	Moreover, METH induced an increase in the protein expression of the tumor suppressor p53 (124.4%) and the cell cycle inhibitor p21(CIP) (1) (p21) (128.1%), resulting in the accumulation of p21 in the nucleus.	Methamphetamine	10-14	KRAS proto-oncogene, GTPase	Rattus norvegicus	127-130
25752339-8	2015	Moreover, METH induced an increase in the protein expression of the tumor suppressor p53 (124.4%) and the cell cycle inhibitor p21(CIP) (1) (p21) (128.1%), resulting in the accumulation of p21 in the nucleus.	Methamphetamine	10-14	KRAS proto-oncogene, GTPase	Rattus norvegicus	141-144
25752339-11	2015	According to these results, we concluded that METH induces a reduction in cell proliferation by upregulating the cell cycle regulators p53/p21 and promoting the accumulation of p21 in the nucleus and that melatonin ameliorates these negative effects of METH.	Methamphetamine	46-50	KRAS proto-oncogene, GTPase	Rattus norvegicus	139-142
25752339-11	2015	According to these results, we concluded that METH induces a reduction in cell proliferation by upregulating the cell cycle regulators p53/p21 and promoting the accumulation of p21 in the nucleus and that melatonin ameliorates these negative effects of METH.	Methamphetamine	46-50	KRAS proto-oncogene, GTPase	Rattus norvegicus	177-180
26273371-2	2015	The combined utilization of KRAS antisense oligodeoxynucleotide (ASODN) and insulin-like growth factor-I receptor (IGF-IR) may inhibit the proliferation of A549 cell lines of lung adenocarcinoma.	Oligodeoxyribonucleotides	43-63	KRAS proto-oncogene, GTPase	Rattus norvegicus	28-32
26273371-2	2015	The combined utilization of KRAS antisense oligodeoxynucleotide (ASODN) and insulin-like growth factor-I receptor (IGF-IR) may inhibit the proliferation of A549 cell lines of lung adenocarcinoma.	asodn	65-70	KRAS proto-oncogene, GTPase	Rattus norvegicus	28-32
25511229-6	2015	CKD rats showed increased protein expression of senescence-associated beta-galactosidase, bone-related proteins, p16 and p21, and increased oxidative stress levels in the calcified area, which were inhibited by both phosphate binders.	Phosphates	216-225	KRAS proto-oncogene, GTPase	Rattus norvegicus	121-124
25490147-8	2015	Isoflavones significantly blocked activations of senescence-associated beta-galactosidase and PPARgamma/p53/p21 by NEFA.	Isoflavones	0-11	KRAS proto-oncogene, GTPase	Rattus norvegicus	108-111
26170892-1	2015	(Du-Zhong) Lignans Inhibit Angiotensin II-Stimulated Proliferation by Affecting P21, P27, and Bax Expression in Rat Mesangial Cells.	Lignans	11-18	KRAS proto-oncogene, GTPase	Rattus norvegicus	80-83
26273643-6	2015	Moreover, resveratrol attenuated pulmonary arterial remodeling, decreased pulmonary arterial pressure, and upregulated SIRT1 and p21 expression but downregulated cyclin D1 expression in MCT induced PAH rat.	Resveratrol	10-21	KRAS proto-oncogene, GTPase	Rattus norvegicus	129-132
26273643-7	2015	Notably, knockdown of SIRT1 eliminated the regulation of resveratrol on p21 and cyclin D1 expression in PDGF-BB treated HPASMCs.	Resveratrol	57-68	KRAS proto-oncogene, GTPase	Rattus norvegicus	72-75
25015661-0	2014	Epigenetic changes in p21 expression in renal cells after exposure to bromate.	Bromates	70-77	KRAS proto-oncogene, GTPase	Rattus norvegicus	22-25
25435978-1	2015	The aim of the present study was to explore the effects of curcumin in combination with bevacizumab on the vascular endothelial growth factor (VEGF)/VEGF receptor (VEGFR)/K-ras pathway in hepatocellular carcinoma.	Curcumin	59-67	KRAS proto-oncogene, GTPase	Rattus norvegicus	171-176
25151216-0	2014	Tangeretin, a citrus pentamethoxyflavone, exerts cytostatic effect via p53/p21 up-regulation and suppresses metastasis in 7,12-dimethylbenz(alpha)anthracene-induced rat mammary carcinoma.	tangeretin	0-10	KRAS proto-oncogene, GTPase	Rattus norvegicus	75-78
25151216-10	2014	Further, tangeretin treatment arrested the cancer cell division at the G1/S phase via p53/p21 up-regulation and inhibited metastasis by suppressing matrix metalloproteinase (MMP)-2, MMP-9 and vascular endothelial growth factor.	tangeretin	9-19	KRAS proto-oncogene, GTPase	Rattus norvegicus	90-93
24998203-1	2014	BACKGROUND & AIMS: Development of pancreatic ductal adenocarcinoma (PDAC) involves activation of c-Ki-ras2 Kirsten rat sarcoma oncogene homolog (KRAS) signaling, but little is known about the roles of proteins that regulate the activity of oncogenic KRAS.	Adenosine Monophosphate	12-15	KRAS proto-oncogene, GTPase	Rattus norvegicus	149-153
25435978-9	2015	Curcumin and the VEGF blocker are each capable of inhibiting hepatocellular carcinoma progression by regulating the VEGF/VEGFR/K-ras pathway.	Curcumin	0-8	KRAS proto-oncogene, GTPase	Rattus norvegicus	127-132
24945428-0	2014	Results of first proficiency test for KRAS testing with formalin-fixed, paraffin-embedded cell lines in China.	Formaldehyde	56-64	KRAS proto-oncogene, GTPase	Rattus norvegicus	38-42
24945428-0	2014	Results of first proficiency test for KRAS testing with formalin-fixed, paraffin-embedded cell lines in China.	Paraffin	72-80	KRAS proto-oncogene, GTPase	Rattus norvegicus	38-42
25015661-5	2014	5-Aza and TSA co-treatment did not alter p38 or p53 phosphorylation, but slightly decreased H2AX phosphorylation and significantly decreased p21 expression.	trichostatin A	10-13	KRAS proto-oncogene, GTPase	Rattus norvegicus	141-144
25015661-3	2014	However, KBrO3 treatment did increase p38, p53 and histone 2AX (H2AX) phosphorylation, and p21 expression.	kbro3	9-14	KRAS proto-oncogene, GTPase	Rattus norvegicus	91-94
25015661-9	2014	Sub-chronic low-dose KBrO3 treatment also induced a biphasic response in p21 expression, with lower concentrations increasing expression, but higher concentrations decreasing expression.	kbro3	21-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	73-76
25015661-10	2014	Methylation-specific PCR demonstrated that sub-chronic KBrO3 treatment altered the methylation of cytosine bases in the p21 gene, as compared with controls, correlating to alterations in p21 protein expression.	kbro3	55-60	KRAS proto-oncogene, GTPase	Rattus norvegicus	120-123
25015661-5	2014	5-Aza and TSA co-treatment did not alter p38 or p53 phosphorylation, but slightly decreased H2AX phosphorylation and significantly decreased p21 expression.	Azacitidine	0-5	KRAS proto-oncogene, GTPase	Rattus norvegicus	141-144
25015661-10	2014	Methylation-specific PCR demonstrated that sub-chronic KBrO3 treatment altered the methylation of cytosine bases in the p21 gene, as compared with controls, correlating to alterations in p21 protein expression.	kbro3	55-60	KRAS proto-oncogene, GTPase	Rattus norvegicus	187-190
25015661-10	2014	Methylation-specific PCR demonstrated that sub-chronic KBrO3 treatment altered the methylation of cytosine bases in the p21 gene, as compared with controls, correlating to alterations in p21 protein expression.	Cytosine	98-106	KRAS proto-oncogene, GTPase	Rattus norvegicus	120-123
24763901-5	2014	Carbon tetrachloride (CCl4) treatment induced IL-20 that further up-regulated the expression of transforming growth factor (TGF)-beta1 and p21(WAF1) and resulted in cell cycle arrest in the Clone-9 rat hepatocyte cell line.	Carbon Tetrachloride	0-20	KRAS proto-oncogene, GTPase	Rattus norvegicus	139-142
25015661-11	2014	Collectively, these data show the novel finding that KBrO3-induced renal cell death is altered by inhibitors of epigenetic modifying enzymes and that KBrO3 itself induces epigenetic changes in the p21 gene.	kbro3	150-155	KRAS proto-oncogene, GTPase	Rattus norvegicus	197-200
25102244-9	2014	Consistent with these phenotypes, we observed decreased expression of the cell cycle-related proteins cyclin D1, cyclin E1, and cyclin B1, and increased expression of p53 and p21 in SAA-treated cells.	salvianolic acid A	182-185	KRAS proto-oncogene, GTPase	Rattus norvegicus	175-178
24863468-6	2014	These DA deficits at P21 were exhibited by a loss of DA and DA metabolite [3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA)] levels and tyrosine hydroxylase (TH) expression in the striatum.	3,4-Dihydroxyphenylacetic Acid	75-105	KRAS proto-oncogene, GTPase	Rattus norvegicus	21-24
24863468-6	2014	These DA deficits at P21 were exhibited by a loss of DA and DA metabolite [3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA)] levels and tyrosine hydroxylase (TH) expression in the striatum.	3,4-Dihydroxyphenylacetic Acid	107-112	KRAS proto-oncogene, GTPase	Rattus norvegicus	21-24
24863468-6	2014	These DA deficits at P21 were exhibited by a loss of DA and DA metabolite [3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA)] levels and tyrosine hydroxylase (TH) expression in the striatum.	Homovanillic Acid	118-135	KRAS proto-oncogene, GTPase	Rattus norvegicus	21-24
24863468-6	2014	These DA deficits at P21 were exhibited by a loss of DA and DA metabolite [3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA)] levels and tyrosine hydroxylase (TH) expression in the striatum.	Homovanillic Acid	137-140	KRAS proto-oncogene, GTPase	Rattus norvegicus	21-24
25009787-3	2014	DMF significantly attenuated neointimal hyperplasia induced by balloon injury in rat carotid arteries via suppression of the G1 to S phase transition resulting from induction of p21 protein in VSMCs.	Dimethyl Fumarate	0-3	KRAS proto-oncogene, GTPase	Rattus norvegicus	178-181
25024745-15	2014	In addition, Mocetinostat treatment of atrial CD90+ cells upregulated cleaved-Caspase3 and activated the p53/p21 axis.	mocetinostat	13-25	KRAS proto-oncogene, GTPase	Rattus norvegicus	109-112
24339278-10	2014	Re-exposed groups had lower corticosterone plasma level (P1P21 M and F, P8P21M) than controls.	Corticosterone	28-42	KRAS proto-oncogene, GTPase	Rattus norvegicus	57-62
24889603-3	2014	We aim to target the guanine nucleotide (GN)-binding pocket because the natural contents of this pocket dictate the signaling state of K-Ras.	Guanine Nucleotides	21-39	KRAS proto-oncogene, GTPase	Rattus norvegicus	135-140
24889603-3	2014	We aim to target the guanine nucleotide (GN)-binding pocket because the natural contents of this pocket dictate the signaling state of K-Ras.	Guanine Nucleotides	41-43	KRAS proto-oncogene, GTPase	Rattus norvegicus	135-140
24889603-4	2014	Here, we characterize the irreversible inhibitor SML-8-73-1 (SML), which targets the GN-binding pocket of K-Ras G12C.	SML-8-73-1	49-59	KRAS proto-oncogene, GTPase	Rattus norvegicus	106-111
24889603-4	2014	Here, we characterize the irreversible inhibitor SML-8-73-1 (SML), which targets the GN-binding pocket of K-Ras G12C.	Guanine Nucleotides	85-87	KRAS proto-oncogene, GTPase	Rattus norvegicus	106-111
24889603-5	2014	We report a high-resolution X-ray crystal structure of G12C K-Ras bound to SML, revealing that the compound binds in a manner similar to GDP, forming a covalent linkage with Cys-12.	Guanosine Diphosphate	137-140	KRAS proto-oncogene, GTPase	Rattus norvegicus	60-65
24889603-5	2014	We report a high-resolution X-ray crystal structure of G12C K-Ras bound to SML, revealing that the compound binds in a manner similar to GDP, forming a covalent linkage with Cys-12.	Cysteine	174-177	KRAS proto-oncogene, GTPase	Rattus norvegicus	60-65
24939301-6	2014	The percentage of cells in G0-G1 and G2-M phases was reduced, and that in S phase increased after treatment for 72 h. The expression of cyclin D1 and B1, p27 and PCNA in VSMCs of paclitaxel-treated group was up-regulated, but that of p21 down-regulated as compared with VECs.	Paclitaxel	179-189	KRAS proto-oncogene, GTPase	Rattus norvegicus	234-237
24535573-12	2014	However, compared to normal control, the expressions of p53 and p21 proteins were decreased in young rat AF cells treated with both high glucoses for one and three days.	Glucose	137-145	KRAS proto-oncogene, GTPase	Rattus norvegicus	64-67
24778007-7	2014	CIMP is the third most commonly involved event, and is defined by widespread methylation of CpG islands of suppressor promoters, with two phenotypes: CIMP-high and CIMP-low which interact with MSI or CIN status V-raf murine sarcoma viral oncogene homolog B (BRAF) is a serine-threonine protein kinase that acts as a downstream effector of the Kirsten rat sarcoma viral oncogene homolog (KRAS) pathway.	Cyclic IMP	0-4	KRAS proto-oncogene, GTPase	Rattus norvegicus	387-391
24412385-9	2014	These effects were coupled with the sequential increase of HO-1 and p21(WAF1) expressions by rosiglitazone.	Rosiglitazone	93-106	KRAS proto-oncogene, GTPase	Rattus norvegicus	68-71
24223793-10	2013	Similarly, p21 antisense oligonucleotide increased the DNA synthesis.	Oligonucleotides	25-40	KRAS proto-oncogene, GTPase	Rattus norvegicus	11-14
24520304-6	2014	During this process, beta-diketone-cobalt complexes decreased cyclin A expression and increased cyclin E and p21 expression.	beta-diketone	21-34	KRAS proto-oncogene, GTPase	Rattus norvegicus	109-112
24520304-6	2014	During this process, beta-diketone-cobalt complexes decreased cyclin A expression and increased cyclin E and p21 expression.	Cobalt	35-41	KRAS proto-oncogene, GTPase	Rattus norvegicus	109-112
25520224-5	2014	Piperonylic acid obviously promoted the protein expressions of P21 and P27 while inhibiting proliferation and DNA synthesis.	piperonylic acid	0-16	KRAS proto-oncogene, GTPase	Rattus norvegicus	63-66
25520224-8	2014	The intervention of piperonylic acid significantly facilitated the gene expressions of P21 and P27, lowered the PCNA expression, and inhibited the formation of intima and the reconstruction of pathological vessels, thus remarkably suppressing luminal stenosis.	piperonylic acid	20-36	KRAS proto-oncogene, GTPase	Rattus norvegicus	87-90
25520224-9	2014	CONCLUSION: Piperonylic acid can inhibit the excessive proliferation of vascular smooth muscle cells and the lumen narrowing after injury of blood vessels, the mechanism of which is associated with the promoted gene expressions of cell cycle key regulators P21 and P27 (Tab.	piperonylic acid	12-28	KRAS proto-oncogene, GTPase	Rattus norvegicus	257-260
24253735-11	2014	Kras2 was also upregulated in TCs, but to a lesser degree than PTHrP.	Technetium	30-33	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-5
23939785-9	2013	Male rats were castrated at P7 and treated with estradiol from P21 to P28; estradiol treatment in castrates resulted in dendritic hypertrophy in SNB motoneurons compared with normal males.	Estradiol	48-57	KRAS proto-oncogene, GTPase	Rattus norvegicus	63-66
23939785-9	2013	Male rats were castrated at P7 and treated with estradiol from P21 to P28; estradiol treatment in castrates resulted in dendritic hypertrophy in SNB motoneurons compared with normal males.	Estradiol	75-84	KRAS proto-oncogene, GTPase	Rattus norvegicus	63-66
24279718-0	2013	Concomitant occurrence of EGFR (epidermal growth factor receptor) and KRAS (V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog) mutations in an ALK (anaplastic lymphoma kinase)-positive lung adenocarcinoma patient with acquired resistance to crizotinib: a case report.	Crizotinib	244-254	KRAS proto-oncogene, GTPase	Rattus norvegicus	70-74
23857431-0	2014	Sulindac and Celecoxib regulate cell cycle progression by p53/p21 up regulation to induce apoptosis during initial stages of experimental colorectal cancer.	Sulindac	0-8	KRAS proto-oncogene, GTPase	Rattus norvegicus	62-65
23857431-0	2014	Sulindac and Celecoxib regulate cell cycle progression by p53/p21 up regulation to induce apoptosis during initial stages of experimental colorectal cancer.	Celecoxib	13-22	KRAS proto-oncogene, GTPase	Rattus norvegicus	62-65
23857431-10	2014	We may conclude that Sulindac and Celecoxib could possibly follow p53/p21 mediated regulation of cell proliferation, where down regulation of NF-kappaB signaling and activation of PPARgamma might serve as important additional events in vivo.	Sulindac	21-29	KRAS proto-oncogene, GTPase	Rattus norvegicus	70-73
23857431-10	2014	We may conclude that Sulindac and Celecoxib could possibly follow p53/p21 mediated regulation of cell proliferation, where down regulation of NF-kappaB signaling and activation of PPARgamma might serve as important additional events in vivo.	Celecoxib	34-43	KRAS proto-oncogene, GTPase	Rattus norvegicus	70-73
24617038-0	2013	Inhibition of beta-catenin and KRAS expressions by Piper betle in azoxymethane-induced colon cancer of male Fischer 344 rats.	Azoxymethane	66-78	KRAS proto-oncogene, GTPase	Rattus norvegicus	31-35
24080207-6	2013	Tumors exposed to raloxifene, bexarotene and/or the combination showed significant suppression of proliferating cell nuclear antigen, cyclin D1, and beta-catenin with an increased apoptotic cells (3-fold) and p21 expression (3.8-fold) as compared tumors of rats fed control diet.	Raloxifene Hydrochloride	18-28	KRAS proto-oncogene, GTPase	Rattus norvegicus	209-212
24080207-6	2013	Tumors exposed to raloxifene, bexarotene and/or the combination showed significant suppression of proliferating cell nuclear antigen, cyclin D1, and beta-catenin with an increased apoptotic cells (3-fold) and p21 expression (3.8-fold) as compared tumors of rats fed control diet.	Bexarotene	30-40	KRAS proto-oncogene, GTPase	Rattus norvegicus	209-212
22623379-8	2013	An increased expression of Bcl2 while other proteins like Bax, Apaf-1, cyt c, and caspases in the apoptotic pathway, and the tumor suppressor proteins, p53 and p21 get down-regulated after DMH treatment which were reverted back to normal with Celecoxib and Dolastatin 15.	1,2-Dimethylhydrazine	189-192	KRAS proto-oncogene, GTPase	Rattus norvegicus	160-163
24204728-7	2013	Interestingly, 1 nmol/L of BK almost completely inhibited the increase in senescent cell number and p21 expression induced by H2O2.	Hydrogen Peroxide	126-130	KRAS proto-oncogene, GTPase	Rattus norvegicus	100-103
23276622-7	2013	In the EGL of the busulfan group, apoptotic granular cells increased at 2 DAT simultaneously with increased numbers of p53- and p21-positive cells while mitotic granular cells decreased, suggesting an occurrence of p53-related apoptosis and depression of proliferative activity in granular cells.	Busulfan	18-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	128-131
25755500-7	2013	Long-term BCAA supplementation significantly reduced expression of CyclinD1, PCNA, thymidine kinase, Bcl-2, and GST-p and increased expression of p21 in the liver.	Amino Acids, Branched-Chain	10-14	KRAS proto-oncogene, GTPase	Rattus norvegicus	146-149
23510080-3	2013	Cisplatin treatment increased p21 and bax and decreased c-myc mRNA expression, which was reversed upon co-culture with BMSCs.	Cisplatin	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	30-33
23907590-4	2013	Both treatments (flaxseed and TNDF) influence the overexpression of genes involved in cell cycle arrest and mitochondrial apoptosis: p53, p21, bcl-2, bax and caspase-3.	tndf	30-34	KRAS proto-oncogene, GTPase	Rattus norvegicus	138-141
23424995-8	2013	KEY RESULTS: Folate up-regulated p21/p27 through a Src/ERK-dependent mechanism that accounted for its anti-proliferative effects on RASMC.	Folic Acid	13-19	KRAS proto-oncogene, GTPase	Rattus norvegicus	33-36
23424995-8	2013	KEY RESULTS: Folate up-regulated p21/p27 through a Src/ERK-dependent mechanism that accounted for its anti-proliferative effects on RASMC.	rasmc	132-137	KRAS proto-oncogene, GTPase	Rattus norvegicus	33-36
23424995-9	2013	Folate protected RASMC from the effects of homocysteine by reducing AKT1, focal adhesion kinase (FAK), paxillin, and p190RhoGAP activation/phosphorylation, along with cytosolic levels of p21 and p27, and increasing RhoA activation.	Folic Acid	0-6	KRAS proto-oncogene, GTPase	Rattus norvegicus	187-190
23424995-9	2013	Folate protected RASMC from the effects of homocysteine by reducing AKT1, focal adhesion kinase (FAK), paxillin, and p190RhoGAP activation/phosphorylation, along with cytosolic levels of p21 and p27, and increasing RhoA activation.	rasmc	17-22	KRAS proto-oncogene, GTPase	Rattus norvegicus	187-190
23424995-9	2013	Folate protected RASMC from the effects of homocysteine by reducing AKT1, focal adhesion kinase (FAK), paxillin, and p190RhoGAP activation/phosphorylation, along with cytosolic levels of p21 and p27, and increasing RhoA activation.	Homocysteine	43-55	KRAS proto-oncogene, GTPase	Rattus norvegicus	187-190
23651544-6	2013	The downregulation of p53 expression with specific small interfering RNA (p53 siRNA) in CoCl2-treated PC12 cells caused reduction in apoptosis, UNC5B expression, and p21 expression.	cobaltous chloride	88-93	KRAS proto-oncogene, GTPase	Rattus norvegicus	166-169
23810908-5	2013	Sulforaphane increased the cyclin-dependent kinase inhibitor p21 and p53 levels, while it decreased CDK2 and cyclin E expression.	sulforaphane	0-12	KRAS proto-oncogene, GTPase	Rattus norvegicus	61-64
23783456-4	2013	SJAMP treatment significantly inhibited DEN-induced HCC by reducing both the number and mean volume of nodules, decreasing serum a-fetoprotein (AFP) levels and proliferating cell nuclear antigen (PCNA) expression in liver, and increasing p21 expression.	Diethylnitrosamine	40-43	KRAS proto-oncogene, GTPase	Rattus norvegicus	238-241
23592481-4	2013	Interestingly, in a screen of multiple cell cycle inhibitors, p21 was dramatically upregulated in INS-1-derived 832/13 cells and rodent islets by two pharmacological inducers of beta-cell stress, dexamethasone and thapsigargin.	Dexamethasone	196-209	KRAS proto-oncogene, GTPase	Rattus norvegicus	62-65
23592481-4	2013	Interestingly, in a screen of multiple cell cycle inhibitors, p21 was dramatically upregulated in INS-1-derived 832/13 cells and rodent islets by two pharmacological inducers of beta-cell stress, dexamethasone and thapsigargin.	Thapsigargin	214-226	KRAS proto-oncogene, GTPase	Rattus norvegicus	62-65
23336931-4	2013	RESULTS: Compared with the single treatment with amlodipine or atorvastatin, the combination of amlodipine plus atorvastatin treatment prevented arteriosclerotic processes, and induced a strong recovery of Sirtuin1 (Sirt1) expression and a marked reduction in p53, p21, and monocyte chemoattractant protein-1 (MCP-1).	Amlodipine	96-106	KRAS proto-oncogene, GTPase	Rattus norvegicus	265-268
23336931-4	2013	RESULTS: Compared with the single treatment with amlodipine or atorvastatin, the combination of amlodipine plus atorvastatin treatment prevented arteriosclerotic processes, and induced a strong recovery of Sirtuin1 (Sirt1) expression and a marked reduction in p53, p21, and monocyte chemoattractant protein-1 (MCP-1).	Atorvastatin	112-124	KRAS proto-oncogene, GTPase	Rattus norvegicus	265-268
23026135-4	2012	This study focused on the effects of v-K-ras and p53 on Methotrexate (MTX)-mediated DHFR amplification.	Methotrexate	56-68	KRAS proto-oncogene, GTPase	Rattus norvegicus	39-44
24399732-11	2013	Western blot analysis showed that MG-132 activated p53, p21, caspase-3 and Bax, and inhibited Bcl-2 in a dose-dependent manner, while p27 expression remained unchanged.	Magnesium	34-36	KRAS proto-oncogene, GTPase	Rattus norvegicus	56-59
23651968-0	2013	[Cilostazol inhibits proliferation and induces apoptosis in rat vascular smooth muscle cells through Rb-p53-p21 pathways].	Cilostazol	1-11	KRAS proto-oncogene, GTPase	Rattus norvegicus	108-111
23651968-8	2013	Low dose of cilostazol (1.0x10(-7), 2.5x10(-7) and 5.0x10(-7) mol/L) significantly upregulated p21 mRNA expression compared to control group (1.86 +- 0.19, 2.20 +- 0.24 and 2.10 +- 0.18 vs. 1.210 +- 0.18, all P < 0.05).	Cilostazol	12-22	KRAS proto-oncogene, GTPase	Rattus norvegicus	95-98
23651968-11	2013	p21 and Rb protein expressions also upregulated at low concentrations of cilostazol and downregulated at high concentrations of cilostazol.	Cilostazol	73-83	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-3
23651968-11	2013	p21 and Rb protein expressions also upregulated at low concentrations of cilostazol and downregulated at high concentrations of cilostazol.	Cilostazol	128-138	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-3
23651968-12	2013	CONCLUSION: Cilostazol could inhibit the proliferation of rat VSMCs through modulating Rb-p53-p21 pathway and induce VSMCs apoptosis through upregulating p53.	Cilostazol	12-22	KRAS proto-oncogene, GTPase	Rattus norvegicus	94-97
22972628-1	2013	BACKGROUND: The authors conducted a systematic review and meta-analysis to examine whether patients who had metastatic colorectal cancer (mCRC) with the v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) p.G13D mutation (an amino acid substitution at position 13 in KRAS from a glycine to an aspartic acid) and received cetuximab treatment had better clinical outcomes than patients who had mCRC tumors with KRAS codon 12 mutations.	Glycine	287-294	KRAS proto-oncogene, GTPase	Rattus norvegicus	207-211
22972628-1	2013	BACKGROUND: The authors conducted a systematic review and meta-analysis to examine whether patients who had metastatic colorectal cancer (mCRC) with the v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) p.G13D mutation (an amino acid substitution at position 13 in KRAS from a glycine to an aspartic acid) and received cetuximab treatment had better clinical outcomes than patients who had mCRC tumors with KRAS codon 12 mutations.	Aspartic Acid	301-314	KRAS proto-oncogene, GTPase	Rattus norvegicus	207-211
23365582-6	2013	EPA increased the mRNA levels of p21(cip1) and p27(kip1), a cyclin-dependent kinase inhibitor, which indicated that EPA induced cell cycle arrest.	Eicosapentaenoic Acid	0-3	KRAS proto-oncogene, GTPase	Rattus norvegicus	33-36
23365582-6	2013	EPA increased the mRNA levels of p21(cip1) and p27(kip1), a cyclin-dependent kinase inhibitor, which indicated that EPA induced cell cycle arrest.	Eicosapentaenoic Acid	116-119	KRAS proto-oncogene, GTPase	Rattus norvegicus	33-36
23026135-4	2012	This study focused on the effects of v-K-ras and p53 on Methotrexate (MTX)-mediated DHFR amplification.	Methotrexate	70-73	KRAS proto-oncogene, GTPase	Rattus norvegicus	39-44
23026135-5	2012	Rat lung epithelial cells expressing v-K-ras or murine lung cancer LKR cells harboring active K-ras continued cell-cycle progression when treated with MTX.	Methotrexate	151-154	KRAS proto-oncogene, GTPase	Rattus norvegicus	39-44
23508728-3	2012	As a continuation of our recent work, we investigated the expressions of cyclin D1 and p21 in NMU-induced breast cancer of Wistar Albino rats.	Methylnitrosourea	94-97	KRAS proto-oncogene, GTPase	Rattus norvegicus	87-90
23268392-4	2012	Treatment of the LPS-challenged cells with QFTLR and benazepril both resulted in significantly attenuated expressions of cyclin D1, CDK2, and P21 and obvious increase of P27 expression (P<0.05 or P<0.01), but QFTLR produced stronger effects than benazepril in regulating of cyclinD1, P21 and P27 protein expressions (P<0.05 or P<0.01).	qftlr	43-48	KRAS proto-oncogene, GTPase	Rattus norvegicus	142-145
23268392-4	2012	Treatment of the LPS-challenged cells with QFTLR and benazepril both resulted in significantly attenuated expressions of cyclin D1, CDK2, and P21 and obvious increase of P27 expression (P<0.05 or P<0.01), but QFTLR produced stronger effects than benazepril in regulating of cyclinD1, P21 and P27 protein expressions (P<0.05 or P<0.01).	qftlr	43-48	KRAS proto-oncogene, GTPase	Rattus norvegicus	290-293
23268392-4	2012	Treatment of the LPS-challenged cells with QFTLR and benazepril both resulted in significantly attenuated expressions of cyclin D1, CDK2, and P21 and obvious increase of P27 expression (P<0.05 or P<0.01), but QFTLR produced stronger effects than benazepril in regulating of cyclinD1, P21 and P27 protein expressions (P<0.05 or P<0.01).	benazepril	53-63	KRAS proto-oncogene, GTPase	Rattus norvegicus	142-145
23268392-4	2012	Treatment of the LPS-challenged cells with QFTLR and benazepril both resulted in significantly attenuated expressions of cyclin D1, CDK2, and P21 and obvious increase of P27 expression (P<0.05 or P<0.01), but QFTLR produced stronger effects than benazepril in regulating of cyclinD1, P21 and P27 protein expressions (P<0.05 or P<0.01).	benazepril	53-63	KRAS proto-oncogene, GTPase	Rattus norvegicus	290-293
23363723-0	2012	[Atorvastatin attenuates parathyroid hormone 1-34 induced cardiomyocytes hypertrophy through downregulating K-Ras-ERK1/2 pathway].	Atorvastatin	1-13	KRAS proto-oncogene, GTPase	Rattus norvegicus	108-113
23363723-8	2012	CONCLUSIONS: Atrovastatin attenuates PTH1-34 induced neonatal rat cardiomyocytes hypertrophy through downregulating K-Ras and ERK1/2 pathway.	atrovastatin	13-25	KRAS proto-oncogene, GTPase	Rattus norvegicus	116-121
22344541-8	2012	ATRA dose-dependently reversed both TGF-beta(1)-induced decreases in p21(Waf1/Cip1) mRNA and protein levels and p27(Kip1) protein level and increases in Skp2 mRNA and protein levels, and inhibited TGF-beta(1)-induced proliferation through G(1) arrest.	Tretinoin	0-4	KRAS proto-oncogene, GTPase	Rattus norvegicus	69-72
22344541-10	2012	CONCLUSION: ATRA inhibited TGF-beta(1)-induced mesangial cell proliferation by up-regulating p21(Waf1/Cip1) mRNA and protein levels, and p27(Kip1) protein level, and down-regulating Skp2 mRNA and protein levels, but it had no significant effect on apoptosis in rat mesangial cells.	Tretinoin	12-16	KRAS proto-oncogene, GTPase	Rattus norvegicus	93-96
23508728-0	2012	High Expression of Cyclin D1 and p21 in N-Nitroso-N-Methylurea-Induced Breast Cancer in Wistar Albino Female Rats.	Methylnitrosourea	40-62	KRAS proto-oncogene, GTPase	Rattus norvegicus	33-36
22804759-12	2012	Inhibiting ERK1/2 phosphorylation with PD98059 completely blocked HG-induced p21 expression and markedly reversed HG-induced inhibition of cell cycle progression in MAPC.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	39-46	KRAS proto-oncogene, GTPase	Rattus norvegicus	77-80
22542654-5	2012	Moreover, in in vivo experiments, P4 and P21, particularly their N-terminally biotinylated peptide compounds (BP4 and BP21), inhibited PAF-induced rat paw oedema dose dependently and markedly, and showed sufficient inhibition of the oedema even at doses 150-300 times less than the doses of PAF antagonists.	Platelet Activating Factor	135-138	KRAS proto-oncogene, GTPase	Rattus norvegicus	41-44
22890553-13	2012	Atorvastatin initiated apoptosis at 10(-4) M and attenuated it at 10(-5) M. Atorvastatin induced p21 protein expression and beta-galactosidase staining of MFB in vitro and in vivo.	Atorvastatin	0-12	KRAS proto-oncogene, GTPase	Rattus norvegicus	97-100
22890553-13	2012	Atorvastatin initiated apoptosis at 10(-4) M and attenuated it at 10(-5) M. Atorvastatin induced p21 protein expression and beta-galactosidase staining of MFB in vitro and in vivo.	Atorvastatin	76-88	KRAS proto-oncogene, GTPase	Rattus norvegicus	97-100
22829592-8	2012	These results demonstrate that Fe(2+)-generated O(2)() mediates p21(ras) and TAK1 activation via PTP inhibition and Lys(63)-polyUb of TRAF6 in caveosomes for proinflammatory M1 activation in HM.	ammonium ferrous sulfate	31-37	KRAS proto-oncogene, GTPase	Rattus norvegicus	64-67
22829592-8	2012	These results demonstrate that Fe(2+)-generated O(2)() mediates p21(ras) and TAK1 activation via PTP inhibition and Lys(63)-polyUb of TRAF6 in caveosomes for proinflammatory M1 activation in HM.	Superoxides	48-52	KRAS proto-oncogene, GTPase	Rattus norvegicus	64-67
22580711-6	2012	Western blot analysis showed that FTY720 induced the downregulation of cyclin D1, cyclin E, CDK2, CDK4, Bcl-2 and E2F1 and the upregulation of Kip1/p27, Cip1/p21, Bax and Rb in GMC in a dose-dependent manner.	Fingolimod Hydrochloride	34-40	KRAS proto-oncogene, GTPase	Rattus norvegicus	158-161
22542671-0	2012	Manganese induces p21 expression in PC12 cells at the transcriptional level.	Manganese	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	18-21
22542671-4	2012	The present studies were initiated to investigate whether p21 are induced after manganese exposure and its potential effects in vitro, with particular attention being given to understand the underlying regulatory mechanism of p21 induction by manganese in this process.	Manganese	80-89	KRAS proto-oncogene, GTPase	Rattus norvegicus	58-61
22542671-4	2012	The present studies were initiated to investigate whether p21 are induced after manganese exposure and its potential effects in vitro, with particular attention being given to understand the underlying regulatory mechanism of p21 induction by manganese in this process.	Manganese	243-252	KRAS proto-oncogene, GTPase	Rattus norvegicus	58-61
22542671-4	2012	The present studies were initiated to investigate whether p21 are induced after manganese exposure and its potential effects in vitro, with particular attention being given to understand the underlying regulatory mechanism of p21 induction by manganese in this process.	Manganese	243-252	KRAS proto-oncogene, GTPase	Rattus norvegicus	226-229
22542671-5	2012	We found that manganese induced DAergic cells injury and upregulation of p21 levels in nigrostriatal regions.	Manganese	14-23	KRAS proto-oncogene, GTPase	Rattus norvegicus	73-76
22542671-8	2012	Moreover, manganese treatment resulted in an increase in the mRNA and protein levels of p21, but did not have the same effect on other related factors.	Manganese	10-19	KRAS proto-oncogene, GTPase	Rattus norvegicus	88-91
22542671-9	2012	Silencing p21 by RNA interference showed a marked reversal of both G2/M arrest and the decrease in cell viability induced by manganese.	Manganese	125-134	KRAS proto-oncogene, GTPase	Rattus norvegicus	10-13
22542671-10	2012	Manganese did not stabilize the p21 protein and mRNA, and caused a marked increase in p21 mRNA levels together with an increase in its promoter activity, indicating a transcriptional mechanism.	Manganese	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	86-89
22542671-11	2012	Overall, the in vivo and in vitro data suggest that exposure to manganese can increase p21 levels.	Manganese	64-73	KRAS proto-oncogene, GTPase	Rattus norvegicus	87-90
22829592-2	2012	Our earlier work demonstrates the role of ferrous iron (Fe(2+)) as a pathogen-associated molecular pattern-independent agonist for activation of IkappaB kinase (IKK) and NF-kappaB in HM via activation and interaction of p21(ras), transforming growth factor beta-activated kinase-1 (TAK1), and phosphatidylinositol 3-kinase (PI3K) in caveosomes.	ammonium ferrous sulfate	42-49	KRAS proto-oncogene, GTPase	Rattus norvegicus	220-223
22829592-2	2012	Our earlier work demonstrates the role of ferrous iron (Fe(2+)) as a pathogen-associated molecular pattern-independent agonist for activation of IkappaB kinase (IKK) and NF-kappaB in HM via activation and interaction of p21(ras), transforming growth factor beta-activated kinase-1 (TAK1), and phosphatidylinositol 3-kinase (PI3K) in caveosomes.	Iron	50-54	KRAS proto-oncogene, GTPase	Rattus norvegicus	220-223
22829592-2	2012	Our earlier work demonstrates the role of ferrous iron (Fe(2+)) as a pathogen-associated molecular pattern-independent agonist for activation of IkappaB kinase (IKK) and NF-kappaB in HM via activation and interaction of p21(ras), transforming growth factor beta-activated kinase-1 (TAK1), and phosphatidylinositol 3-kinase (PI3K) in caveosomes.	ammonium ferrous sulfate	56-63	KRAS proto-oncogene, GTPase	Rattus norvegicus	220-223
22829592-6	2012	Fe(2+)-induced p21(ras) activity is abrogated with the Src inhibitor PP2 and SOD.	ammonium ferrous sulfate	0-6	KRAS proto-oncogene, GTPase	Rattus norvegicus	15-18
21940155-5	2012	TB and TB+VA-treated rats, but not VA-treated rats, exhibited higher levels of H3K9 acetylation and p21 protein expression.	tributyrin	0-2	KRAS proto-oncogene, GTPase	Rattus norvegicus	100-103
21940155-5	2012	TB and TB+VA-treated rats, but not VA-treated rats, exhibited higher levels of H3K9 acetylation and p21 protein expression.	tributyrin	7-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	100-103
21940155-5	2012	TB and TB+VA-treated rats, but not VA-treated rats, exhibited higher levels of H3K9 acetylation and p21 protein expression.	Vitamin A	10-12	KRAS proto-oncogene, GTPase	Rattus norvegicus	100-103
22555846-0	2012	Indoxyl sulfate promotes vascular smooth muscle cell senescence with upregulation of p53, p21, and prelamin A through oxidative stress.	Indican	0-15	KRAS proto-oncogene, GTPase	Rattus norvegicus	90-93
22555846-4	2012	The IS-induced expression of p53 and p21 was suppressed by N-acetylcysteine, an antioxidant.	Acetylcysteine	59-75	KRAS proto-oncogene, GTPase	Rattus norvegicus	37-40
22726273-11	2012	De novo lipogenesis with rosiglitazone treatment at p21 was studied using 50% U13C-glucose and gas chromatography/mass spectrometry.	Rosiglitazone	25-38	KRAS proto-oncogene, GTPase	Rattus norvegicus	52-55
22726273-18	2012	p21 SGA adipocytes revealed increased fatty acid de novo synthesis through a complex relationship with glucose metabolism.	Fatty Acids	38-48	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-3
22542654-5	2012	Moreover, in in vivo experiments, P4 and P21, particularly their N-terminally biotinylated peptide compounds (BP4 and BP21), inhibited PAF-induced rat paw oedema dose dependently and markedly, and showed sufficient inhibition of the oedema even at doses 150-300 times less than the doses of PAF antagonists.	Platelet Activating Factor	291-294	KRAS proto-oncogene, GTPase	Rattus norvegicus	41-44
22301686-1	2012	AIMS: The aim of this study was to determine the effect of chronic ethanol feeding on acetylation of histone H3 at lysine 9 (H3-Lys9) at promoter and coding regions of genes for class I alcohol dehydrogenase (ADH I), inducible nitric oxide synthase (iNOS), Bax, p21, c-met and hepatocyte growth factor in the rat liver.	Ethanol	67-74	KRAS proto-oncogene, GTPase	Rattus norvegicus	262-265
22036941-7	2012	The cinacalcet-mediated decrease in parathyroid gland size was accompanied by increased expression of the cyclin-dependent kinase inhibitor p21.	Cinacalcet	4-14	KRAS proto-oncogene, GTPase	Rattus norvegicus	140-143
22449373-8	2012	The expression of P-p53 and p21 was increased in cisplatin-induced nephropathy.	Cisplatin	49-58	KRAS proto-oncogene, GTPase	Rattus norvegicus	28-31
22301686-1	2012	AIMS: The aim of this study was to determine the effect of chronic ethanol feeding on acetylation of histone H3 at lysine 9 (H3-Lys9) at promoter and coding regions of genes for class I alcohol dehydrogenase (ADH I), inducible nitric oxide synthase (iNOS), Bax, p21, c-met and hepatocyte growth factor in the rat liver.	Lysine	115-121	KRAS proto-oncogene, GTPase	Rattus norvegicus	262-265
22113172-1	2012	BACKGROUND: We recently reported that aldosterone-induced cellular senescence via an increase in p21, a cyclin-dependent kinase (CDK) inhibitor, in rat kidney and cultured human proximal tubular cells.	Aldosterone	38-49	KRAS proto-oncogene, GTPase	Rattus norvegicus	97-100
22345314-5	2012	In males, exposure to PCBs and PBDEs at 1.7, 5, 10, 20, 40, and 60 mumol/kg/day induced equivalent and dose-dependent reductions in T4 from p 7 to p 21.	Polychlorinated Biphenyls	22-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	147-151
22345314-5	2012	In males, exposure to PCBs and PBDEs at 1.7, 5, 10, 20, 40, and 60 mumol/kg/day induced equivalent and dose-dependent reductions in T4 from p 7 to p 21.	Halogenated Diphenyl Ethers	31-36	KRAS proto-oncogene, GTPase	Rattus norvegicus	147-151
22345314-6	2012	Exposure to equimolar mixtures of PCBs and PBDEs at 3.4, 10, 20, 40, and 80 mumol/kg/day additively reduced T4 from p 7 to p 21 in males.	Polychlorinated Biphenyls	34-38	KRAS proto-oncogene, GTPase	Rattus norvegicus	123-127
22345314-6	2012	Exposure to equimolar mixtures of PCBs and PBDEs at 3.4, 10, 20, 40, and 80 mumol/kg/day additively reduced T4 from p 7 to p 21 in males.	Halogenated Diphenyl Ethers	43-48	KRAS proto-oncogene, GTPase	Rattus norvegicus	123-127
22308472-7	2012	OSS up-regulated cyclin A and down-regulated p21(CIP1) in ECs and induced their proliferation; these effects were mediated by HDAC-1/2/3.	OSS	0-3	KRAS proto-oncogene, GTPase	Rattus norvegicus	45-48
22194422-10	2012	The increase of p21(Cip1) was associated with increased acetylation of both histone H3 and H4 and decreased trimethylation of histone H3 lysine-27 at the p21(Cip1) promoter.	Lysine	137-143	KRAS proto-oncogene, GTPase	Rattus norvegicus	16-19
22194422-10	2012	The increase of p21(Cip1) was associated with increased acetylation of both histone H3 and H4 and decreased trimethylation of histone H3 lysine-27 at the p21(Cip1) promoter.	Lysine	137-143	KRAS proto-oncogene, GTPase	Rattus norvegicus	154-157
22194422-11	2012	In the p21(Cip1) coding region, dimethylation of histone H3 lysine-4 was significantly higher (P <0.05) in livers of OP rats compared with OR rats.	Lysine	60-66	KRAS proto-oncogene, GTPase	Rattus norvegicus	7-10
22076566-9	2012	Western blotting showed that MMC treatment increased the levels of activated forms of p53 and p21, whereas levels of the activated forms of Akt and caspase-3 were unchanged.	Mitomycin	29-32	KRAS proto-oncogene, GTPase	Rattus norvegicus	94-97
22582138-9	2012	We also found increases in hippocampal NGF and plasma corticosterone following MDMA treatment on P16 and P21, respectively.	Corticosterone	54-68	KRAS proto-oncogene, GTPase	Rattus norvegicus	105-108
22244893-6	2012	Doxorubicin induced p53 and p21 was suppressed by treatment with AG1478, an EGFR and ErbB4 kinase inhibitor, or suppression of ErbB4 expression with small interfering RNA.	Doxorubicin	0-11	KRAS proto-oncogene, GTPase	Rattus norvegicus	28-31
22244893-6	2012	Doxorubicin induced p53 and p21 was suppressed by treatment with AG1478, an EGFR and ErbB4 kinase inhibitor, or suppression of ErbB4 expression with small interfering RNA.	RTKI cpd	65-71	KRAS proto-oncogene, GTPase	Rattus norvegicus	28-31
22200425-6	2012	Administration of indoxyl sulfate to hypertensive rats reduces renal expression of Klotho and promotes cell senescence, with expression of senescence-associated beta-galactosidase, p53, p21, p16, and retinoblastoma protein, accompanied by kidney fibrosis.	Indican	18-33	KRAS proto-oncogene, GTPase	Rattus norvegicus	186-189
22074740-5	2012	In this study, we used gene therapy in the form of antisense oligonucleotides (ASOs) specifically to silence Kras (alias Ki-ras) expression in a rat model of renal fibrosis caused by unilateral ureteric obstruction.	Oligonucleotides	61-77	KRAS proto-oncogene, GTPase	Rattus norvegicus	109-113
22074740-5	2012	In this study, we used gene therapy in the form of antisense oligonucleotides (ASOs) specifically to silence Kras (alias Ki-ras) expression in a rat model of renal fibrosis caused by unilateral ureteric obstruction.	Oligonucleotides, Antisense	79-83	KRAS proto-oncogene, GTPase	Rattus norvegicus	109-113
22156682-4	2011	Animal model of depression was developed by chronic administration of Clomipramine and/or Melipramine in rat pups from postnatal day 7 (P7) and/or 14 (P14) to P21 and/or P28, respectively.	Clomipramine	70-82	KRAS proto-oncogene, GTPase	Rattus norvegicus	159-162
21780161-11	2011	Together, lack of magnesium may increase p21(Cip1) and p27(Kip1) levels mediated by the decrease in ATP content and the activation of p53, resulting in the suppression of cell cycle progression from G1 to S phase in NRK-52E cells.	Magnesium	18-27	KRAS proto-oncogene, GTPase	Rattus norvegicus	41-44
21832251-8	2011	NF-kappaB inhibitors suppressed indoxyl sulfate-induced p21 expression, whereas NF-kappaB p65 siRNA enhanced its expression.	Indican	32-47	KRAS proto-oncogene, GTPase	Rattus norvegicus	56-59
22201090-1	2011	Animal model of depression was developed by means of chronic exposure of rat pups to anticholinergic drugs (Atropine, Scopolamine) during the early life period from postnatal day 7 (P7) and/or 14 (P14) to P21 and/or P28, respectively.	Atropine	108-116	KRAS proto-oncogene, GTPase	Rattus norvegicus	205-208
22201090-1	2011	Animal model of depression was developed by means of chronic exposure of rat pups to anticholinergic drugs (Atropine, Scopolamine) during the early life period from postnatal day 7 (P7) and/or 14 (P14) to P21 and/or P28, respectively.	Scopolamine	118-129	KRAS proto-oncogene, GTPase	Rattus norvegicus	205-208
21652547-10	2012	In contrast, the expression of p27(Kip1) and p21(Cip1) was significantly increased in DM-SG compared to DM-LG and C-SG (P < 0.05).	dm	86-88	KRAS proto-oncogene, GTPase	Rattus norvegicus	45-48
21780161-0	2011	Magnesium deficiency suppresses cell cycle progression mediated by increase in transcriptional activity of p21(Cip1)  and p27(Kip1)  in renal epithelial NRK-52E cells.	Magnesium	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	107-110
21780161-5	2011	After serum addition, the expression levels of p21(Cip1) and p27(Kip1) in the absence of MgCl(2) were higher than those in the presence of MgCl(2) .	mgcl	89-93	KRAS proto-oncogene, GTPase	Rattus norvegicus	47-50
21780161-5	2011	After serum addition, the expression levels of p21(Cip1) and p27(Kip1) in the absence of MgCl(2) were higher than those in the presence of MgCl(2) .	mgcl	139-143	KRAS proto-oncogene, GTPase	Rattus norvegicus	47-50
21780161-7	2011	The mRNA levels and promoter activities of p21(Cip1) and p27(Kip1) in the absence of MgCl(2) were higher than those in the presence of MgCl(2) .	mgcl	85-89	KRAS proto-oncogene, GTPase	Rattus norvegicus	43-46
21780161-7	2011	The mRNA levels and promoter activities of p21(Cip1) and p27(Kip1) in the absence of MgCl(2) were higher than those in the presence of MgCl(2) .	mgcl	135-139	KRAS proto-oncogene, GTPase	Rattus norvegicus	43-46
21780161-9	2011	Pifithrin-alpha, a p53 inhibitor, decreased the p-p53, p21(Cip1) and p27(Kip1) levels, and the percentage in G1 phase in the absence of MgCl(2) .	pifithrin	0-15	KRAS proto-oncogene, GTPase	Rattus norvegicus	55-58
21763782-9	2011	Treatment with TSA or transfection of KLF4 increased the expression of both p21 and p27 and promoter activity.	trichostatin A	15-18	KRAS proto-oncogene, GTPase	Rattus norvegicus	76-79
21763782-11	2011	These data demonstrate that TSA inhibits neointimal thickening and VSMC proliferation via activation of the KLF4/p21/p27 signaling pathway.	trichostatin A	28-31	KRAS proto-oncogene, GTPase	Rattus norvegicus	113-116
21738012-6	2011	The cells transformed by K-Ras (V12)  maintained cellular ATP level mainly through glycolytic ATP production without induction of GLUT1, the low Km glucose transporter.	Adenosine Triphosphate	58-61	KRAS proto-oncogene, GTPase	Rattus norvegicus	25-30
21738012-6	2011	The cells transformed by K-Ras (V12)  maintained cellular ATP level mainly through glycolytic ATP production without induction of GLUT1, the low Km glucose transporter.	Adenosine Triphosphate	94-97	KRAS proto-oncogene, GTPase	Rattus norvegicus	25-30
21738012-7	2011	Finally, K-Ras (V12) -triggered LC3-II formation was modulated by extracellular glucose levels, and LC3-II formation increased only in hepatocellular carcinoma tissues exhibiting low glucose uptake and increased K-Ras expression.	Glucose	80-87	KRAS proto-oncogene, GTPase	Rattus norvegicus	9-14
21738012-7	2011	Finally, K-Ras (V12) -triggered LC3-II formation was modulated by extracellular glucose levels, and LC3-II formation increased only in hepatocellular carcinoma tissues exhibiting low glucose uptake and increased K-Ras expression.	Glucose	183-190	KRAS proto-oncogene, GTPase	Rattus norvegicus	9-14
22156682-4	2011	Animal model of depression was developed by chronic administration of Clomipramine and/or Melipramine in rat pups from postnatal day 7 (P7) and/or 14 (P14) to P21 and/or P28, respectively.	Imipramine	90-101	KRAS proto-oncogene, GTPase	Rattus norvegicus	159-162
21370285-0	2011	Accumulation of K-Ras codon 12 mutations in the F344 rat distal colon following azoxymethane exposure.	Azoxymethane	80-92	KRAS proto-oncogene, GTPase	Rattus norvegicus	16-21
21642617-0	2011	Aristolochic acid-induced carcinogenesis examined by ACB-PCR quantification of H-Ras and K-Ras mutant fraction.	aristolochic acid I	0-17	KRAS proto-oncogene, GTPase	Rattus norvegicus	89-94
21912060-2	2011	The aim of this study was to investigate the gene expression of p53, p21 and B-cell lymphoma-2 (bcl-2) using preventive and therapeutic approaches of selenium in chemically induced hepatocarcinogenesis in rats.	Selenium	150-158	KRAS proto-oncogene, GTPase	Rattus norvegicus	69-72
21586513-3	2011	Stearate also increases cell cycle inhibitor p21(CIP1/WAF1) and p27(KIP1) levels and concomitantly decreases cyclin-dependent kinase 2 (Cdk2) phosphorylation.	Stearates	0-8	KRAS proto-oncogene, GTPase	Rattus norvegicus	45-48
21586513-5	2011	The MEK1 inhibitor, PD98059, reversed stearate-induced p21(CIP1/WAF1) upregulation, but only partially restored stearate-induced dephosphorylation of Cdk2.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	20-27	KRAS proto-oncogene, GTPase	Rattus norvegicus	55-58
21586513-5	2011	The MEK1 inhibitor, PD98059, reversed stearate-induced p21(CIP1/WAF1) upregulation, but only partially restored stearate-induced dephosphorylation of Cdk2.	Stearates	38-46	KRAS proto-oncogene, GTPase	Rattus norvegicus	55-58
21533767-9	2011	Berberine induces cell cycle arrest and potentiates the inhibitory effect of DHEAS through disrupting the binding of p27, p21 with Skp2.	Berberine	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	122-125
21533767-9	2011	Berberine induces cell cycle arrest and potentiates the inhibitory effect of DHEAS through disrupting the binding of p27, p21 with Skp2.	Dehydroepiandrosterone Sulfate	77-82	KRAS proto-oncogene, GTPase	Rattus norvegicus	122-125
21533767-11	2011	Being treated with berberine and DHEAS also promoted p27 and p21 bind to CDK2, so the proliferation of A7r5 cells induced by PDGF-BB was inhibited.	Berberine	19-28	KRAS proto-oncogene, GTPase	Rattus norvegicus	61-64
21533767-11	2011	Being treated with berberine and DHEAS also promoted p27 and p21 bind to CDK2, so the proliferation of A7r5 cells induced by PDGF-BB was inhibited.	Dehydroepiandrosterone Sulfate	33-38	KRAS proto-oncogene, GTPase	Rattus norvegicus	61-64
21533767-12	2011	The data provide evidence that berberine acts through the inhibition of p27-Skp2 and p21-Skp2 with subsequent activation of the cell cycle arrest, which leads to the increase in sensitivity to DHEAS.	Berberine	31-40	KRAS proto-oncogene, GTPase	Rattus norvegicus	85-88
21533767-12	2011	The data provide evidence that berberine acts through the inhibition of p27-Skp2 and p21-Skp2 with subsequent activation of the cell cycle arrest, which leads to the increase in sensitivity to DHEAS.	Dehydroepiandrosterone Sulfate	193-198	KRAS proto-oncogene, GTPase	Rattus norvegicus	85-88
21514281-7	2011	In VSMCs from SHR, aspirin increased p53 and p21 expression and inhibited the expression of cell cycle associated proteins, such as p-Rb, cyclin D, and cyclin E.	Aspirin	19-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	45-48
21171965-5	2011	Each protein in this subset of SP/KLF members individually inhibits BrdU (5-bromo-2-deoxyuridine) incorporation in KRAS oncogenic-mutant cancer cells.	Bromodeoxyuridine	68-72	KRAS proto-oncogene, GTPase	Rattus norvegicus	115-119
21171965-5	2011	Each protein in this subset of SP/KLF members individually inhibits BrdU (5-bromo-2-deoxyuridine) incorporation in KRAS oncogenic-mutant cancer cells.	Bromodeoxyuridine	74-96	KRAS proto-oncogene, GTPase	Rattus norvegicus	115-119
21300357-5	2011	Pull-down assay or Western blot analysis revealed that pre-administration of 10(-8)mol/L E(2) significantly reduced the H(2)O(2)-induced activation of oncogene Ras, as well as activity of p16 and p38 MAPK, and expression of PRAK, p53, p21 and p-Rb.	Hydrogen Peroxide	120-128	KRAS proto-oncogene, GTPase	Rattus norvegicus	235-238
21544732-6	2011	Along with these changes, SDS-SWCNT treatment elevated protein levels for p53 and p21 with a concomitant increase in the single strand DNA breakage.	sds	26-29	KRAS proto-oncogene, GTPase	Rattus norvegicus	82-85
21779580-6	2011	Quercetin restrained the proliferation of aHSCs rather than quiescent HSCs and heptotcytes by inducing a G(1) arrest as examined by cell cycle analysis and evidenced by increased levels of p53, p21(CIP1/WAF1), as well as p27(KIP1), and decreased abundance of cyclins (D(1), D(2), A, E).	Quercetin	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	194-197
21401759-9	2011	Finally, AG1478 injection decreased p21 levels in the gastric mucosa at 17 days, while no changes were detected in p27, cyclin E, CDK2, cyclin D1 and CDK4 concentrations.	RTKI cpd	9-15	KRAS proto-oncogene, GTPase	Rattus norvegicus	36-39
21721157-0	2011	1"-Acetoxychavicol acetate enhances the phase II enzyme activities via the increase in intranuclear Nrf2 level and cytosolic p21 level.	1'-acetoxychavicol acetate	0-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	125-128
21167829-13	2011	Western blotting analysis showed decreased ERK1/2 MAP kinase phosphorylation level, significantly increased p21(cip1) expression and reduced retinoblastoma protein (pRb) phosphorylation after 24h of triptolide treatment.	triptolide	199-209	KRAS proto-oncogene, GTPase	Rattus norvegicus	108-111
21167829-15	2011	CONCLUSIONS: Our study indicates that triptolide exert inhibitory effect on VSMC proliferation, inactivation of MAPK pathway and modulation of cell cycle proteins p21(cip1) and Rb are relating mechanisms.	triptolide	38-48	KRAS proto-oncogene, GTPase	Rattus norvegicus	163-166
21226888-1	2011	BACKGROUND: The aim of this study was to investigate whether mutations in the genes H-ras and K-ras were related to the mechanism of invasion as a result of the immunoexpression of H-Ras, Ki-67, alpha-smooth muscle actin (SMA) and vascular endothelial growth factor (VEGF) during 4-nitroquinoline 1-oxide (4NQO)-induced rat tongue carcinogenesis.	4-Nitroquinoline-1-oxide	280-304	KRAS proto-oncogene, GTPase	Rattus norvegicus	94-99
21226888-1	2011	BACKGROUND: The aim of this study was to investigate whether mutations in the genes H-ras and K-ras were related to the mechanism of invasion as a result of the immunoexpression of H-Ras, Ki-67, alpha-smooth muscle actin (SMA) and vascular endothelial growth factor (VEGF) during 4-nitroquinoline 1-oxide (4NQO)-induced rat tongue carcinogenesis.	4-Nitroquinoline-1-oxide	306-310	KRAS proto-oncogene, GTPase	Rattus norvegicus	94-99
21251947-5	2011	In this work, we showed the in vitro inhibitory effects of BF on luteinizing hormone (LH)-inducible ovulatory gene expression in rat ovarian granulosa cells, including genes P450scc, StAR, PR, AREG, EREG, TGF-beta1, C/EBP beta, RUNX1, p21, cyclin E1, CYP19a1, SULT1E1 and PTGS2.	bifenthrin	59-61	KRAS proto-oncogene, GTPase	Rattus norvegicus	235-238
21721157-4	2011	ACA induced glutathione S-transferase (GST) and NAD (P)H: quinone oxidoreductase 1 (NQO1) activities, increased intracellular glutathione (GSH) level, and upregulated intranuclear Nrf2 and cytosolic p21.	4-amylcinnamoylanthranilic acid	0-3	KRAS proto-oncogene, GTPase	Rattus norvegicus	199-202
20964789-0	2011	Low-dose carcinogenicity of 2-amino-3-methylimidazo[4,5-f ]quinoline in rats: Evidence for the existence of no-effect levels and a mechanism involving p21(Cip / WAF1).	2-amino-3-methylimidazo(4,5-f)quinoline	28-68	KRAS proto-oncogene, GTPase	Rattus norvegicus	151-154
21719999-6	2011	Furthermore, bufalin not only inhibited upregulation of cyclin D1 and CDK4, but also downregulation of p21 in both mRNA and protein levels.	bufalin	13-20	KRAS proto-oncogene, GTPase	Rattus norvegicus	103-106
21467636-6	2011	Cell cycle arrest and increase in p21 expression were significantly inhibited by 1,2-bis(o-aminophenoxy)ethane-N,N,N",N"-tetraacetic acid tetra (acetoxymethyl) ester (BAPTA-AM), an intracellular calcium chelator.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	167-175	KRAS proto-oncogene, GTPase	Rattus norvegicus	34-37
21467636-6	2011	Cell cycle arrest and increase in p21 expression were significantly inhibited by 1,2-bis(o-aminophenoxy)ethane-N,N,N",N"-tetraacetic acid tetra (acetoxymethyl) ester (BAPTA-AM), an intracellular calcium chelator.	Calcium	195-202	KRAS proto-oncogene, GTPase	Rattus norvegicus	34-37
21712954-13	2011	Moreover, the expression of gamma-H2A.X, a molecular marker of DNA damage response, p16(INK4a), p53, and p21 is increased in senescent MSCs induced with ORS, and is also reversed by DKK1 or by beta-catenin siRNA.	World Health Organization oral rehydration solution	153-156	KRAS proto-oncogene, GTPase	Rattus norvegicus	105-108
21195930-6	2011	RESULTS: DH + IS rats showed decreased expression of klotho, increased expression of senescence-associated beta-galactosidase, p16(INK4a), p21(WAF1/CIP1), p53, and Rb in renal tubular cells, and increased tubulointerstitial fibrosis and mesangial expansion as compared with DH rats.	dh +	9-13	KRAS proto-oncogene, GTPase	Rattus norvegicus	139-142
21195930-8	2011	CONCLUSION: Administration of indoxyl sulfate to hypertensive rats reduced renal expression of klotho and promoted cell senescence with expression of senescence-related proteins, such as p16(INK4a), p21(WAF1/CIP1), p53, and Rb, which was accompanied by renal fibrosis.	Indican	30-45	KRAS proto-oncogene, GTPase	Rattus norvegicus	199-202
21128180-0	2011	Dietary supplementation of lutein reduces colon carcinogenesis in DMH-treated rats by modulating K-ras, PKB, and beta-catenin proteins.	Dimethylhydrazines	66-69	KRAS proto-oncogene, GTPase	Rattus norvegicus	97-102
21128180-4	2011	The results showed a significant increase in protein expression for K-ras and beta-catenin in tumors of DMH-treated rats.	Dimethylhydrazines	104-107	KRAS proto-oncogene, GTPase	Rattus norvegicus	68-73
20170653-8	2010	Interestingly, prenatal ethanol exposure did affect the pattern of the change in neuronal number over time; total neuronal number was stable in the ethanol-treated pups after P12, but it continued to rise in the controls until P21.	Ethanol	24-31	KRAS proto-oncogene, GTPase	Rattus norvegicus	227-230
21368868-4	2010	Dex upregulates cell cycle-related genes p16 and p21 in a glucocorticoid receptor(GR)-dependent manner.	Dexamethasone	0-3	KRAS proto-oncogene, GTPase	Rattus norvegicus	49-52
20696760-5	2010	In addition, Dyrk1A-induced p53 phosphorylation at Ser-15 led to a robust induction of p53 target genes (e.g. p21(CIP1)) and impaired G(1)/G(0)-S phase transition, resulting in attenuated proliferation of H19-7 cells and human embryonic stem cell-derived neural precursor cells.	Serine	51-54	KRAS proto-oncogene, GTPase	Rattus norvegicus	110-113
20691162-9	2010	More notably, DH+IS rats showed significantly increased aortic calcification and wall thickness, and significantly increased expression of SA-beta-gal, p16(INK4a), p21(WAF1/CIP1), p53 and Rb in the cells embedded in the calcification area as compared with DH rats.	dh+	14-17	KRAS proto-oncogene, GTPase	Rattus norvegicus	164-167
20495008-11	2010	Local activation of ERK1/2 by Ki-Ras stimulates mitochondrial SOD, which reduces reactive oxygen species and produces H(2)O(2).	Reactive Oxygen Species	81-104	KRAS proto-oncogene, GTPase	Rattus norvegicus	30-36
20495008-11	2010	Local activation of ERK1/2 by Ki-Ras stimulates mitochondrial SOD, which reduces reactive oxygen species and produces H(2)O(2).	Hydrogen Peroxide	118-126	KRAS proto-oncogene, GTPase	Rattus norvegicus	30-36
20526188-8	2010	RESULTS: Intrathecal injection of 3 mg/kg ketamine at P3 and 15 mg/kg at P21 reverses carrageenan-induced hyperalgesia.	Ketamine	42-50	KRAS proto-oncogene, GTPase	Rattus norvegicus	73-76
20526188-8	2010	RESULTS: Intrathecal injection of 3 mg/kg ketamine at P3 and 15 mg/kg at P21 reverses carrageenan-induced hyperalgesia.	Carrageenan	86-97	KRAS proto-oncogene, GTPase	Rattus norvegicus	73-76
20526189-12	2010	CONCLUSIONS: The therapeutic ratio for intrathecal morphine (toxic dose/antinociceptive dose) was at least 300 at P3 and at least 20 at P21 (latter doses limited by side effects).	Morphine	51-59	KRAS proto-oncogene, GTPase	Rattus norvegicus	136-139
20553906-10	2010	EGCG significantly inhibited telomere attrition, TRF(2) loss and p53, p21 upregulation induced by H(2)O(2).	epigallocatechin gallate	0-4	KRAS proto-oncogene, GTPase	Rattus norvegicus	70-73
20553906-10	2010	EGCG significantly inhibited telomere attrition, TRF(2) loss and p53, p21 upregulation induced by H(2)O(2).	Water	98-103	KRAS proto-oncogene, GTPase	Rattus norvegicus	70-73
20522637-10	2010	Ex vivo, EFS-induced contractile responses increased significantly over time and were significantly reduced by atropine starting at P14 but were sensitive to l-NAME only after P21.	NG-Nitroarginine Methyl Ester	158-164	KRAS proto-oncogene, GTPase	Rattus norvegicus	176-179
20649565-8	2010	KEY RESULTS: Mycophenolic acid dose-dependently inhibited steady-state proliferation of 49F cells by up-regulation of p21, p27 and p53, in association with a decrease in cyclins D2 and E.	Mycophenolic Acid	13-30	KRAS proto-oncogene, GTPase	Rattus norvegicus	118-121
20429050-9	2010	Our data also showed both that EMs inhibited cell apoptosis and cell cycle G1 arrest induced by STZ and ALX through down-regulaing p53 and p21 expression.	Streptozocin	96-99	KRAS proto-oncogene, GTPase	Rattus norvegicus	139-142
20429050-9	2010	Our data also showed both that EMs inhibited cell apoptosis and cell cycle G1 arrest induced by STZ and ALX through down-regulaing p53 and p21 expression.	Alloxan	104-107	KRAS proto-oncogene, GTPase	Rattus norvegicus	139-142
20148315-3	2010	Ceramide can induce cell-cycle arrest by up-regulation of cyclin-dependent kinase (Cdk) inhibitors p21 and p27 through activation of protein phosphatase 2A (PP2A).	Ceramides	0-8	KRAS proto-oncogene, GTPase	Rattus norvegicus	99-102
20054021-2	2010	P21 is a cell cycle inhibitor that may be induced by oxygen-free radicals and may have a protective effect in ischaemic acute kidney injury (AKI).	oxygen-free radicals	53-73	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-3
20368687-9	2010	In contrast, knockdown of endogenous Egr-1 by small interference RNA attenuated CPZ-induced p21(Waf1/Cip1) promoter activity.	Chlorpromazine	80-83	KRAS proto-oncogene, GTPase	Rattus norvegicus	92-95
20368687-12	2010	Finally, stable silencing of Egr-1 expression lead to attenuated CPZ-inducible p21(Waf1/Cip1) expression and inhibited G2/M phase cell-cycle arrest.	Chlorpromazine	65-68	KRAS proto-oncogene, GTPase	Rattus norvegicus	79-82
20368687-13	2010	These results demonstrate that a functional link between ERK and JNK MAP kinase pathways and p21(Waf1/Cip1) induction via Egr-1 contributes to CPZ-induced anticancer activity in C6 glioma cells.	Chlorpromazine	143-146	KRAS proto-oncogene, GTPase	Rattus norvegicus	93-96
20112250-7	2010	PAs induced mutations in the cII gene of rat liver and in the p53 and K-ras genes of mouse liver tumors.	Pyrrolizidine Alkaloids	0-3	KRAS proto-oncogene, GTPase	Rattus norvegicus	70-75
20424134-8	2010	Methylselenocysteine also induced rhythmic expression of Trp53, p21, and Gadd45alpha mRNAs with peak levels at ZT12, when c-Myc expression was at its lowest level.	selenomethylselenocysteine	0-20	KRAS proto-oncogene, GTPase	Rattus norvegicus	64-67
20223627-14	2010	In VSMC, this inhibition was associated with an S-phase cell cycle arrest and increased expression of cyclin A, cyclin D1, and the cyclin-dependent kinase inhibitor p21.	vsmc	3-7	KRAS proto-oncogene, GTPase	Rattus norvegicus	165-168
20053955-7	2010	The p38 MAPK inhibitor 4-(4-flurophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)imidazole (SB203580) abolished the inhibitory effect of CORM-2 on PSC proliferation and prevented both CORM-2-induced HO-1 and p21(Waf1/Cip1) up-regulation.	4-(4-flurophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)imidazole	23-90	KRAS proto-oncogene, GTPase	Rattus norvegicus	208-211
20053955-7	2010	The p38 MAPK inhibitor 4-(4-flurophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)imidazole (SB203580) abolished the inhibitory effect of CORM-2 on PSC proliferation and prevented both CORM-2-induced HO-1 and p21(Waf1/Cip1) up-regulation.	SB 203580	92-100	KRAS proto-oncogene, GTPase	Rattus norvegicus	208-211
20053955-8	2010	Treatment with tin protoporphyrin IX, an HO inhibitor, or transfection of HO-1 small interfering RNA abolished the inductive effect of CORM-2 on p21(Waf1/Cip1) and reversed the suppressive effect of CORM-2 on PSC growth.	tin protoporphyrin IX	15-36	KRAS proto-oncogene, GTPase	Rattus norvegicus	145-148
20163460-7	2010	Like loss of HO-1, loss of p21(WAF1) through siRNA transfection also reversed the inhibitory effect of rosiglitazone on PASMC proliferation triggered by serotonin.	Rosiglitazone	103-116	KRAS proto-oncogene, GTPase	Rattus norvegicus	27-30
20361309-7	2010	KR62776 increased the levels of Gadd45, p27, p21 and PPARgamma proteins but decreased the cell cyclerelated proteins, such as cdk2, cyclin B and cyclin D1.	KR 62776	0-7	KRAS proto-oncogene, GTPase	Rattus norvegicus	45-48
20163460-6	2010	In addition, rosiglitazone stimulated p21(WAF1) expression in PASMCs, a 2.34-fold increase in the p21(WAF1) protein level being achieved with 5 microm rosiglitazone; again, this effect was blocked by knockdown of HO-1.	Rosiglitazone	13-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	38-41
20163460-6	2010	In addition, rosiglitazone stimulated p21(WAF1) expression in PASMCs, a 2.34-fold increase in the p21(WAF1) protein level being achieved with 5 microm rosiglitazone; again, this effect was blocked by knockdown of HO-1.	Rosiglitazone	13-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	98-101
20163460-7	2010	Like loss of HO-1, loss of p21(WAF1) through siRNA transfection also reversed the inhibitory effect of rosiglitazone on PASMC proliferation triggered by serotonin.	pasmc	120-125	KRAS proto-oncogene, GTPase	Rattus norvegicus	27-30
20163460-6	2010	In addition, rosiglitazone stimulated p21(WAF1) expression in PASMCs, a 2.34-fold increase in the p21(WAF1) protein level being achieved with 5 microm rosiglitazone; again, this effect was blocked by knockdown of HO-1.	pasmcs	62-68	KRAS proto-oncogene, GTPase	Rattus norvegicus	38-41
20163460-6	2010	In addition, rosiglitazone stimulated p21(WAF1) expression in PASMCs, a 2.34-fold increase in the p21(WAF1) protein level being achieved with 5 microm rosiglitazone; again, this effect was blocked by knockdown of HO-1.	pasmcs	62-68	KRAS proto-oncogene, GTPase	Rattus norvegicus	98-101
20163460-6	2010	In addition, rosiglitazone stimulated p21(WAF1) expression in PASMCs, a 2.34-fold increase in the p21(WAF1) protein level being achieved with 5 microm rosiglitazone; again, this effect was blocked by knockdown of HO-1.	Rosiglitazone	151-164	KRAS proto-oncogene, GTPase	Rattus norvegicus	38-41
20163460-7	2010	Like loss of HO-1, loss of p21(WAF1) through siRNA transfection also reversed the inhibitory effect of rosiglitazone on PASMC proliferation triggered by serotonin.	Serotonin	153-162	KRAS proto-oncogene, GTPase	Rattus norvegicus	27-30
20163460-6	2010	In addition, rosiglitazone stimulated p21(WAF1) expression in PASMCs, a 2.34-fold increase in the p21(WAF1) protein level being achieved with 5 microm rosiglitazone; again, this effect was blocked by knockdown of HO-1.	Rosiglitazone	151-164	KRAS proto-oncogene, GTPase	Rattus norvegicus	98-101
20163460-8	2010	Taken together, our findings suggest that activation of PPARgamma induces HO-1 expression, and that this in turn stimulates p21(WAF1) expression to suppress PASMC proliferation.	pasmc	157-162	KRAS proto-oncogene, GTPase	Rattus norvegicus	124-127
19923417-5	2010	Cell-cycle analysis indicated an arrest in G(0)/G(1) phase in response to TSA, which was accompanied by elevation in synthesis of the cyclin-dependent kinase inhibitors (CDKIs) p21/Waf1 and p27/Kip1.	trichostatin A	74-77	KRAS proto-oncogene, GTPase	Rattus norvegicus	177-180
19602127-1	2009	BACKGROUND AND OBJECTIVE: We reported previously that cyclosporine A induces a high level of expression of p21 in rat gingival keratinocytes and in OECM1 cells.	Cyclosporine	54-68	KRAS proto-oncogene, GTPase	Rattus norvegicus	107-110
19674922-10	2010	Both drugs suppressed GHBP in serum at P7 and P14; and liver at P4 and P7, but a rebound increase in serum GHBP was noted at P21 with Ibuprofen only.	ghbp	107-111	KRAS proto-oncogene, GTPase	Rattus norvegicus	125-128
20118535-3	2010	Hypothemycin normalized the morphology and inhibited anchorage-independent growth of Ki-ras transformed normal rat kidney (NRK) cells with selectivity and potency comparable to or greater than that of the MEK inhibitor U0126.	hypothemycin	0-12	KRAS proto-oncogene, GTPase	Rattus norvegicus	85-91
20118535-4	2010	In Ki-ras-transformed and phorbol 12-myristate 13-acetate (PMA)-treated NRK cells, hypothemycin blocked ERK activation but showed a minimal effect on autophosphorylation of protein kinase D1 (PKD1), another kinase containing the conserved cysteine.	hypothemycin	83-95	KRAS proto-oncogene, GTPase	Rattus norvegicus	3-9
20051375-9	2010	ACFs in rats treated with Frondanol A5 showed significant upregulation of p21(WAF1/CIP1) and downregulation of proliferating cell nuclear antigen compared with control group.	frondanol a5	26-38	KRAS proto-oncogene, GTPase	Rattus norvegicus	74-77
21472213-5	2010	In addition, incidences of Egfr and Kras gene mutations in rat and mouse lung tumors induced by the chemical carcinogens NNK, MeIQx and N-bis(2?hydroxypropyl)nitrosamine (DHPN) were examined.	2-amino-3,8-dimethylimidazo(4,5-f)quinoxaline	126-131	KRAS proto-oncogene, GTPase	Rattus norvegicus	36-40
21472213-5	2010	In addition, incidences of Egfr and Kras gene mutations in rat and mouse lung tumors induced by the chemical carcinogens NNK, MeIQx and N-bis(2?hydroxypropyl)nitrosamine (DHPN) were examined.	diisopropanolnitrosamine	171-175	KRAS proto-oncogene, GTPase	Rattus norvegicus	36-40
19808102-6	2009	Apamin blockade of SK calcium-dependent currents and iberiotoxin blockade of BK calcium-dependent currents in the P21 MD rat demonstrated reduced outward current due to dysfunction of these channels.	iberiotoxin	53-64	KRAS proto-oncogene, GTPase	Rattus norvegicus	114-117
19674922-9	2010	Indomethacin resulted in a sustained elevation in corticosterone levels at P21, while ibuprofen increased serum and hepatic GH levels.	Indomethacin	0-12	KRAS proto-oncogene, GTPase	Rattus norvegicus	75-78
19674922-9	2010	Indomethacin resulted in a sustained elevation in corticosterone levels at P21, while ibuprofen increased serum and hepatic GH levels.	Corticosterone	50-64	KRAS proto-oncogene, GTPase	Rattus norvegicus	75-78
19829098-6	2010	T11TS induces downregulation of the cyclin-D (1 and 3) expression with the concurrent upregulation of p21 and p27 and their concomitant association with cyclin-dependent kinase 4, proliferating cell nuclear antigen and cyclin E respectively leading to a decrease in cyclin-dependent kinase 4 kinase activity.	t11ts	0-5	KRAS proto-oncogene, GTPase	Rattus norvegicus	102-105
20023236-1	2009	This study was undertaken to investigate, by immunohistochemistry, the expression of some tumor suppressor genes such as p16, p21 and Retinoblastoma (Rb) during 4-Nitroquinoline 1-oxide induced rat tongue carcinogenesis.	4-Nitroquinoline-1-oxide	161-185	KRAS proto-oncogene, GTPase	Rattus norvegicus	126-129
19912332-3	2009	At all ages [postnatal day (P)8, P14, P21] the bAP-evoked calcium transient amplitude increased with distance from the soma with a peak at around 50 microm, followed by a gradual decline in amplitude.	benzylaminopurine	47-50	KRAS proto-oncogene, GTPase	Rattus norvegicus	38-41
19912332-3	2009	At all ages [postnatal day (P)8, P14, P21] the bAP-evoked calcium transient amplitude increased with distance from the soma with a peak at around 50 microm, followed by a gradual decline in amplitude.	Calcium	58-65	KRAS proto-oncogene, GTPase	Rattus norvegicus	38-41
19826045-10	2009	Rats that were fed the high-dose CP-31398 or a combination of low-dose CP-31398 and celecoxib showed considerable enhancement of p53 and p21(WAF1/CIP) expression, apoptosis, and reduced tumor cell proliferation in colonic tumors.	CP 31398	33-41	KRAS proto-oncogene, GTPase	Rattus norvegicus	137-140
19826045-10	2009	Rats that were fed the high-dose CP-31398 or a combination of low-dose CP-31398 and celecoxib showed considerable enhancement of p53 and p21(WAF1/CIP) expression, apoptosis, and reduced tumor cell proliferation in colonic tumors.	CP 31398	71-79	KRAS proto-oncogene, GTPase	Rattus norvegicus	137-140
19721228-5	2009	Real-time and Western blotting revealed that both p21 and p27 expression was markedly reduced by berberine.	Berberine	97-106	KRAS proto-oncogene, GTPase	Rattus norvegicus	50-53
19826045-10	2009	Rats that were fed the high-dose CP-31398 or a combination of low-dose CP-31398 and celecoxib showed considerable enhancement of p53 and p21(WAF1/CIP) expression, apoptosis, and reduced tumor cell proliferation in colonic tumors.	Celecoxib	84-93	KRAS proto-oncogene, GTPase	Rattus norvegicus	137-140
19585671-7	2009	Addition of parthenolide also increased cell population at G(0)/G(1) phase by 19.2%~65.7% (P<0.05) and decreased cell population at S phase by 50.7%~84.8% (P<0.05), which is consistent with its stimulatory effects on p21 and p27.	parthenolide	12-24	KRAS proto-oncogene, GTPase	Rattus norvegicus	223-226
19418558-9	2009	However, TbetaRI/pSmad3C/p21(WAF1) was impaired as DEN-induced HCC developed and progressed.	Diethylnitrosamine	51-54	KRAS proto-oncogene, GTPase	Rattus norvegicus	25-28
19343784-0	2009	Arecoline-induced phosphorylated p53 and p21(WAF1) protein expression is dependent on ATM/ATR and phosphatidylinositol-3-kinase in clone-9 cells.	Arecoline	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	41-44
19195022-11	2009	TB increased (p < 0.05) hepatic nuclear histone H3K9 hyperacetylation specifically in PNL and p21 protein expression, which could be associated with inhibitory HDAC effects.	tributyrin	0-2	KRAS proto-oncogene, GTPase	Rattus norvegicus	97-100
19418558-10	2009	The specific inhibition of JNK activity by SP600125 suppressed pSmad3L/c-Myc in the damaged hepatocytes and enhanced pSmad3C/p21(WAF1), acting as a tumor suppressor in normal hepatocytes.	pyrazolanthrone	43-51	KRAS proto-oncogene, GTPase	Rattus norvegicus	125-128
19343784-7	2009	ATM shRNA attenuated arecoline-induced p-p53Ser15 and p21(WAF1) at 24 h. Arecoline (0.5 mM) increased phosphorylation levels of p-AktSer473 and p-mTORSer2448 at 30-60 min.	Arecoline	21-30	KRAS proto-oncogene, GTPase	Rattus norvegicus	54-57
19343784-7	2009	ATM shRNA attenuated arecoline-induced p-p53Ser15 and p21(WAF1) at 24 h. Arecoline (0.5 mM) increased phosphorylation levels of p-AktSer473 and p-mTORSer2448 at 30-60 min.	Arecoline	73-82	KRAS proto-oncogene, GTPase	Rattus norvegicus	54-57
19343784-1	2009	Betel-quid use is associated with liver cancer whereas its constituent arecoline is cytotoxic, genotoxic, and induces p53-dependent p21(WAF1) protein expression in Clone-9 cells (rat hepatocytes).	Arecoline	71-80	KRAS proto-oncogene, GTPase	Rattus norvegicus	132-135
19343784-8	2009	Dominant-negative PI3K plasmids attenuated arecoline-induced p21(WAF1), but not p-p53Ser15, at 24 h. Rapamycin attenuated arecoline-induced phosphrylated p-p53Ser15, but not p21(WAF1), at 24 h. ATM shRNA, but not dominant-negative PI3K plasmids, attenuated arecoline-induced p21(WAF1) gene transcription.	Arecoline	43-52	KRAS proto-oncogene, GTPase	Rattus norvegicus	61-64
19343784-8	2009	Dominant-negative PI3K plasmids attenuated arecoline-induced p21(WAF1), but not p-p53Ser15, at 24 h. Rapamycin attenuated arecoline-induced phosphrylated p-p53Ser15, but not p21(WAF1), at 24 h. ATM shRNA, but not dominant-negative PI3K plasmids, attenuated arecoline-induced p21(WAF1) gene transcription.	Arecoline	43-52	KRAS proto-oncogene, GTPase	Rattus norvegicus	174-177
19343784-3	2009	Thus, we studied the role of ATM/ATR and PI3K in arecoline-induced p53 and p21(WAF1) protein expression in Clone-9 cells.	Arecoline	49-58	KRAS proto-oncogene, GTPase	Rattus norvegicus	75-78
19343784-8	2009	Dominant-negative PI3K plasmids attenuated arecoline-induced p21(WAF1), but not p-p53Ser15, at 24 h. Rapamycin attenuated arecoline-induced phosphrylated p-p53Ser15, but not p21(WAF1), at 24 h. ATM shRNA, but not dominant-negative PI3K plasmids, attenuated arecoline-induced p21(WAF1) gene transcription.	Arecoline	43-52	KRAS proto-oncogene, GTPase	Rattus norvegicus	174-177
19233274-2	2009	PTU was administered from birth to postnatal day 10 (P10) or P21, leading to decreased neural stem cell/progenitor proliferation in the dentate gyrus, as well as significantly fewer granule cells and reduced hippocampal volume.	Propylthiouracil	0-3	KRAS proto-oncogene, GTPase	Rattus norvegicus	61-64
19343784-8	2009	Dominant-negative PI3K plasmids attenuated arecoline-induced p21(WAF1), but not p-p53Ser15, at 24 h. Rapamycin attenuated arecoline-induced phosphrylated p-p53Ser15, but not p21(WAF1), at 24 h. ATM shRNA, but not dominant-negative PI3K plasmids, attenuated arecoline-induced p21(WAF1) gene transcription.	Sirolimus	101-110	KRAS proto-oncogene, GTPase	Rattus norvegicus	61-64
19343784-8	2009	Dominant-negative PI3K plasmids attenuated arecoline-induced p21(WAF1), but not p-p53Ser15, at 24 h. Rapamycin attenuated arecoline-induced phosphrylated p-p53Ser15, but not p21(WAF1), at 24 h. ATM shRNA, but not dominant-negative PI3K plasmids, attenuated arecoline-induced p21(WAF1) gene transcription.	Sirolimus	101-110	KRAS proto-oncogene, GTPase	Rattus norvegicus	174-177
19343784-8	2009	Dominant-negative PI3K plasmids attenuated arecoline-induced p21(WAF1), but not p-p53Ser15, at 24 h. Rapamycin attenuated arecoline-induced phosphrylated p-p53Ser15, but not p21(WAF1), at 24 h. ATM shRNA, but not dominant-negative PI3K plasmids, attenuated arecoline-induced p21(WAF1) gene transcription.	Sirolimus	101-110	KRAS proto-oncogene, GTPase	Rattus norvegicus	174-177
19343784-8	2009	Dominant-negative PI3K plasmids attenuated arecoline-induced p21(WAF1), but not p-p53Ser15, at 24 h. Rapamycin attenuated arecoline-induced phosphrylated p-p53Ser15, but not p21(WAF1), at 24 h. ATM shRNA, but not dominant-negative PI3K plasmids, attenuated arecoline-induced p21(WAF1) gene transcription.	Arecoline	122-131	KRAS proto-oncogene, GTPase	Rattus norvegicus	174-177
19343784-8	2009	Dominant-negative PI3K plasmids attenuated arecoline-induced p21(WAF1), but not p-p53Ser15, at 24 h. Rapamycin attenuated arecoline-induced phosphrylated p-p53Ser15, but not p21(WAF1), at 24 h. ATM shRNA, but not dominant-negative PI3K plasmids, attenuated arecoline-induced p21(WAF1) gene transcription.	Arecoline	122-131	KRAS proto-oncogene, GTPase	Rattus norvegicus	174-177
19343784-8	2009	Dominant-negative PI3K plasmids attenuated arecoline-induced p21(WAF1), but not p-p53Ser15, at 24 h. Rapamycin attenuated arecoline-induced phosphrylated p-p53Ser15, but not p21(WAF1), at 24 h. ATM shRNA, but not dominant-negative PI3K plasmids, attenuated arecoline-induced p21(WAF1) gene transcription.	Arecoline	122-131	KRAS proto-oncogene, GTPase	Rattus norvegicus	174-177
19343784-8	2009	Dominant-negative PI3K plasmids attenuated arecoline-induced p21(WAF1), but not p-p53Ser15, at 24 h. Rapamycin attenuated arecoline-induced phosphrylated p-p53Ser15, but not p21(WAF1), at 24 h. ATM shRNA, but not dominant-negative PI3K plasmids, attenuated arecoline-induced p21(WAF1) gene transcription.	Arecoline	122-131	KRAS proto-oncogene, GTPase	Rattus norvegicus	174-177
19343784-9	2009	We conclude that arecoline activates the ATM/ATR-p53-p21(WAF1) and the PI3K/Akt-mTOR-p53 pathways in Clone-9 cells.	Arecoline	17-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	53-56
19343784-10	2009	Arecoline-induced phosphorylated p-p53Ser15 expression is dependent on ATM whereas arecoline-induced p21(WAF1) protein expression is dependent on ATM and PI3K.	Arecoline	83-92	KRAS proto-oncogene, GTPase	Rattus norvegicus	101-104
19343784-11	2009	Moreover, p21(WAF1) gene is transcriptionally induced by arecoline-activated ATM.	Arecoline	57-66	KRAS proto-oncogene, GTPase	Rattus norvegicus	10-13
19171550-9	2009	Immunoblot analyses revealed that FA2H silencing prevented db-cAMP-induced upregulation of cyclin-dependent kinase inhibitors p21 and p27.	Bucladesine	59-66	KRAS proto-oncogene, GTPase	Rattus norvegicus	126-129
19164802-6	2009	Moreover, treatment of VSMCs with BEC or L-OHNA, or knockdown of arginase I protein, arrested cells in the G(0)/G(1) phase of the cell cycle and induced the expression of the cyclin-dependent protein kinase inhibitor, p21.	vsmcs	23-28	KRAS proto-oncogene, GTPase	Rattus norvegicus	218-221
19154760-6	2009	In addition, carnosine could reverse high glucose-induced down-regulation of cyclin-dependent kinase inhibitor p21 but not that of p27.	Glucose	42-49	KRAS proto-oncogene, GTPase	Rattus norvegicus	111-114
19164802-6	2009	Moreover, treatment of VSMCs with BEC or L-OHNA, or knockdown of arginase I protein, arrested cells in the G(0)/G(1) phase of the cell cycle and induced the expression of the cyclin-dependent protein kinase inhibitor, p21.	(2-boronoethyl)-cysteine	34-37	KRAS proto-oncogene, GTPase	Rattus norvegicus	218-221
19956429-11	2009	Levels of expression of cyclin D1, p21, cleaved PARP, and cleaved caspase 3 proteins indicated the presence of cell cycle arrest and apoptosis following NaB treatment.	nab	153-156	KRAS proto-oncogene, GTPase	Rattus norvegicus	35-38
19292920-12	2009	The cyclin dependent kinase inhibitors p21 and p27 responded differently to GLA, p27 expression was increased (27 +/- 7.3%) while p21 remained unchanged.	gamma-Linolenic Acid	76-79	KRAS proto-oncogene, GTPase	Rattus norvegicus	39-42
19292920-12	2009	The cyclin dependent kinase inhibitors p21 and p27 responded differently to GLA, p27 expression was increased (27 +/- 7.3%) while p21 remained unchanged.	gamma-Linolenic Acid	76-79	KRAS proto-oncogene, GTPase	Rattus norvegicus	130-133
18847333-8	2009	EtOH also transactivated the luciferase activity of the p21 promoter region independent of additional exogenous ERalpha, activated p21 and p53, and stimulated senescence-associated beta-galactosidase activity in rat stromal osteoblasts.	Ethanol	0-4	KRAS proto-oncogene, GTPase	Rattus norvegicus	56-59
18847333-8	2009	EtOH also transactivated the luciferase activity of the p21 promoter region independent of additional exogenous ERalpha, activated p21 and p53, and stimulated senescence-associated beta-galactosidase activity in rat stromal osteoblasts.	Ethanol	0-4	KRAS proto-oncogene, GTPase	Rattus norvegicus	131-134
18847333-10	2009	We conclude that inhibitory cross-talk between EtOH and E2 in osteoblasts on ERs, p53/p21, and cell senescence provides a pathophysiologic mechanism underlying bone loss and the protective effects of estrogens in alcohol-exposed females.	Ethanol	47-51	KRAS proto-oncogene, GTPase	Rattus norvegicus	86-89
19224154-3	2009	The expression of P21 and P27 in preadipocytes treated with diazoxide or glibenclamide was assayed by Western blot.	Diazoxide	60-69	KRAS proto-oncogene, GTPase	Rattus norvegicus	18-21
19224154-3	2009	The expression of P21 and P27 in preadipocytes treated with diazoxide or glibenclamide was assayed by Western blot.	Glyburide	73-86	KRAS proto-oncogene, GTPase	Rattus norvegicus	18-21
19224154-5	2009	After treatment of preadipocytes with diazoxide, the expression levels of P21 and P27 were obviously higher than those in control group, but the expression levels of P21 and P27 in glibenclamide-treated group were lower than those in control group.	Diazoxide	38-47	KRAS proto-oncogene, GTPase	Rattus norvegicus	74-77
19224154-5	2009	After treatment of preadipocytes with diazoxide, the expression levels of P21 and P27 were obviously higher than those in control group, but the expression levels of P21 and P27 in glibenclamide-treated group were lower than those in control group.	Diazoxide	38-47	KRAS proto-oncogene, GTPase	Rattus norvegicus	166-169
19224154-5	2009	After treatment of preadipocytes with diazoxide, the expression levels of P21 and P27 were obviously higher than those in control group, but the expression levels of P21 and P27 in glibenclamide-treated group were lower than those in control group.	Glyburide	181-194	KRAS proto-oncogene, GTPase	Rattus norvegicus	166-169
19037103-4	2009	Expression of K-Ras resulted in extracellular signal-regulated kinase (ERK) activation, which mediated induction of cyclooxygenase (COX)-2 and increased prostaglandin E(2) production.	Dinoprostone	153-171	KRAS proto-oncogene, GTPase	Rattus norvegicus	14-19
20192116-6	2009	mRNA expression of p21 and p27 was determined in vitro at 100 and 150 microM of fatty acids and in tumors of rats supplemented with LA or DHA oils.	Fatty Acids	80-91	KRAS proto-oncogene, GTPase	Rattus norvegicus	19-22
20192116-6	2009	mRNA expression of p21 and p27 was determined in vitro at 100 and 150 microM of fatty acids and in tumors of rats supplemented with LA or DHA oils.	dha oils	138-146	KRAS proto-oncogene, GTPase	Rattus norvegicus	19-22
20192116-7	2009	In vitro, DHA, but not LA, had cytotoxic effect on C6 cells at 200 and 400 microM and DHA increased mRNA expression of p21 at 150 microM (p < 0.05).	Docosahexaenoic Acids	86-89	KRAS proto-oncogene, GTPase	Rattus norvegicus	119-122
20192116-9	2009	p21 and p27 mRNA expression in tumors of DHA oil group did not differ with LA oil group.	dha oil	41-48	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-3
18779944-0	2008	Lovastatin induces apoptosis of k-ras-transformed thyroid cells via inhibition of ras farnesylation and by modulating redox state.	Lovastatin	0-10	KRAS proto-oncogene, GTPase	Rattus norvegicus	32-37
18779944-3	2008	In FRTL-5-K-Ras cells, the product of K-ras gene is implicated in the scavenging of reactive oxygen species (ROS) through the activation of extracellular-signal-regulated kinase (ERK)1/2 kinases.	Reactive Oxygen Species	84-107	KRAS proto-oncogene, GTPase	Rattus norvegicus	10-15
19105244-9	2008	Rapamycin also inhibited betacellulin- and IGF-I-induced entry of cells into S phase and 5"-Bromo-2"-deoxyuridine incorporation as well as the effect of betacellulin and IGF-I on cyclin D1 expression and nuclear exclusion of p21(Cip1) and p(27Kip1).	Sirolimus	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	225-228
18779944-3	2008	In FRTL-5-K-Ras cells, the product of K-ras gene is implicated in the scavenging of reactive oxygen species (ROS) through the activation of extracellular-signal-regulated kinase (ERK)1/2 kinases.	Reactive Oxygen Species	84-107	KRAS proto-oncogene, GTPase	Rattus norvegicus	38-43
18779944-3	2008	In FRTL-5-K-Ras cells, the product of K-ras gene is implicated in the scavenging of reactive oxygen species (ROS) through the activation of extracellular-signal-regulated kinase (ERK)1/2 kinases.	Reactive Oxygen Species	109-112	KRAS proto-oncogene, GTPase	Rattus norvegicus	10-15
18779944-3	2008	In FRTL-5-K-Ras cells, the product of K-ras gene is implicated in the scavenging of reactive oxygen species (ROS) through the activation of extracellular-signal-regulated kinase (ERK)1/2 kinases.	Reactive Oxygen Species	109-112	KRAS proto-oncogene, GTPase	Rattus norvegicus	38-43
18779944-7	2008	Lovastatin antitumor efficacy in K-ras-dependent thyroid tumors was further confirmed in vivo, proposing a new therapeutic strategy for those tumor diseases that are sustained by an inappropriate K-ras expression.	Lovastatin	0-10	KRAS proto-oncogene, GTPase	Rattus norvegicus	33-38
18779944-7	2008	Lovastatin antitumor efficacy in K-ras-dependent thyroid tumors was further confirmed in vivo, proposing a new therapeutic strategy for those tumor diseases that are sustained by an inappropriate K-ras expression.	Lovastatin	0-10	KRAS proto-oncogene, GTPase	Rattus norvegicus	196-201
18824008-4	2008	We used statistical analyses to search for sets of dinucleotide sequences (designated target sequences) that are present at and in close proximity to mutation sites in four genes associated with human colorectal tumourigenesis (adenomatosis polyposis coli (APC), v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS), phosphoinositide-3-kinase, catalytic, alpha polypeptide (PIK3CA), and tumour protein p53 (TP53)).	Dinucleoside Phosphates	51-63	KRAS proto-oncogene, GTPase	Rattus norvegicus	317-321
18784252-5	2008	The first, which corresponds to nanoclusters occupied by GTP-loaded H-, N- or K-Ras, supports Raf activation and amplifies low Raf kinase input to generate a digital ERKpp output.	Guanosine Triphosphate	57-60	KRAS proto-oncogene, GTPase	Rattus norvegicus	78-83
18680741-7	2008	S-diclofenac treatment also resulted in stabilization of p53 coupled with the induction of downstream proteins such as p21, p53AIP1 and Bax.	Diclofenac	2-12	KRAS proto-oncogene, GTPase	Rattus norvegicus	119-122
18264122-7	2008	CONCLUSIONS AND IMPLICATIONS: There was over-activity of the hexosamine pathway in MCGT1 cells, which may explain the higher expression of TGF-beta1 and p21, the cellular hypertrophy and the increased expression of extracellular matrix (ECM) components in the cells.	Hexosamines	61-71	KRAS proto-oncogene, GTPase	Rattus norvegicus	153-156
18503560-9	2008	At P14 and P21, but not at P35, pretreatment with RTG prevented the establishment of kindling-induced enhanced seizure susceptibility.	ezogabine	50-53	KRAS proto-oncogene, GTPase	Rattus norvegicus	11-14
18621849-14	2008	Changes in the levels of p21 and ROS might also participate in the cellular effects of hemin.	Hemin	87-92	KRAS proto-oncogene, GTPase	Rattus norvegicus	25-28
18295995-4	2008	We found that LiPC induced SE resulted in ceramide increases and DNA fragmentation in the hippocampus of adult, P21, and P7 rats.	lipc	14-18	KRAS proto-oncogene, GTPase	Rattus norvegicus	112-115
18454179-2	2008	Here we describe that ablation of the Nox1 activity by Nox1 small-interference RNAs (siRNAs) or diphenylene iodonium (DPI) inhibited synthesis of both VEGF proteins and VEGF mRNAs in K-Ras transformed normal rat kidney (KNRK) cells.	diphenyleneiodonium	96-116	KRAS proto-oncogene, GTPase	Rattus norvegicus	183-188
18567619-5	2008	AOM injection repressed p21 expression, which was reversed by butyrate supplementation.	Butyrates	62-70	KRAS proto-oncogene, GTPase	Rattus norvegicus	24-27
18567619-6	2008	Although butyrate enhanced p21 expression with both dietary lipid sources, the increase in p21 resulted in an increase in apoptosis and decrease in ACF with fish oil, but had no effect on apoptosis and increased ACF with corn oil.	Butyrates	9-17	KRAS proto-oncogene, GTPase	Rattus norvegicus	27-30
18486258-13	2008	Doxorubicin stimulated p21 expression and the phosphorylation of MAPKAP kinase-2 in endothelial cells.	Doxorubicin	0-11	KRAS proto-oncogene, GTPase	Rattus norvegicus	23-26
18058808-5	2008	18.K-Ras(V12) cells exhibited increased phosphorylation of MAP kinases and CREB, proliferation rates, COX-2 and microsomal prostaglandin E synthase (mPGES)-1 expression and PGE(2) and PGI(2) levels.	Prostaglandins E	150-153	KRAS proto-oncogene, GTPase	Rattus norvegicus	3-12
18058808-5	2008	18.K-Ras(V12) cells exhibited increased phosphorylation of MAP kinases and CREB, proliferation rates, COX-2 and microsomal prostaglandin E synthase (mPGES)-1 expression and PGE(2) and PGI(2) levels.	Prostaglandins I	184-187	KRAS proto-oncogene, GTPase	Rattus norvegicus	3-12
18395440-8	2008	We found a G(1) cell cycle arrest mediated by an increase of cyclin/cyclin-dependent kinase inhibitor p21(WAF1/CIP1) protein after dexamethasone treatment and incremental change in amyloid beta protein and glutamate toxicity.	Dexamethasone	131-144	KRAS proto-oncogene, GTPase	Rattus norvegicus	102-105
18395440-8	2008	We found a G(1) cell cycle arrest mediated by an increase of cyclin/cyclin-dependent kinase inhibitor p21(WAF1/CIP1) protein after dexamethasone treatment and incremental change in amyloid beta protein and glutamate toxicity.	Glutamic Acid	206-215	KRAS proto-oncogene, GTPase	Rattus norvegicus	102-105
18263706-0	2008	HSP27 regulates p53 transcriptional activity in doxorubicin-treated fibroblasts and cardiac H9c2 cells: p21 upregulation and G2/M phase cell cycle arrest.	Doxorubicin	48-59	KRAS proto-oncogene, GTPase	Rattus norvegicus	104-107
18263706-8	2008	Moreover, upregulation of p21 was observed in HSF-1(+/+) and H9c2 cells, indicating that HSP27 binding transactivates p53 and enhances transcription of p21 in response to Dox treatment.	Doxorubicin	171-174	KRAS proto-oncogene, GTPase	Rattus norvegicus	26-29
18263706-8	2008	Moreover, upregulation of p21 was observed in HSF-1(+/+) and H9c2 cells, indicating that HSP27 binding transactivates p53 and enhances transcription of p21 in response to Dox treatment.	Doxorubicin	171-174	KRAS proto-oncogene, GTPase	Rattus norvegicus	152-155
18263706-9	2008	Further analysis with flow cytometry showed that increased expression of p21 results in G(2)/M phase cell cycle arrest in Dox-treated cells.	Doxorubicin	122-125	KRAS proto-oncogene, GTPase	Rattus norvegicus	73-76
18264122-8	2008	By inhibiting the increased activity the hexosamine pathway, rhein decreased TGF-beta1 and p21 expression and thus contributed to the decreased cellular hypertrophy and ECM synthesis.	Hexosamines	41-51	KRAS proto-oncogene, GTPase	Rattus norvegicus	91-94
18336467-0	2008	p21(Cip1) expression is increased in ambient oxygen, compared to estimated physiological (5%) levels in rat muscle precursor cell culture.	Oxygen	45-51	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-3
18336467-3	2008	In the present study, we hypothesized that 20% O2 in culture represents a sufficient stimulus to cause increased expression of two key negative regulators of the cell-cycle Cip/Kip family of cyclin-dependent kinase inhibitors, p21(Cip1) and p27(Kip1), in MPCs.	Oxygen	47-49	KRAS proto-oncogene, GTPase	Rattus norvegicus	227-230
17996031-7	2008	Ten-day treatment with either drug increased dopamine utilization in the neostriatum on P21, whereas 5-day treatment had no effect.	Dopamine	45-53	KRAS proto-oncogene, GTPase	Rattus norvegicus	88-91
18336467-8	2008	Furthermore, 20% O2 caused an increase in p21(Cip1) mRNA stability and p53 transcription factor activity.	Oxygen	17-19	KRAS proto-oncogene, GTPase	Rattus norvegicus	42-45
17882567-5	2007	RESULTS: Chromanol 293B, a blocker of KCNQ1/KCNE1 K(+) channel, inhibited short-circuit currents (I ( sc )) from P1 to P21.	2,2,5,7,8-pentamethyl-1-hydroxychroman	9-18	KRAS proto-oncogene, GTPase	Rattus norvegicus	119-122
17847023-0	2008	K-ras mutations and mucin profile in preneoplastic lesions and colon tumors induced in rats by 1,2-dimethylhydrazine.	1,2-Dimethylhydrazine	95-116	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-5
17976369-4	2007	We found that FAK Tyr-407 phosphorylation was lower in H-Ras transformed NIH3T3 and K-Ras transformed rat-2 fibroblasts than in the respective untransformed control cells.	Tyrosine	18-21	KRAS proto-oncogene, GTPase	Rattus norvegicus	84-89
18230104-0	2008	Expression of p21 and p53 in rat gingival and human oral epithelial cells after cyclosporine A treatment.	Cyclosporine	80-94	KRAS proto-oncogene, GTPase	Rattus norvegicus	14-17
18230104-1	2008	BACKGROUND AND OBJECTIVE: Expression of p21 and p53 were examined, at gene and protein levels, in edentulous gingival epithelial cells from rats and from a human oral epidermoid carcinoma cell line, OECM1, after cyclosporine A therapy.	Cyclosporine	212-226	KRAS proto-oncogene, GTPase	Rattus norvegicus	40-43
17997002-6	2008	Arecoline (0.5mM) also increased p21(WAF1) protein expression and p21(WAF1) gene transcription.	Arecoline	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	33-36
17997002-6	2008	Arecoline (0.5mM) also increased p21(WAF1) protein expression and p21(WAF1) gene transcription.	Arecoline	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	66-69
17997002-8	2008	Pifithrin-alpha (p53 inhibitor) and the loss of the two p53-binding elements in the p21(WAF1) gene promoter attenuated arecoline-induced p21(WAF1) gene transcription at 24h.	Arecoline	119-128	KRAS proto-oncogene, GTPase	Rattus norvegicus	84-87
17997002-8	2008	Pifithrin-alpha (p53 inhibitor) and the loss of the two p53-binding elements in the p21(WAF1) gene promoter attenuated arecoline-induced p21(WAF1) gene transcription at 24h.	Arecoline	119-128	KRAS proto-oncogene, GTPase	Rattus norvegicus	137-140
17997002-10	2008	We concluded that arecoline induces cytotoxicity, DNA damage, G(0)/G(1) cell cycle arrest, TGF-beta1, p21(WAF1) and activates p53 in Clone-9 cells.	Arecoline	18-27	KRAS proto-oncogene, GTPase	Rattus norvegicus	102-105
17997002-11	2008	Moreover, arecoline-induced p21(WAF1) is dependent on p53 while arecoline-inhibited growth is dependent on both TGF-beta and p53.	Arecoline	10-19	KRAS proto-oncogene, GTPase	Rattus norvegicus	28-31
17654247-6	2007	Results showed that the levels of pRB, cyclin D, CDK2, cyclin E, and CDK4 were significantly lower in rats given 500 and 750 mg/kg/d DEHP, while levels of p21 were significantly higher in rat testes.	Diethylhexyl Phthalate	133-137	KRAS proto-oncogene, GTPase	Rattus norvegicus	155-158
17698922-7	2007	Small interfering RNA (siRNA) knockdown of K-Ras but not Rac1 abolished PtdIns(3,4,5)P(3) production at the leading edge and inhibited EGF-stimulated protrusion.	phosphatidylinositol 3,4,5-triphosphate	72-89	KRAS proto-oncogene, GTPase	Rattus norvegicus	43-48
17554252-6	2007	Calcitriol treatment upregulated the PTH/PTHrP receptor but also increased inhibitors of cell proliferation such as p21(Waf1/Cip1), IGFBP3, and FGFR3.	Calcitriol	0-10	KRAS proto-oncogene, GTPase	Rattus norvegicus	116-119
16916990-3	2006	We combined OCEAN with peptide-nucleic-acid (PNA)-based variant enrichment to detect and simultaneously genotype v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) codon 12 sequence variants in human tissue specimens.	ocean	12-17	KRAS proto-oncogene, GTPase	Rattus norvegicus	167-171
17462539-5	2007	NAC is shown to decrease glioma cell proliferation, inducing a cell cycle arrest in the G(0)/G(1) phase and markedly up-regulating p21 expression.	Acetylcysteine	0-3	KRAS proto-oncogene, GTPase	Rattus norvegicus	131-134
17439406-15	2007	In addition, EDDF inhibited the phosphorylation of ERK1/2 and decreased the expression of cyclin D1 and CDK4; p21 (Cip1) levels were increased after treatment with EDDF.	eddf	13-17	KRAS proto-oncogene, GTPase	Rattus norvegicus	110-113
17439406-15	2007	In addition, EDDF inhibited the phosphorylation of ERK1/2 and decreased the expression of cyclin D1 and CDK4; p21 (Cip1) levels were increased after treatment with EDDF.	eddf	164-168	KRAS proto-oncogene, GTPase	Rattus norvegicus	110-113
17487067-0	2007	Differential protection and transactivation of P53, P21, Bcl2, PCNA, cyclin G, and MDM2 genes in rat liver and the HepG2 cell line upon exposure to pifithrin.	pifithrin	148-157	KRAS proto-oncogene, GTPase	Rattus norvegicus	52-55
17487067-11	2007	PFT-alpha inhibited the transactivation of p53 in rat liver cells and resulted in repression of Bcl2, PCNA, MDM2, Cyclin G and P21 genes by arsenic trioxide.	Arsenic Trioxide	140-156	KRAS proto-oncogene, GTPase	Rattus norvegicus	127-130
16916940-4	2006	In the FRTL-5 rat cell line, cAMP cross-signals with transduction pathways of growth factors to induce cyclin D1 and p21(cip1) and down-regulate p27(kip1).	Cyclic AMP	29-33	KRAS proto-oncogene, GTPase	Rattus norvegicus	117-120
16876216-8	2006	5-Aza-deoxycytidine restored the loss of expression of p21 in CAsE cells to control levels, but did not restore the expression of p16, IGF-II, or FGFR1, indicating the loss of expression of these genes is due to factors other than DNA methylation changes.	Decitabine	0-19	KRAS proto-oncogene, GTPase	Rattus norvegicus	55-58
17603281-5	2007	The antiproliferative effect of curcumin in VSMCs was accompanied by the increased expression of p21(WAF1/CIP1).	Curcumin	32-40	KRAS proto-oncogene, GTPase	Rattus norvegicus	97-100
17603281-6	2007	Inhibition of VSMC growth and expression of p21(WAF1/CIP1) by curcumin were partially, but not completely, abolished when the cells were co- incubated with the HO inhibitor tin protoporphyrin.	Curcumin	62-70	KRAS proto-oncogene, GTPase	Rattus norvegicus	44-47
17603281-6	2007	Inhibition of VSMC growth and expression of p21(WAF1/CIP1) by curcumin were partially, but not completely, abolished when the cells were co- incubated with the HO inhibitor tin protoporphyrin.	tin protoporphyrin IX	173-191	KRAS proto-oncogene, GTPase	Rattus norvegicus	44-47
16875883-7	2007	An examination of the suppressive effects of NQ304 on PDGF-BB-stimulated VSMC cycle progression showed that NQ304 (10 microM) induced the G1 phase arrest of PDGF-BB-stimulated cell cycle progression by elevating p21(cip1) mRNA expression.	NQ304	108-113	KRAS proto-oncogene, GTPase	Rattus norvegicus	212-215
17012303-0	2006	ACB-PCR measurement of K-ras codon 12 mutant fractions in livers of Big Blue rats treated with N-hydroxy-2-acetylaminofluorene.	Hydroxyacetylaminofluorene	95-126	KRAS proto-oncogene, GTPase	Rattus norvegicus	23-28
17012303-9	2006	This data raises the possibility that N-OH-AAF may not only induce mutations by a genotoxic mechanism, but also by amplification of both de novo and pre-existing K-ras mutation.	n-oh-aaf	38-46	KRAS proto-oncogene, GTPase	Rattus norvegicus	162-167
16809631-8	2006	Maximum tetanic tension was lower for the AR group at P21 and P41-2 compared with their dam-reared counterparts.	Argon	42-44	KRAS proto-oncogene, GTPase	Rattus norvegicus	54-57
16916990-3	2006	We combined OCEAN with peptide-nucleic-acid (PNA)-based variant enrichment to detect and simultaneously genotype v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) codon 12 sequence variants in human tissue specimens.	Peptide Nucleic Acids	23-43	KRAS proto-oncogene, GTPase	Rattus norvegicus	167-171
16712893-0	2006	The farnesyltransferase inhibitor, LB42708, inhibits growth and induces apoptosis irreversibly in H-ras and K-ras-transformed rat intestinal epithelial cells.	LB42708	35-42	KRAS proto-oncogene, GTPase	Rattus norvegicus	108-113
17062926-3	2006	The expression of P21 in renal tubular epithelial cells on the process was detected by immunohistochemistry at different time spots (7, 14, 21 d after UUO, sham-surgery or enalapril treatment).	Enalapril	172-181	KRAS proto-oncogene, GTPase	Rattus norvegicus	18-21
16901471-7	2006	p53 activation by H2O2 was evidenced by elevated Ser15 phosphorylation, increased luciferase p53 reporter activity and upregulation of the downstream p53 targets p21(waf1) and apoptotic proteins, bax, Noxa and PUMA.	Hydrogen Peroxide	18-22	KRAS proto-oncogene, GTPase	Rattus norvegicus	162-165
16908950-0	2006	Trichostatin A, an inhibitor of histone deacetylase, inhibits smooth muscle cell proliferation via induction of p21(WAF1).	trichostatin A	0-14	KRAS proto-oncogene, GTPase	Rattus norvegicus	112-115
16797887-6	2006	The arsenite-injection markedly increased the phosphorylated forms of c-Jun and ATF-2 and the protein levels of c-Jun, p53 and p21(WAF1/CIP1) in the partially hepatectomized liver.	arsenite	4-12	KRAS proto-oncogene, GTPase	Rattus norvegicus	127-130
16797887-7	2006	These results suggested that arsenite induced apoptosis in the hepatocytes in vivo, through the enhancement of the activation of JNK and p38 MAPK caused by partial hepatectomy and the p53-dependent p21(WAF1/CIP1) protein expression.	arsenite	29-37	KRAS proto-oncogene, GTPase	Rattus norvegicus	198-201
16794187-7	2006	In rats, treatment with 2-ME abrogated injury-induced neointima formation; decreased proliferating SMCs; downregulated expression of proliferating-cell nuclear antigen (PCNA), c-myc, cyclin D(1), cyclin B(1), phosphorylated Akt, phosphorylated ERK1/2, p21, and pRb; inhibited cdk-1 and cdk-4 activity; and upregulated expression of cyclooxygenase (COX)-2 and p27.	2-Methoxyestradiol	24-28	KRAS proto-oncogene, GTPase	Rattus norvegicus	252-255
16908950-7	2006	TSA treatment also induced the expression of p21(WAF1) but not of p16(INK4), p27(KIP1) or p53.	trichostatin A	0-3	KRAS proto-oncogene, GTPase	Rattus norvegicus	45-48
16908950-9	2006	In conclusion, TSA inhibits VSMC proliferation via the induction of p21(WAF1) expression and subsequent cell-cycle arrest with reduction of the phosphorylation of Rb protein at the G1-S phase.	trichostatin A	15-18	KRAS proto-oncogene, GTPase	Rattus norvegicus	68-71
16730872-5	2006	Further investigation into the mechanism revealed that Cd treatment led to down-modulation of cyclin-dependent kinases, Cdk1 and Cdk2, apparently by elevating the expression of cyclin kinase inhibitors, KIP1/p27 and WAF1/p21.	Cadmium	55-57	KRAS proto-oncogene, GTPase	Rattus norvegicus	221-224
16730872-7	2006	Based on these observations, it appears that Cd causes G2/M phase arrest in NRK-52E cells via elevation of p53 activity, increasing the expression of cyclin kinase inhibitors p27 and p21, and decreasing the expression of cyclin-dependent kinases Cdk1 and 2, and of cyclins A and B.	Cadmium	45-47	KRAS proto-oncogene, GTPase	Rattus norvegicus	183-186
16438962-6	2006	Our data suggest that IL-1beta (10 ng/ml) causes an enhancement of U46619-mediated basilar artery contraction that probably involves TTX-sensitive neuronal release of an alpha1-adrenoceptor agonist and activation of p42/p44 and p38 mitogen-activated protein kinases/p21(ras) pathways.	15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid	67-73	KRAS proto-oncogene, GTPase	Rattus norvegicus	266-269
16467127-0	2006	Inhibition of p21 modifies the response of cortical proximal tubules to cisplatin in rats.	Cisplatin	72-81	KRAS proto-oncogene, GTPase	Rattus norvegicus	14-17
16467127-1	2006	The purpose of this study was to evaluate whether upregulated p21, a cell cycle-inhibitory protein, contributes to cisplatin (CDDP)-induced acute renal failure (ARF) and to acquired resistance to rechallenge injury with CDDP in rats.	Cisplatin	115-124	KRAS proto-oncogene, GTPase	Rattus norvegicus	62-65
16467127-1	2006	The purpose of this study was to evaluate whether upregulated p21, a cell cycle-inhibitory protein, contributes to cisplatin (CDDP)-induced acute renal failure (ARF) and to acquired resistance to rechallenge injury with CDDP in rats.	Cisplatin	126-130	KRAS proto-oncogene, GTPase	Rattus norvegicus	62-65
16467127-1	2006	The purpose of this study was to evaluate whether upregulated p21, a cell cycle-inhibitory protein, contributes to cisplatin (CDDP)-induced acute renal failure (ARF) and to acquired resistance to rechallenge injury with CDDP in rats.	Cisplatin	220-224	KRAS proto-oncogene, GTPase	Rattus norvegicus	62-65
16467127-3	2006	Rats were treated with p21 antisense oligodeoxynucleotide (ODN) or its vehicle, p21 sense ODN, every 36 h from days 0 to 5 for single CDDP and from days 13 to 19 for rechallenge injury and killed at day 3, 5, 16, or 19.	Oligodeoxyribonucleotides	37-57	KRAS proto-oncogene, GTPase	Rattus norvegicus	23-26
16467127-3	2006	Rats were treated with p21 antisense oligodeoxynucleotide (ODN) or its vehicle, p21 sense ODN, every 36 h from days 0 to 5 for single CDDP and from days 13 to 19 for rechallenge injury and killed at day 3, 5, 16, or 19.	Oligodeoxyribonucleotides	59-62	KRAS proto-oncogene, GTPase	Rattus norvegicus	23-26
16467127-4	2006	The uptake of FITC-labeled p21 antisense ODNs by cortical proximal tubule (PT) cells was much greater than by PT cells in the outer stripe of outer medulla (OSOM).	Fluorescein-5-isothiocyanate	14-18	KRAS proto-oncogene, GTPase	Rattus norvegicus	27-30
16467127-5	2006	Administration of antisense induced partial downregulation of p21 mRNA and protein levels in whole kidneys with single CDDP treatment and its rechallenge injury.	Cisplatin	119-123	KRAS proto-oncogene, GTPase	Rattus norvegicus	62-65
16467127-6	2006	Antisense significantly aggravated PT necrosis and decreased the number of p21-positive PT cells in the cortex but not in the OSOM in both CDDP-induced ARF and its rechallenge injury.	Cisplatin	139-143	KRAS proto-oncogene, GTPase	Rattus norvegicus	75-78
16467127-8	2006	Our findings suggested that p21 plays, at least in part, a cytoprotective role in cortical PTs exposed to CDDP, although this does not contribute to renal dysfunction when judged by Scr and BUN levels.	Cisplatin	106-110	KRAS proto-oncogene, GTPase	Rattus norvegicus	28-31
16467127-9	2006	Because antisense may not adequately be taken up and/or function in PTs in the OSOM, the role of p21 in PTs in the OSOM in CDDP-induced ARF remains to be clarified.	Cisplatin	123-127	KRAS proto-oncogene, GTPase	Rattus norvegicus	97-100
21162245-0	2006	[Effect of repeated + Gz exposure on HO-1, p21 and LCAD expressions in rat heart and aorta].	gz	22-24	KRAS proto-oncogene, GTPase	Rattus norvegicus	43-46
16438962-6	2006	Our data suggest that IL-1beta (10 ng/ml) causes an enhancement of U46619-mediated basilar artery contraction that probably involves TTX-sensitive neuronal release of an alpha1-adrenoceptor agonist and activation of p42/p44 and p38 mitogen-activated protein kinases/p21(ras) pathways.	Tetrodotoxin	133-136	KRAS proto-oncogene, GTPase	Rattus norvegicus	266-269
16395258-1	2006	Early 1,25-dihydroxyvitamin D(3) (VD(3)) therapy during the course of renal failure prevents the downregulation of VD(3) receptor (VDR), calcium-sensing receptor (CaSR) or p21, and the parathyroid (PT) growth.	1,25-dihydroxyvitamin D	6-29	KRAS proto-oncogene, GTPase	Rattus norvegicus	172-175
16426843-0	2006	Celecoxib leads to G2/M arrest by induction of p21 and down-regulation of cyclin B1 expression in a p53-independent manner.	Celecoxib	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	47-50
16706023-4	2006	RESULT: There was the tendency that mica monomer granule preparation with three different dosage could decrease the expression of p53 as well as p21, and mica had the obvious regulative effects on deletion of p16 and high-expression of bcl-2.	mica	36-40	KRAS proto-oncogene, GTPase	Rattus norvegicus	145-148
16474204-7	2006	Treatment with benidipine for 2 days increased the level of p21 protein and partially reduced p70 S6 kinase 1 (p70S6K1) activity.	benidipine	15-25	KRAS proto-oncogene, GTPase	Rattus norvegicus	60-63
16420421-3	2006	Neonatal and 21-day-old (P21) rats were intrathecally treated with one of the GABA(A)R antagonists bicuculline and gabazine, with both compounds dose-dependently decreasing hindpaw mechanical and thermal withdrawal thresholds in P21 rats but increasing them in P3 neonates.	Bicuculline	99-110	KRAS proto-oncogene, GTPase	Rattus norvegicus	229-232
16420421-3	2006	Neonatal and 21-day-old (P21) rats were intrathecally treated with one of the GABA(A)R antagonists bicuculline and gabazine, with both compounds dose-dependently decreasing hindpaw mechanical and thermal withdrawal thresholds in P21 rats but increasing them in P3 neonates.	gabazine	115-123	KRAS proto-oncogene, GTPase	Rattus norvegicus	229-232
16420421-4	2006	Intrathecal gabazine also produced an increase in the cutaneous evoked electromyography (EMG) response of the biceps femoris in P21 rates but lowering the response in neonates.	gabazine	12-20	KRAS proto-oncogene, GTPase	Rattus norvegicus	128-131
16898871-10	2006	Increased phosphorylation of p53, as well as higher mRNA and protein levels of p21(WAF1/CIP1), PTEN, and mdm2, and lower levels of IGF-IR were detected in tumors of GLN-supplemented rats vs. controls.	Glutamine	165-168	KRAS proto-oncogene, GTPase	Rattus norvegicus	79-82
17178689-13	2006	These pathways controlled cholesterol metabolism, activation of nuclear receptors, and N-ras and K-ras signaling.	Cholesterol	26-37	KRAS proto-oncogene, GTPase	Rattus norvegicus	97-102
16141400-0	2005	Single perivascular delivery of mitomycin C stimulates p21 expression and inhibits neointima formation in rat arteries.	Mitomycin	32-43	KRAS proto-oncogene, GTPase	Rattus norvegicus	55-58
16293243-8	2005	These results suggested that the activation of JNK and the upregulation of c-Jun, p53 and p21(WAF1/CIP1) were involved in the apoptosis of hepatocytes induced by partial hepatectomy with manganese.	Manganese	187-196	KRAS proto-oncogene, GTPase	Rattus norvegicus	90-93
16309217-3	2005	The expressions of p53, p21 and 14-3-3sigma in glioma cells treated with GL331 were investigated by Western blot analysis.	GL 331	73-78	KRAS proto-oncogene, GTPase	Rattus norvegicus	24-43
16309217-5	2005	GL331 also caused the glioma cells to accumulate in the G2/M-phase of the cell cycle and increased the expressions of p53, p21 and 14-3-3sigma.	GL 331	0-5	KRAS proto-oncogene, GTPase	Rattus norvegicus	123-142
16309217-6	2005	CONCLUSION: GL331 exerts cytotoxic effects and induces apoptosis in C6 glioma cells, accompanied by cell accumulation in the G2/M-phase and activation of p53, p21 and 14-3-3sigma.	GL 331	12-17	KRAS proto-oncogene, GTPase	Rattus norvegicus	159-178
16141400-5	2005	The antiproliferative action of MMc was associated with a selective increase in the expression of the cyclin-dependent kinase inhibitor p21, and with a decrease in cyclin B1-cyclin-dependent kinase-1 complex activity.	Mitomycin	32-35	KRAS proto-oncogene, GTPase	Rattus norvegicus	136-139
16190877-5	2005	Further, ethanol exposure antagonized the anti-proliferative action of TGFbeta1 and blocked TGFbeta1-dependent increases in cell cycle inhibitor p21.	Ethanol	9-16	KRAS proto-oncogene, GTPase	Rattus norvegicus	145-148
16155410-10	2005	p21(Cip/WAF1) was decreased significantly in DMN-treated HSCs compared to control cells (88%, P<0.001).	Dimethylnitrosamine	45-48	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-3
15240344-4	2004	In wild-type VSMCs, exogenously added L-PGDS delayed serum-induced cell cycle progression from the G1 to S phase, as determined by gene array analysis and the decreased protein expressions of cyclin-dependent kinase-2, p21(Cip1), and cyclin D1.	l-pgds	38-44	KRAS proto-oncogene, GTPase	Rattus norvegicus	219-222
16046856-2	2005	Unilateral HI was induced by ligation of the right common carotid artery and exposure to 8% O(2)/92% N(2) for 120 (P7) or 90 (P21) min.	hi	11-13	KRAS proto-oncogene, GTPase	Rattus norvegicus	126-129
16046856-7	2005	Differential effects of HI on phosphorylation of the NMDA receptor at P7 and P21 may contribute to age-related changes in sensitivity to HI.	hi	137-139	KRAS proto-oncogene, GTPase	Rattus norvegicus	77-80
16457693-10	2005	The DHEA-induced cellular effects were associated with increased expression of p16 and p21, but not p53 expression, implicating a p53-independent mechanism in their action.	Dehydroepiandrosterone	4-8	KRAS proto-oncogene, GTPase	Rattus norvegicus	87-90
16457693-11	2005	CONCLUSION: We provide evidence that DHEA and DHEA 8354 can suppress mammary carcinogenesis by altering various cellular functions, inducing cellular senescence, in tumor cells with the potential involvement of p16 and p21 in mediating these effects.	Dehydroepiandrosterone	37-41	KRAS proto-oncogene, GTPase	Rattus norvegicus	219-222
16457693-11	2005	CONCLUSION: We provide evidence that DHEA and DHEA 8354 can suppress mammary carcinogenesis by altering various cellular functions, inducing cellular senescence, in tumor cells with the potential involvement of p16 and p21 in mediating these effects.	Dehydroepiandrosterone	46-50	KRAS proto-oncogene, GTPase	Rattus norvegicus	219-222
16113589-12	2005	mRNA renal expression for p27 and TGF-beta did not change between groups, but p21 mRNA renal expression, highly induced in this model, significantly decreased with SIMV treatment (31.6 +/- 6.6 vs. 50.2 +/- 5.8 OD, p < 0.05).	Simvastatin	164-168	KRAS proto-oncogene, GTPase	Rattus norvegicus	78-81
15869744-12	2005	We further showed that chrysin induced p38-MAPK activation, and using a specific p38-MAPK inhibitor, SB203580, attenuated chrysin-induced p21(Waf1/Cip1) expression.	SB 203580	101-109	KRAS proto-oncogene, GTPase	Rattus norvegicus	138-141
15939090-2	2005	Pups subjected to chronic hypoxia (10% O2 from P0 to P21) had increased aggression, hyperactivity (open-field test), and decreased CA1 cell counts.	Oxygen	39-41	KRAS proto-oncogene, GTPase	Rattus norvegicus	53-56
15769867-17	2005	Rapamycin influences the cell cycle by up-regulation of p27, down-regulation of p21, and inhibition of p70(s6k) phosphorylation.	Sirolimus	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	80-83
15557822-7	2004	Hydroxyurea treatment induced G1 arrest and a senescence-like changes in rat hepatoma McA-RH7777 cells may be the likely results of signal disruption of MAP kinases (ERK, JNK, and p38 MAP kinase) and p21(Waf1) over-expression.	Hydroxyurea	0-11	KRAS proto-oncogene, GTPase	Rattus norvegicus	200-203
15581186-5	2004	Western blot analyses demonstrated that MNU exposure caused progressive reduction of p21 protein levels, an increase of Rb phosphorylation, activation of AKT and CDK2, and upregulation of FGF receptors.	Methylnitrosourea	40-43	KRAS proto-oncogene, GTPase	Rattus norvegicus	85-88
15325252-6	2004	In OC15-5 cells treated with 15d-PGJ2, the expression of CDK inhibitor, p27(Kip1), was up-regulated, while that of p21(WAF1/Cip1), p18(INK4C) CDK2, CDK4, and cyclin E was unchanged.	15-deoxy-delta(12,14)-prostaglandin J2	29-37	KRAS proto-oncogene, GTPase	Rattus norvegicus	115-118
15337841-0	2004	Protein kinase B, P34cdc2 kinase, and p21 ras GTP-binding in kidneys of aging rats.	Guanosine Triphosphate	46-49	KRAS proto-oncogene, GTPase	Rattus norvegicus	38-41
15203180-3	2004	Histopathological examinations revealed marked induction of apoptotic cell death and decrease of mitosis in neuroepithelial cells in the brain of Ara-C-treated fetus, and these changes were most prominent from 9 to 12 h. Expression of p53 protein, which mediates apoptosis and cell cycle arrest after DNA damage, was elevated remarkably and peaked at 3 h. p21, a cyclin-dependent kinase inhibitor responsible for p53-mediated cell cycle arrest, showed intense overexpression in protein and mRNA levels following the increase of p53 protein.	Cytarabine	146-151	KRAS proto-oncogene, GTPase	Rattus norvegicus	356-359
15271584-6	2004	Acute or chronic quinpirole treatment on P14 produced a larger increase in CORT than controls and produced larger increases in CORT than control rats on P21.	Quinpirole	17-27	KRAS proto-oncogene, GTPase	Rattus norvegicus	153-156
15207644-4	2004	The inhibitory effect of (Ac)5-GP on the cell cycle progression of C6 glioma cells which arrested cells at the G0/G1 phase was associated with a marked decrease in the protein expression of cyclin D1, and an induction in the content of cyclin-dependent kinase (cdk) inhibitor p21 protein.	Pentaacetyl geniposide	25-33	KRAS proto-oncogene, GTPase	Rattus norvegicus	276-279
15051933-9	2004	There was a two- fold induction of the cyclin-dependent kinase inhibitor p21 in PMVSMC treated with NO donors.	pmvsmc	80-86	KRAS proto-oncogene, GTPase	Rattus norvegicus	73-76
15130764-7	2004	Combined exposure to RTX and ROPA produced a sustained and complete cell cycle blockade in IEC-18 cells, associated with depletion of cyclin D1 and sustained enhancement of p21(Waf1/Cip1) levels.	resiniferatoxin	21-24	KRAS proto-oncogene, GTPase	Rattus norvegicus	173-176
15051933-12	2004	The ability of NO to induce p21 upregulation may be a mechanism by which it exerts antiproliferative effects in PMVSMC.	pmvsmc	112-118	KRAS proto-oncogene, GTPase	Rattus norvegicus	28-31
14975736-8	2004	While p27(Kip1), p53, and p21(Waf1) were slightly increased by menadione in both groups, the basal induction level in the old was considerably higher.	Vitamin K 3	63-72	KRAS proto-oncogene, GTPase	Rattus norvegicus	26-29
15099639-14	2004	In conclusion, ibuprofen inhibits tendon cell proliferation in a process that is probably mediated by the upregulation of p21(CIP1) and reduced phosphorylation of Rb protein.	Ibuprofen	15-24	KRAS proto-oncogene, GTPase	Rattus norvegicus	122-125
15087391-6	2004	Moreover, inhibition of the MEK-MAPK pathway by the specific inhibitor, UO126, rescued the cells from apoptosis, whereas the inhibition of phosphoinositide 3-kinase by its specific inhibitor, LY294002, promoted apoptosis in RENT4 cells expressing activated K-Ras.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	192-200	KRAS proto-oncogene, GTPase	Rattus norvegicus	257-262
15067513-6	2004	rhIGF-I significantly increased the numbers of p21-positive nuclei (5.15 +/- 0.19 vs 3.45 +/- 0.42/x400 high-power field (HPF); P < 0.05) and proliferating cell nuclear antigen (PCNA)-positive nuclei (28.61 +/- 1.89 vs 18.26 +/- 2.14/x400 HPF; P < 0.05), but decreased the number of cyclin D1-positive cells (3.3 +/- 0.3 vs 6.3 +/- 1.7/x400 HPF; P < 0.05) on day 3. rhIGF-I did not alter 5-bromo-3-deoxyuridine (BrdU) incorporation.	5-bromo-3-deoxyuridine	397-419	KRAS proto-oncogene, GTPase	Rattus norvegicus	47-50
15067513-6	2004	rhIGF-I significantly increased the numbers of p21-positive nuclei (5.15 +/- 0.19 vs 3.45 +/- 0.42/x400 high-power field (HPF); P < 0.05) and proliferating cell nuclear antigen (PCNA)-positive nuclei (28.61 +/- 1.89 vs 18.26 +/- 2.14/x400 HPF; P < 0.05), but decreased the number of cyclin D1-positive cells (3.3 +/- 0.3 vs 6.3 +/- 1.7/x400 HPF; P < 0.05) on day 3. rhIGF-I did not alter 5-bromo-3-deoxyuridine (BrdU) incorporation.	Bromodeoxyuridine	421-425	KRAS proto-oncogene, GTPase	Rattus norvegicus	47-50
14751676-5	2004	Following 24 h of culture both compounds caused a statistically significant increase in the mRNA levels of the cell cycle inhibitory protein, gadd153, whereas p21 was statistically altered by etoposide only.	Etoposide	192-201	KRAS proto-oncogene, GTPase	Rattus norvegicus	159-162
15053237-0	2004	Ki-ras mutational analysis in rat follicular-cell proliferative lesions of the thyroid gland induced by radioactive iodine and potassium perchlorate.	radioactive iodine	104-122	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-6
14712206-11	2004	Elevated Bax translocation following ionizing irradiation in 12V-Ki-Ras-overexpressing cells is completely inhibited by PD169316 or dominant-negative p38 MAPK.	2-(4-nitrophenyl)-4-(4-fluorophenyl)-5-(4-pyridinyl)-1H-imidazole	120-128	KRAS proto-oncogene, GTPase	Rattus norvegicus	65-71
14707007-4	2004	In the presence of 0.1% FBS media, hemin induced p21 through an HO-dependent, p53-independent mechanism; certain products of HO activity (iron and carbon monoxide), but not others (ferritin, apoferritin, bilirubin), recapitulated these inductive effects on p21 expression.	Hemin	35-40	KRAS proto-oncogene, GTPase	Rattus norvegicus	49-52
14707007-4	2004	In the presence of 0.1% FBS media, hemin induced p21 through an HO-dependent, p53-independent mechanism; certain products of HO activity (iron and carbon monoxide), but not others (ferritin, apoferritin, bilirubin), recapitulated these inductive effects on p21 expression.	Hemin	35-40	KRAS proto-oncogene, GTPase	Rattus norvegicus	257-260
14707007-4	2004	In the presence of 0.1% FBS media, hemin induced p21 through an HO-dependent, p53-independent mechanism; certain products of HO activity (iron and carbon monoxide), but not others (ferritin, apoferritin, bilirubin), recapitulated these inductive effects on p21 expression.	Holmium	64-66	KRAS proto-oncogene, GTPase	Rattus norvegicus	49-52
14707007-4	2004	In the presence of 0.1% FBS media, hemin induced p21 through an HO-dependent, p53-independent mechanism; certain products of HO activity (iron and carbon monoxide), but not others (ferritin, apoferritin, bilirubin), recapitulated these inductive effects on p21 expression.	Holmium	125-127	KRAS proto-oncogene, GTPase	Rattus norvegicus	49-52
14707007-4	2004	In the presence of 0.1% FBS media, hemin induced p21 through an HO-dependent, p53-independent mechanism; certain products of HO activity (iron and carbon monoxide), but not others (ferritin, apoferritin, bilirubin), recapitulated these inductive effects on p21 expression.	Iron	138-142	KRAS proto-oncogene, GTPase	Rattus norvegicus	49-52
14707007-4	2004	In the presence of 0.1% FBS media, hemin induced p21 through an HO-dependent, p53-independent mechanism; certain products of HO activity (iron and carbon monoxide), but not others (ferritin, apoferritin, bilirubin), recapitulated these inductive effects on p21 expression.	Carbon Monoxide	147-162	KRAS proto-oncogene, GTPase	Rattus norvegicus	49-52
14707007-4	2004	In the presence of 0.1% FBS media, hemin induced p21 through an HO-dependent, p53-independent mechanism; certain products of HO activity (iron and carbon monoxide), but not others (ferritin, apoferritin, bilirubin), recapitulated these inductive effects on p21 expression.	Bilirubin	204-213	KRAS proto-oncogene, GTPase	Rattus norvegicus	49-52
14707007-6	2004	In IRPTCs maintained in 5% FBS, hemin induced HO-dependent p21 expression, provoked cell cycle arrest, and inhibited cell growth without inducing apoptosis; this inhibitory effect of hemin on cell growth was blocked by the concomitant inhibition of HO activity and loss of p21 expression.	Hemin	32-37	KRAS proto-oncogene, GTPase	Rattus norvegicus	59-62
14707007-6	2004	In IRPTCs maintained in 5% FBS, hemin induced HO-dependent p21 expression, provoked cell cycle arrest, and inhibited cell growth without inducing apoptosis; this inhibitory effect of hemin on cell growth was blocked by the concomitant inhibition of HO activity and loss of p21 expression.	Hemin	32-37	KRAS proto-oncogene, GTPase	Rattus norvegicus	273-276
14707007-6	2004	In IRPTCs maintained in 5% FBS, hemin induced HO-dependent p21 expression, provoked cell cycle arrest, and inhibited cell growth without inducing apoptosis; this inhibitory effect of hemin on cell growth was blocked by the concomitant inhibition of HO activity and loss of p21 expression.	Hemin	183-188	KRAS proto-oncogene, GTPase	Rattus norvegicus	59-62
14707007-6	2004	In IRPTCs maintained in 5% FBS, hemin induced HO-dependent p21 expression, provoked cell cycle arrest, and inhibited cell growth without inducing apoptosis; this inhibitory effect of hemin on cell growth was blocked by the concomitant inhibition of HO activity and loss of p21 expression.	Hemin	183-188	KRAS proto-oncogene, GTPase	Rattus norvegicus	273-276
14707007-7	2004	We conclude that hemin is a potent HO-dependent inducer of p21 and that hemin increases the sensitivity to apoptosis in serum-deplete conditions and decreases cell growth in serum-replete conditions; inhibiting HO activity and concomitantly ablating p21 expression exacerbate apoptosis and reverse the growth-inhibitory actions of hemin.	Hemin	17-22	KRAS proto-oncogene, GTPase	Rattus norvegicus	59-62
14707007-7	2004	We conclude that hemin is a potent HO-dependent inducer of p21 and that hemin increases the sensitivity to apoptosis in serum-deplete conditions and decreases cell growth in serum-replete conditions; inhibiting HO activity and concomitantly ablating p21 expression exacerbate apoptosis and reverse the growth-inhibitory actions of hemin.	Hemin	17-22	KRAS proto-oncogene, GTPase	Rattus norvegicus	250-253
14707007-7	2004	We conclude that hemin is a potent HO-dependent inducer of p21 and that hemin increases the sensitivity to apoptosis in serum-deplete conditions and decreases cell growth in serum-replete conditions; inhibiting HO activity and concomitantly ablating p21 expression exacerbate apoptosis and reverse the growth-inhibitory actions of hemin.	Hemin	72-77	KRAS proto-oncogene, GTPase	Rattus norvegicus	250-253
14707007-7	2004	We conclude that hemin is a potent HO-dependent inducer of p21 and that hemin increases the sensitivity to apoptosis in serum-deplete conditions and decreases cell growth in serum-replete conditions; inhibiting HO activity and concomitantly ablating p21 expression exacerbate apoptosis and reverse the growth-inhibitory actions of hemin.	Hemin	72-77	KRAS proto-oncogene, GTPase	Rattus norvegicus	250-253
15114044-5	2004	Increased expression of p21 and Bax, decreased expression of Bcl-2, cytochrome C release from the mitochondria into the cytosol and subsequent activation of caspase-9 and -3 were identified in the cells treated with ammonia, although there was no apparent change in p53 expression.	Ammonia	216-223	KRAS proto-oncogene, GTPase	Rattus norvegicus	24-27
15053237-0	2004	Ki-ras mutational analysis in rat follicular-cell proliferative lesions of the thyroid gland induced by radioactive iodine and potassium perchlorate.	potassium perchlorate	127-148	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-6
15053237-2	2004	The present paper reports, using direct sequencing, the incidence of Ki-ras mutations (codons 12 and 13) in follicular-cell carcinomas of the thyroid gland in Wistar rats induced by administration of radioactive iodine and potassium perchlorate.	radioactive iodine	200-218	KRAS proto-oncogene, GTPase	Rattus norvegicus	69-75
15053237-2	2004	The present paper reports, using direct sequencing, the incidence of Ki-ras mutations (codons 12 and 13) in follicular-cell carcinomas of the thyroid gland in Wistar rats induced by administration of radioactive iodine and potassium perchlorate.	potassium perchlorate	223-244	KRAS proto-oncogene, GTPase	Rattus norvegicus	69-75
14647002-3	2003	The aim of our study was to examine the influence of late-afternoon (1600-1800) subcutaneous (s.c.) melatonin (Mel) injections, administered for 2 weeks, on the p21 expression in male Wistar rat thyroid follicular cells (TFC).	Melatonin	100-109	KRAS proto-oncogene, GTPase	Rattus norvegicus	161-164
14576830-10	2003	These results suggest that an activating mutation of K-ras can markedly enhance the iNOS expression mediated by IL-1beta or LPS, through the activation of promoters on NF-kappaB, C/EBP, and CRE-like sites, and that nitric oxide contributes to the colony formation and tumor growth of K-ras-transformed cells.	Nitric Oxide	215-227	KRAS proto-oncogene, GTPase	Rattus norvegicus	53-58
12960065-6	2003	This was confirmed by a pull-down assay that quantifies the binding of activated (i.e. GTP-bound) Rac to p21-activated kinase.	Guanosine Triphosphate	87-90	KRAS proto-oncogene, GTPase	Rattus norvegicus	105-108
14647002-3	2003	The aim of our study was to examine the influence of late-afternoon (1600-1800) subcutaneous (s.c.) melatonin (Mel) injections, administered for 2 weeks, on the p21 expression in male Wistar rat thyroid follicular cells (TFC).	Melatonin	111-114	KRAS proto-oncogene, GTPase	Rattus norvegicus	161-164
12972064-8	2003	At P3, MDMA offspring showed reductions in the dopamine metabolite homovanillic acid which persisted through P21, along with reductions in the serotonin (5-HT) metabolite, 5-HIAA.	N-Methyl-3,4-methylenedioxyamphetamine	7-11	KRAS proto-oncogene, GTPase	Rattus norvegicus	109-112
12972064-8	2003	At P3, MDMA offspring showed reductions in the dopamine metabolite homovanillic acid which persisted through P21, along with reductions in the serotonin (5-HT) metabolite, 5-HIAA.	Homovanillic Acid	67-84	KRAS proto-oncogene, GTPase	Rattus norvegicus	109-112
12972064-9	2003	Prenatally exposed MDMA animals at P21 also had reduced dopamine and 5-HT turnover in the nucleus accumbens.	Dopamine	56-64	KRAS proto-oncogene, GTPase	Rattus norvegicus	35-38
12972064-11	2003	In addition, prenatal MDMA significantly increased locomotor activity of P21 pups in a 20-min novel cage environment.	N-Methyl-3,4-methylenedioxyamphetamine	22-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	73-76
12960143-11	2003	celecoxib induces cell cycle arrest at the G(1)-S phase transition point and modifies cell cycle regulatory proteins such as cyclin D1, retinoblastoma (Rb), and phosphorylated Rb, cyclin E, p27(KIP1), and p21(WAF1/CIP1).	Celecoxib	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	205-208
12715917-4	2003	The expression of Mullerian inhibiting substance (MIS) was transiently increased in small growing follicles in the ovary of DES-treated rats at postnatal day 7 (P7), and the expression profile in the ovary differed between DES- and vehicle oil-treated rats at P14 and P21.	Diethylstilbestrol	124-127	KRAS proto-oncogene, GTPase	Rattus norvegicus	268-271
12807724-10	2003	Levels of cyclin D1, cyclin E, cyclin-dependent kinase (CDK)-2 and CDK-4 were reduced in carcinomas from corticosterone treated rats; whereas, levels of cyclin-dependent kinase inhibitors (CKI) Kip1/p27 and Cip1/p21 were elevated.	Corticosterone	105-119	KRAS proto-oncogene, GTPase	Rattus norvegicus	212-215
12810531-4	2003	Western blotting analysis revealed that the protein levels of cyclin A, cyclin E, and cyclin-dependent-kinase (CDK) 2 but not cyclin D1 and CDK4 decreased after progesterone treatment, but those of CDK-inhibitory proteins, p21 and p27, increased.	Progesterone	161-173	KRAS proto-oncogene, GTPase	Rattus norvegicus	223-226
12810531-5	2003	Immunoprecipitation showed that the formations of the CDK2-p21 and CDK2-p27 complex were increased and the assayable CDK2 kinase activity was decreased in the progesterone-treated RASMCs.	Progesterone	159-171	KRAS proto-oncogene, GTPase	Rattus norvegicus	59-62
12810531-5	2003	Immunoprecipitation showed that the formations of the CDK2-p21 and CDK2-p27 complex were increased and the assayable CDK2 kinase activity was decreased in the progesterone-treated RASMCs.	rasmcs	180-186	KRAS proto-oncogene, GTPase	Rattus norvegicus	59-62
12810531-7	2003	Pretreatment of RASMCs with a p21 or p27 antisense oligonucleotide reduced the progesterone-induced inhibition of [(3)H]thymidine incorporation into RASMCs.	rasmcs	16-22	KRAS proto-oncogene, GTPase	Rattus norvegicus	30-33
12810531-7	2003	Pretreatment of RASMCs with a p21 or p27 antisense oligonucleotide reduced the progesterone-induced inhibition of [(3)H]thymidine incorporation into RASMCs.	Progesterone	79-91	KRAS proto-oncogene, GTPase	Rattus norvegicus	30-33
12810531-7	2003	Pretreatment of RASMCs with a p21 or p27 antisense oligonucleotide reduced the progesterone-induced inhibition of [(3)H]thymidine incorporation into RASMCs.	Thymidine	120-129	KRAS proto-oncogene, GTPase	Rattus norvegicus	30-33
12810531-7	2003	Pretreatment of RASMCs with a p21 or p27 antisense oligonucleotide reduced the progesterone-induced inhibition of [(3)H]thymidine incorporation into RASMCs.	rasmcs	149-155	KRAS proto-oncogene, GTPase	Rattus norvegicus	30-33
12809946-6	2003	The rise in the p53 protein level after partial hepatectomy with selenite injection was followed by the upregulation of p21(WAF1/CIP1) mRNA and protein expression.	Selenious Acid	65-73	KRAS proto-oncogene, GTPase	Rattus norvegicus	120-123
12809946-7	2003	These results suggested that selenite induced apoptosis accompanied by the activation of caspase-3 and JNK and the upregulation of c-jun, c-fos, p53 and p21(WAF1/CIP1) at the early stage of liver regeneration.	Selenious Acid	29-37	KRAS proto-oncogene, GTPase	Rattus norvegicus	153-156
12746943-7	2003	However, high Dex exposure resulted in elevated lung MMP-9 levels at P21 and P45.	Dexamethasone	14-17	KRAS proto-oncogene, GTPase	Rattus norvegicus	69-72
12594205-4	2003	SCOP interacted directly through its LRR domain with a subset of K-Ras in the guanine nucleotide-free form that was present in the raft fraction.	Guanine Nucleotides	78-96	KRAS proto-oncogene, GTPase	Rattus norvegicus	65-70
12594205-5	2003	This interaction interfered with the binding of added guanine nucleotide to K-Ras in vitro.	Guanine Nucleotides	54-72	KRAS proto-oncogene, GTPase	Rattus norvegicus	76-81
12640114-6	2003	Stable transfectants of the K-ras oncogene in intestinal epithelial IEC18 cells were generated which show little alpha-catenin-beta-catenin association with respect to control clones; this effect is accompanied by increased Tyr-142 phosphorylation and activation of Fer and Fyn kinases.	Tyrosine	224-227	KRAS proto-oncogene, GTPase	Rattus norvegicus	28-33
12640114-7	2003	As reported for Fer, Fyn kinase is constitutively bound to p120 catenin; expression of K-ras induces the phosphorylation of p120 catenin on tyrosine residues increasing its affinity for E-cadherin and, consequently, promotes the association of Fyn with the adherens junction complex.	Tyrosine	140-148	KRAS proto-oncogene, GTPase	Rattus norvegicus	87-92
12839936-9	2003	K-ras mutations were assessed by primer-mediated RFLP, allele-specific oligonucleotide hybridization, and direct DNA sequencing.	Oligonucleotides	71-86	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-5
12809946-0	2003	Jun N-terminal kinase activation and upregulation of p53 and p21(WAF1/CIP1) in selenite-induced apoptosis of regenerating liver.	Selenious Acid	79-87	KRAS proto-oncogene, GTPase	Rattus norvegicus	61-64
12713563-0	2003	Overexpression of p21, cyclin E and decreased expression of p27 in DMBA (7, 12-dimethylbenzanthracene)-induced rat ovarian carcinogenesis.	6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene	67-71	KRAS proto-oncogene, GTPase	Rattus norvegicus	18-21
12713563-0	2003	Overexpression of p21, cyclin E and decreased expression of p27 in DMBA (7, 12-dimethylbenzanthracene)-induced rat ovarian carcinogenesis.	9,10-Dimethyl-1,2-benzanthracene	73-101	KRAS proto-oncogene, GTPase	Rattus norvegicus	18-21
12713563-10	2003	These results suggest that the increased expression of cyclin E and p21, and the decreased expression of p27, occur in DMBA-induced rat ovarian carcinogenesis and result in tumor progression.	6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene	119-123	KRAS proto-oncogene, GTPase	Rattus norvegicus	68-71
12480138-11	2002	Prenatal ethanol exposure caused the down-regulation of p27(Kip) between P0 and P21.	Ethanol	9-16	KRAS proto-oncogene, GTPase	Rattus norvegicus	80-83
11943200-1	2002	p21-activated protein kinase gamma-PAK phosphorylates prolactin (PRL) in rat pituitary secretory granules on Ser-177 and on the equivalent site, Ser-179, in recombinant human PRL.	Serine	109-112	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-3
12242526-4	2002	In conclusion, K- ras mutation plays an important role in DIPN-induced rat thyroid tumorigenesis, possibly regarded as an early event in the tumorigenic process.	diisopropanolnitrosamine	58-62	KRAS proto-oncogene, GTPase	Rattus norvegicus	15-21
12444545-4	2002	When cells were synchronized in S phase with aphidicolin and then released, activation of Delta MEKK3:ER* resulted in the up-regulation of p21(CIP1) and a pronounced inhibition of cyclin A/CDK2 and cyclin B1/CDK1 kinase activity.	Aphidicolin	45-56	KRAS proto-oncogene, GTPase	Rattus norvegicus	139-142
12498791-3	2002	Here we demonstrate that embryonic and adult rat neural stem cells (NSC) express ERalpha and ERbeta, 17beta-Estradiol treatment decreased the proliferation of NSC stimulated by epidermal growth factor (EGF), which was due to the upregulation of the cyclin-dependent kinase (CDK) inhibitor, p21(Cip1).	Estradiol	101-117	KRAS proto-oncogene, GTPase	Rattus norvegicus	290-293
12417091-1	2002	OBJECTIVE: To investigate the roles of p53 and K-ras gene in carcinogenesis and development of the lung carcinoma induced by 3-methylcholanthrene (MCA) and diethylinitrosamine (DEN) in Wistar rats, and to elucidate the relationships between the protein expression and gene mutation of p53 and K-ras.	Methylcholanthrene	125-145	KRAS proto-oncogene, GTPase	Rattus norvegicus	47-52
12417091-1	2002	OBJECTIVE: To investigate the roles of p53 and K-ras gene in carcinogenesis and development of the lung carcinoma induced by 3-methylcholanthrene (MCA) and diethylinitrosamine (DEN) in Wistar rats, and to elucidate the relationships between the protein expression and gene mutation of p53 and K-ras.	diethylinitrosamine	156-175	KRAS proto-oncogene, GTPase	Rattus norvegicus	47-52
12417091-1	2002	OBJECTIVE: To investigate the roles of p53 and K-ras gene in carcinogenesis and development of the lung carcinoma induced by 3-methylcholanthrene (MCA) and diethylinitrosamine (DEN) in Wistar rats, and to elucidate the relationships between the protein expression and gene mutation of p53 and K-ras.	Diethylnitrosamine	177-180	KRAS proto-oncogene, GTPase	Rattus norvegicus	47-52
12417091-11	2002	CONCLUSIONS: p53 gene mutation and K-ras overexpression were early events in the carcinogenesis and development of rat lung carcinoma induced by MCA and DEN, while K-ras mutation does not play any important role.	Diethylnitrosamine	153-156	KRAS proto-oncogene, GTPase	Rattus norvegicus	35-40
12048257-0	2002	3-Hydroxy-3-methylglutaryl CoA reductase inhibitors prevent high glucose-induced proliferation of mesangial cells via modulation of Rho GTPase/ p21 signaling pathway: Implications for diabetic nephropathy.	Glucose	65-72	KRAS proto-oncogene, GTPase	Rattus norvegicus	144-147
12048257-8	2002	Simvastatin reversed the down-regulation of p21 protein expression and decreased CDK4 and CDK2 kinase activities.	Simvastatin	0-11	KRAS proto-oncogene, GTPase	Rattus norvegicus	44-47
12048257-12	2002	Our data suggest that simvastatin represses the HG-induced Rho GTPase/p21 signaling in glomerular MCs.	Simvastatin	22-33	KRAS proto-oncogene, GTPase	Rattus norvegicus	70-73
11981032-8	2002	Increases of RXR levels by YFP-RXR expression, drug treatments, or the combination of the two, however, restored the growth-inhibitory effects of calcitriol and 9-cis-RA and restored p21 induction by calcitriol.	Calcitriol	200-210	KRAS proto-oncogene, GTPase	Rattus norvegicus	183-186
11943200-1	2002	p21-activated protein kinase gamma-PAK phosphorylates prolactin (PRL) in rat pituitary secretory granules on Ser-177 and on the equivalent site, Ser-179, in recombinant human PRL.	Serine	145-148	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-3
11940356-12	2002	The expression of p21(cip1) and p27(kip1) showed an inverse gradient to that of Ki67.	ki67	80-84	KRAS proto-oncogene, GTPase	Rattus norvegicus	18-21
12014640-0	2002	Expression of p53 and p21 Ki-ras proteins in rat thyroid gland tumors induced by 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX).	3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone	81-133	KRAS proto-oncogene, GTPase	Rattus norvegicus	22-25
12014640-0	2002	Expression of p53 and p21 Ki-ras proteins in rat thyroid gland tumors induced by 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX).	3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone	81-133	KRAS proto-oncogene, GTPase	Rattus norvegicus	26-32
12014640-0	2002	Expression of p53 and p21 Ki-ras proteins in rat thyroid gland tumors induced by 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX).	3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone	135-137	KRAS proto-oncogene, GTPase	Rattus norvegicus	22-25
12014640-0	2002	Expression of p53 and p21 Ki-ras proteins in rat thyroid gland tumors induced by 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX).	3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone	135-137	KRAS proto-oncogene, GTPase	Rattus norvegicus	26-32
11906706-10	2002	These results suggested that the inhibition of the JNK-AP-1 pathway and concurrent up-regulation of p53 and p21(WAF1/CIP1) were involved in hepatocyte apoptosis induced by partial hepatectomy with methotrexate.	Methotrexate	197-209	KRAS proto-oncogene, GTPase	Rattus norvegicus	108-111
11872643-7	2002	Increased 8-OHdG formation is caused by developing oxidative stress or apoptotic degradation of DNA and coordinated with enhanced expression of CD1 mRNA and cell proliferation, subsequent increase of p21(WAF1/Cip1) mRNA expression, cell-cycle arrest and apoptosis, while activation of 8-OHdG repair mechanisms contributes to protection of tissue against reactive oxygen species-induced cell death.	8-ohdg	10-16	KRAS proto-oncogene, GTPase	Rattus norvegicus	200-203
11598137-2	2001	PPARgamma ligands troglitazone (TRO, 10 microm) and rosiglitazone (RSG, 10 microm) attenuated the induction of p21(Cip1) protein by platelet-derived growth factor (PDGF) and insulin without affecting cognate mRNA levels in rat aortic smooth muscle cells (RASMC).	Troglitazone	18-30	KRAS proto-oncogene, GTPase	Rattus norvegicus	111-114
11872643-0	2002	Formation of 8-hydroxydeoxyguanosine and cell-cycle arrest in the rat liver via generation of oxidative stress by phenobarbital: association with expression profiles of p21(WAF1/Cip1), cyclin D1 and Ogg1.	8-ohdg	13-36	KRAS proto-oncogene, GTPase	Rattus norvegicus	169-172
11872643-0	2002	Formation of 8-hydroxydeoxyguanosine and cell-cycle arrest in the rat liver via generation of oxidative stress by phenobarbital: association with expression profiles of p21(WAF1/Cip1), cyclin D1 and Ogg1.	Phenobarbital	114-127	KRAS proto-oncogene, GTPase	Rattus norvegicus	169-172
12017282-0	2002	Effect of vaccination with mutant KRAS peptides on rat colon carcinogenesis induced by azoxymethane.	Azoxymethane	87-99	KRAS proto-oncogene, GTPase	Rattus norvegicus	34-38
12401947-11	2002	The neuronal transferrin receptor expression by P21 coincides with a drop in transferrin-IR and iron transport into the brain at this age, suggesting that neuronal transferrin receptor mRNA is posttranscriptionally regulated by the lowered iron availability from this developmental stage onwards.	Iron	96-100	KRAS proto-oncogene, GTPase	Rattus norvegicus	48-51
12401947-11	2002	The neuronal transferrin receptor expression by P21 coincides with a drop in transferrin-IR and iron transport into the brain at this age, suggesting that neuronal transferrin receptor mRNA is posttranscriptionally regulated by the lowered iron availability from this developmental stage onwards.	Iron	240-244	KRAS proto-oncogene, GTPase	Rattus norvegicus	48-51
11747551-8	2002	Although no overall increase could be observed in whole testis samples of the etoposide-treated rat, stage-specific analysis revealed an induction of p21 expression in stages XIII-I.	Etoposide	78-87	KRAS proto-oncogene, GTPase	Rattus norvegicus	150-153
12201671-0	2002	Verapamil reverts resistance to drug-induced apoptosis in Ki-ras-transformed cells by altering the cell membrane and the mitochondrial transmembrane potentials.	Verapamil	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	58-64
11598137-2	2001	PPARgamma ligands troglitazone (TRO, 10 microm) and rosiglitazone (RSG, 10 microm) attenuated the induction of p21(Cip1) protein by platelet-derived growth factor (PDGF) and insulin without affecting cognate mRNA levels in rat aortic smooth muscle cells (RASMC).	Rosiglitazone	52-65	KRAS proto-oncogene, GTPase	Rattus norvegicus	111-114
11598137-2	2001	PPARgamma ligands troglitazone (TRO, 10 microm) and rosiglitazone (RSG, 10 microm) attenuated the induction of p21(Cip1) protein by platelet-derived growth factor (PDGF) and insulin without affecting cognate mRNA levels in rat aortic smooth muscle cells (RASMC).	Rosiglitazone	67-70	KRAS proto-oncogene, GTPase	Rattus norvegicus	111-114
11598137-3	2001	The protein kinase Cdelta (PKCdelta) inhibitor rottlerin also blocked the induction of p21(Cip1) protein, whereas the conventional PKC isotype inhibitor Go 6976 had no effect.	rottlerin	47-56	KRAS proto-oncogene, GTPase	Rattus norvegicus	87-90
11598137-4	2001	Kinetic studies using the protein synthesis inhibitor cycloheximide showed that TRO, RSG, and rottlerin shortened the half-life of p21(Cip1) protein.	Cycloheximide	54-67	KRAS proto-oncogene, GTPase	Rattus norvegicus	131-134
11598137-4	2001	Kinetic studies using the protein synthesis inhibitor cycloheximide showed that TRO, RSG, and rottlerin shortened the half-life of p21(Cip1) protein.	Rosiglitazone	85-88	KRAS proto-oncogene, GTPase	Rattus norvegicus	131-134
11598137-4	2001	Kinetic studies using the protein synthesis inhibitor cycloheximide showed that TRO, RSG, and rottlerin shortened the half-life of p21(Cip1) protein.	rottlerin	94-103	KRAS proto-oncogene, GTPase	Rattus norvegicus	131-134
11598137-5	2001	TRO, RSG, and rottlerin inhibited PDGF-induced expression of p21(Cip1), but they did not affect insulin-induced expression of p21(Cip1).	Troglitazone	0-3	KRAS proto-oncogene, GTPase	Rattus norvegicus	61-64
11598137-5	2001	TRO, RSG, and rottlerin inhibited PDGF-induced expression of p21(Cip1), but they did not affect insulin-induced expression of p21(Cip1).	Rosiglitazone	5-8	KRAS proto-oncogene, GTPase	Rattus norvegicus	61-64
11598137-5	2001	TRO, RSG, and rottlerin inhibited PDGF-induced expression of p21(Cip1), but they did not affect insulin-induced expression of p21(Cip1).	rottlerin	14-23	KRAS proto-oncogene, GTPase	Rattus norvegicus	61-64
11598137-7	2001	Adenovirus-mediated overexpression of PKCdelta rescued the down-regulation of p21(Cip1) expression both by TRO and RSG in PDGF-treated RASMC.	rasmc	135-140	KRAS proto-oncogene, GTPase	Rattus norvegicus	78-81
11598137-12	2001	Both inhibitors also reversed PPARgamma ligand effects on p21(Cip1) expression in PDGF-treated RASMC.	rasmc	95-100	KRAS proto-oncogene, GTPase	Rattus norvegicus	58-61
11745690-1	2001	The p21 proteins encoded by N-, Ki-, and H-ras are small guanine nucleotide-binding proteins that act as switches in several signal transduction pathways.	Guanine Nucleotides	57-75	KRAS proto-oncogene, GTPase	Rattus norvegicus	4-7
11687506-1	2001	We investigated the effect of 2-methyl-arachidonyl-2"-fluoro-ethylamide (Met-F-AEA), a stable analog of the endocannabinoid anandamide, on a rat thyroid epithelial cell line (FRTL-5) transformed by the K-ras oncogene, and on epithelial tumors derived from these cells.	2-methylarachidonyl-2'-fluoroethylamide	30-71	KRAS proto-oncogene, GTPase	Rattus norvegicus	202-207
11687506-4	2001	This effect was inhibited by the CB1 receptor antagonist SR141716A (0.7 mg/kg/dose) and was accompanied by a strong reduction of K-ras activity.	Rimonabant	57-66	KRAS proto-oncogene, GTPase	Rattus norvegicus	129-134
11687506-6	2001	Met-F-AEA inhibited (IC50 ~5 mM) the proliferation in vitro and the transition to the S phase of KiMol cells and it reduced K-ras activity; these effects were antagonized by SR141716A.	Rimonabant	174-183	KRAS proto-oncogene, GTPase	Rattus norvegicus	124-129
11745690-2	2001	Recently, evidence has been accumulating to suggest that valine-12 mutation in the Ki-Ras protein is associated with lung and colorectal tumours that are more aggressive than those carrying aspartate-12 mutation.	Valine	57-63	KRAS proto-oncogene, GTPase	Rattus norvegicus	83-89
11737585-3	2001	Since 1,25(OH)2D3-antiproliferative action in various cell types involve increases in p21, we studied whether induction of p21 by 1,25(OH)2D3 or the vitamin D analog, 19-Nor-1,25(OH)2D2, could counteract the PT hyperplasia induced by high dietary P in early uremia.	Calcitriol	130-141	KRAS proto-oncogene, GTPase	Rattus norvegicus	123-126
11737585-9	2001	Both vitamin D compounds enhanced PT p21 expression and prevented high P-induced increases in PT TGF-alpha content.	Vitamin D	5-14	KRAS proto-oncogene, GTPase	Rattus norvegicus	37-40
11737585-11	2001	CONCLUSIONS: In early uremia, vitamin D suppression of high P-induced PT hyperplasia and high dietary Ca arrest of PT growth involve induction of PT p21 and prevention of increases in TGF-alpha.	Vitamin D	30-39	KRAS proto-oncogene, GTPase	Rattus norvegicus	149-152
11676881-1	2001	OBJECTIVE: To study the effects of retinoic acid on regulation of expressions of cyclin-dependent kinase inhibitors, i.e. p16, p21 and p27 in cultured rat hepatic stellate cells.	Tretinoin	35-48	KRAS proto-oncogene, GTPase	Rattus norvegicus	127-130
11676881-6	2001	In addition, retinoic acid increased the protein level of p16 (218.75%, P <0.05) and induced p21 protein expression; meanwhile, p27 was undetectable by immunocytochemistry in both control and retinoic acid-treated hepatic stellate cells.	Tretinoin	13-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	96-99
11676881-8	2001	CONCLUSIONS: Up-regulation of p16 and p21 on post-transcriptional level may contribute, in part, to retinoic acid inhibition of transforming growth factor beta 1-initiated rat hepatic stellate cells activation in vitro.	Tretinoin	100-113	KRAS proto-oncogene, GTPase	Rattus norvegicus	38-41
11463487-3	2001	The administration of TAM markedly decreased the tumor development and showed decreased expression of bromodeoxyuridine, cyclin D1, cyclin E, and p21(Cip1) when compared with those of the DMBA-control group; however, a few tumors showed progressive growth in spite of TAM treatment.	Tamoxifen	22-25	KRAS proto-oncogene, GTPase	Rattus norvegicus	146-149
11732210-0	2001	Possible role of K-ras oncogene in mutagenic activity of ethylnitrosourea on lymphocyte hyperproliferation in rat colon.	Ethylnitrosourea	57-73	KRAS proto-oncogene, GTPase	Rattus norvegicus	17-22
11463487-0	2001	Chemically induced rat mammary tumor treated with tamoxifen showed decreased expression of cyclin D1, cyclin E, and p21(Cip1).	Tamoxifen	50-59	KRAS proto-oncogene, GTPase	Rattus norvegicus	116-119
11769610-0	2001	[Effect of calcium and temperature on adhesion of K-ras transformed rat lung cells].	Calcium	11-18	KRAS proto-oncogene, GTPase	Rattus norvegicus	50-55
11513834-6	2001	These results suggest that baicalein inhibits the proliferation of rat heart endothelial cells via G1 and G2 arrest in association with the down-regulation of the expression and function of Cdk1, Cdk2, cyclin D2 and cyclin A proteins, and up-regulation of cyclin E, p15(Ink4B), p53 and p21(CIP1/Waf1).	baicalein	27-36	KRAS proto-oncogene, GTPase	Rattus norvegicus	286-289
11487646-2	2001	Whole-cell patch clamping in the superficial superior collicular layers (sSCs) from P10 to P21 demonstrated a severe decrease in spontaneous EPSC frequency after chronic NMDA treatment.	N-Methylaspartate	170-174	KRAS proto-oncogene, GTPase	Rattus norvegicus	91-94
11476966-11	2001	These results suggested that the enhanced and sustained JNK activation and the upregulation of p53 and p21(WAF1/CIP1) were involved in hepatocyte apoptosis induced by PH with cisplatin.	Cisplatin	175-184	KRAS proto-oncogene, GTPase	Rattus norvegicus	103-106
11724347-7	2001	All three types of the above-mentioned treatments (PMEDAP, DXT, DXT+PMEDAP) increased significantly the number of p21-positive cells, compared with untreated tumours.	dxt	59-62	KRAS proto-oncogene, GTPase	Rattus norvegicus	114-117
11369699-5	2001	This study is to discern the biological effects of p21(Cip1) gene transfer into RSF and its therapeutic effects on AA.	(3r,3as,6ar)-Hexahydrofuro[2,3-B]furan-3-Ol	80-83	KRAS proto-oncogene, GTPase	Rattus norvegicus	51-54
11369699-12	2001	The adenoviral p21(Cip1) gene transfer inhibited growth of RSF without inducing apoptosis.	(3r,3as,6ar)-Hexahydrofuro[2,3-B]furan-3-Ol	59-62	KRAS proto-oncogene, GTPase	Rattus norvegicus	15-18
11318941-5	2001	Dexamethasone stimulated CAT activity of the p21(CIP1) promoter 4.5-fold.	Dexamethasone	0-13	KRAS proto-oncogene, GTPase	Rattus norvegicus	45-48
11316848-0	2001	Role of the increase in p21 in cisplatin-induced acute renal failure in rats.	Cisplatin	31-40	KRAS proto-oncogene, GTPase	Rattus norvegicus	24-27
11316848-2	2001	This was accomplished with the examination of the renal expression of p21 in cisplatin (CDDP)-induced ARF and in rechallenge injury with CDDP.	Cisplatin	77-86	KRAS proto-oncogene, GTPase	Rattus norvegicus	70-73
11316848-2	2001	This was accomplished with the examination of the renal expression of p21 in cisplatin (CDDP)-induced ARF and in rechallenge injury with CDDP.	Cisplatin	88-92	KRAS proto-oncogene, GTPase	Rattus norvegicus	70-73
11316848-5	2001	The first CDDP dose significantly increased p53-positive nuclei at day 1, which disappeared by day 5, and the number of p21-positive nuclei, which had two peaks on days 3 and 9.	Cisplatin	10-14	KRAS proto-oncogene, GTPase	Rattus norvegicus	120-123
11318941-7	2001	Dexamethasone inducibility of p21(CIP1) promoter activity requires the presence of the C/EBP alpha DNA binding site in the GRE of the p21(CIP1) promoter and C/EBP alpha protein.	Dexamethasone	0-13	KRAS proto-oncogene, GTPase	Rattus norvegicus	30-33
11318941-7	2001	Dexamethasone inducibility of p21(CIP1) promoter activity requires the presence of the C/EBP alpha DNA binding site in the GRE of the p21(CIP1) promoter and C/EBP alpha protein.	Dexamethasone	0-13	KRAS proto-oncogene, GTPase	Rattus norvegicus	134-137
11318941-10	2001	The glomerular-sieving method revealed that prednisolone increased p21(CIP1) expression in glomeruli.	Prednisolone	44-56	KRAS proto-oncogene, GTPase	Rattus norvegicus	67-70
11231340-2	2001	To identify potential mechanisms mediating these opposing effects of dietary P on PT growth, this study first focused on p21(WAF1) (p21) because high P reduces while low P enhances serum 1,25-dihydroxyvitamin D, whose potent antiproliferative properties result from the induction of p21.	1,25-dihydroxyvitamin D	187-210	KRAS proto-oncogene, GTPase	Rattus norvegicus	132-135
11181050-0	2001	Ethanol infusion increases ANP and p21 gene expression in isolated perfused rat heart.	Ethanol	0-7	KRAS proto-oncogene, GTPase	Rattus norvegicus	35-38
11181050-3	2001	Ethanol infusion of 150 min duration significantly induced both ANP and p21 mRNA expression of ventricular myocardium compared with hearts infused with vehicle (n = 8).	Ethanol	0-7	KRAS proto-oncogene, GTPase	Rattus norvegicus	72-75
11084022-7	2001	Thymidine incorporation assays revealed an anti-proliferative effect of ALK7 activation in PC12 cells, which correlated with increased transcription from the promoters of cycline-dependent kinase inhibitors p15(INK4B) and p21.	Thymidine	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	222-225
11038236-3	2000	Immunoblotting analysis showed that CCM strongly inhibited DEN-mediated the increased expression of oncogenic p21(ras) and p53 proteins in liver tissues of rats.	Curcumin	36-39	KRAS proto-oncogene, GTPase	Rattus norvegicus	110-113
11819701-2	2000	Anti-inflammatory activities of BR were studied by xylene and croton oil-induced mouse ear edema, carrageenin, histamine and hot scald-induced rat pow edema, adjuvant-induced rat arthritis and cotton pellet induced mouse granuloma formation methods.RESULTS:The 500mg/kg of BR-H2O extract frac-tionated from BR-Methanol extract had inhibitory effect on the formation of DEN-induced GST-P-positive foci in rat liver (GST-P staining was 78% positive in DEN+AAF group vs 20% positive in DEN+AAF+BR group, P<0.05) and the expression of mutant p53 and p21(ras) protein was lower than that of hepatic preneoplastic lesions (33% and 22% positive respectively in DEN+AAF group vs negative in DEN+AAF+BR group).	Bromine	32-34	KRAS proto-oncogene, GTPase	Rattus norvegicus	549-552
11819702-1	2000	AIM:To study the molecular mechanisms of retinoic acid (RA)on prolix-feration and expression of cyclin-dependent kinase inhibitors (CKI), i.e.p16, p21 and p27 in cultured rat hepatic stellate cells (HSC) stimulated with transforming growth factor beta 1 (TGF-beta1).METHODS:HSC were isolated from healthy rat livers and cultured.After stimulated with 1mg/L TGF-beta1, subcultured HSC were treated with or without 1nmol/L RA.	Tretinoin	41-54	KRAS proto-oncogene, GTPase	Rattus norvegicus	147-150
11819702-1	2000	AIM:To study the molecular mechanisms of retinoic acid (RA)on prolix-feration and expression of cyclin-dependent kinase inhibitors (CKI), i.e.p16, p21 and p27 in cultured rat hepatic stellate cells (HSC) stimulated with transforming growth factor beta 1 (TGF-beta1).METHODS:HSC were isolated from healthy rat livers and cultured.After stimulated with 1mg/L TGF-beta1, subcultured HSC were treated with or without 1nmol/L RA.	Radium	56-58	KRAS proto-oncogene, GTPase	Rattus norvegicus	147-150
11038236-3	2000	Immunoblotting analysis showed that CCM strongly inhibited DEN-mediated the increased expression of oncogenic p21(ras) and p53 proteins in liver tissues of rats.	Diethylnitrosamine	59-62	KRAS proto-oncogene, GTPase	Rattus norvegicus	110-113
10969813-1	2000	Azoxymethane (AOM)-induced colonic carcinogenesis involves a number of mutations, including those in the K-ras gene and CTNNB1, that codes for beta-catenin.	Azoxymethane	0-12	KRAS proto-oncogene, GTPase	Rattus norvegicus	105-110
11004662-0	2000	K-ras point mutation is associated with enhancement by deoxycholic acid of colon carcinogenesis induced by azoxymethane, but not with its attenuation by all-trans-retinoic acid.	Deoxycholic Acid	55-71	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-5
11004662-0	2000	K-ras point mutation is associated with enhancement by deoxycholic acid of colon carcinogenesis induced by azoxymethane, but not with its attenuation by all-trans-retinoic acid.	Azoxymethane	107-119	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-5
11004662-6	2000	Administration of DCA significantly increased the incidence of K-ras point mutation in colon tumors and the labeling index in the colon mucosa.	Deoxycholic Acid	18-21	KRAS proto-oncogene, GTPase	Rattus norvegicus	63-68
11819677-5	2000	The results also showed that DMH increased labeling index (LI) of proliferating cell nuclear antigen (PCNA) of intestinal mucosa and the expression of ras-p21.	1,2-Dimethylhydrazine	29-32	KRAS proto-oncogene, GTPase	Rattus norvegicus	155-158
10893439-4	2000	Additionally, CAPE inhibited growth in soft agar and decreased the protein level of p21(ras).	caffeic acid phenethyl ester	14-18	KRAS proto-oncogene, GTPase	Rattus norvegicus	84-87
10969813-1	2000	Azoxymethane (AOM)-induced colonic carcinogenesis involves a number of mutations, including those in the K-ras gene and CTNNB1, that codes for beta-catenin.	Azoxymethane	14-17	KRAS proto-oncogene, GTPase	Rattus norvegicus	105-110
10912792-9	2000	Finally, we report that p21CIP1 was not absolutely required for the genistein-induced G2 arrest, as the isoflavone caused at least partial G2 arrest in p21-deficient Rat-1 fibroblasts as well as in p21-/- mouse embryo fibroblasts.	Isoflavones	104-114	KRAS proto-oncogene, GTPase	Rattus norvegicus	152-155
10926548-7	2000	Heparin induces production of p21, a potent inhibitor of cyclin-dependent kinases, thereby potentially identifying a fundamental mechanism by which heparin inhibits proliferation in smooth muscle-like cells.	Heparin	0-7	KRAS proto-oncogene, GTPase	Rattus norvegicus	30-33
10926548-7	2000	Heparin induces production of p21, a potent inhibitor of cyclin-dependent kinases, thereby potentially identifying a fundamental mechanism by which heparin inhibits proliferation in smooth muscle-like cells.	Heparin	148-155	KRAS proto-oncogene, GTPase	Rattus norvegicus	30-33
10910967-0	2000	Resveratrol depresses the growth of colorectal aberrant crypt foci by affecting bax and p21(CIP) expression.	Resveratrol	0-11	KRAS proto-oncogene, GTPase	Rattus norvegicus	88-91
10910967-7	2000	In conclusion, the results suggest a protective role of RV in colon carcinogenesis with a mechanism involving changes in bax and p21 expression.	Resveratrol	56-58	KRAS proto-oncogene, GTPase	Rattus norvegicus	129-132
10952156-6	2000	Cultured cardiac myocytes treated with Ang II and infected with either control or recombinant adenovirus indicated that expression of p21 and p16 inhibited Ang II-induced cardiac myocyte hypertrophy, [3H]leucine incorporation into total cellular proteins, and skeletal alpha-actin (SK-A) and atrial natriuretic peptide (ANP) mRNA accumulation.	Tritium	201-203	KRAS proto-oncogene, GTPase	Rattus norvegicus	134-137
11819702-3	2000	In addition, RA increased the protein level of p16 (218.75%, P <0.05) and induced p21 protein expression; meanwhile, p27 was undetectable by ICC in both control and RA-treated HSC.	Radium	13-15	KRAS proto-oncogene, GTPase	Rattus norvegicus	85-88
10801895-8	2000	TRO and rosiglitazone attenuated both the mitogen-induced degradation of p27(kip1) and the mitogenic induction of p21(cip1).	Troglitazone	0-3	KRAS proto-oncogene, GTPase	Rattus norvegicus	114-117
10801895-8	2000	TRO and rosiglitazone attenuated both the mitogen-induced degradation of p27(kip1) and the mitogenic induction of p21(cip1).	Rosiglitazone	8-21	KRAS proto-oncogene, GTPase	Rattus norvegicus	114-117
10820188-2	2000	Bacterial lipopolysaccharides induced the GTP loading of p21(ras), and the expression of a dominant-negative mutant of p21(ras) (Deltap21(ras)) inhibited lipopolysaccharide-induced GTP loading in rat primary astrocytes.	Guanosine Triphosphate	42-45	KRAS proto-oncogene, GTPase	Rattus norvegicus	57-60
10771097-0	2000	Treatment of v-Ki-ras-transformed SVC1 cells with low retinoic acid induces malignancy reversion associated with ras p21 down-regulation.	Tretinoin	54-67	KRAS proto-oncogene, GTPase	Rattus norvegicus	117-120
10775445-7	2000	Pretreatment of pancreatic acini with Clostridium botulinum C3 transferase, which specifically inactivates p21(rho), partially inhibited carbachol-induced p125(FAK), p130(cas), and paxillin tyrosine phosphorylation.	Carbachol	137-146	KRAS proto-oncogene, GTPase	Rattus norvegicus	107-110
10775445-7	2000	Pretreatment of pancreatic acini with Clostridium botulinum C3 transferase, which specifically inactivates p21(rho), partially inhibited carbachol-induced p125(FAK), p130(cas), and paxillin tyrosine phosphorylation.	paxillin tyrosine	181-198	KRAS proto-oncogene, GTPase	Rattus norvegicus	107-110
10754208-1	2000	To clarify the involvement of tumor suppressor genes in exogenous and endogenous liver carcinogenesis, alterations of p16, p21 and p53 in hepatocellular carcinomas (HCCs) induced by N-nitrosodiethylamine (DEN) and a choline deficient L-amino acid-defined (CDAA) diet in rats were investigated.	Diethylnitrosamine	182-203	KRAS proto-oncogene, GTPase	Rattus norvegicus	123-126
10888235-7	2000	Regarding suppressor gene expression, both p21 and TGF-beta1 mRNA expression in ethanol-treated rats were similar to those obtained in saline-treated controls.	Ethanol	80-87	KRAS proto-oncogene, GTPase	Rattus norvegicus	43-46
10666051-3	2000	This study was aimed at determining the relationship between inhibition of colorectal cancer by sulindac and sulindac sulfone and the presence of activating K-ras mutations in the 1,2-dimethylhydrazine dihydrochloride rat model.	Sulindac	96-104	KRAS proto-oncogene, GTPase	Rattus norvegicus	157-162
10666051-3	2000	This study was aimed at determining the relationship between inhibition of colorectal cancer by sulindac and sulindac sulfone and the presence of activating K-ras mutations in the 1,2-dimethylhydrazine dihydrochloride rat model.	1,2-DIMETHYLHYDRAZINE DIHYDROCHLORIDE	180-217	KRAS proto-oncogene, GTPase	Rattus norvegicus	157-162
10820188-2	2000	Bacterial lipopolysaccharides induced the GTP loading of p21(ras), and the expression of a dominant-negative mutant of p21(ras) (Deltap21(ras)) inhibited lipopolysaccharide-induced GTP loading in rat primary astrocytes.	Guanosine Triphosphate	42-45	KRAS proto-oncogene, GTPase	Rattus norvegicus	119-122
10820188-2	2000	Bacterial lipopolysaccharides induced the GTP loading of p21(ras), and the expression of a dominant-negative mutant of p21(ras) (Deltap21(ras)) inhibited lipopolysaccharide-induced GTP loading in rat primary astrocytes.	Guanosine Triphosphate	181-184	KRAS proto-oncogene, GTPase	Rattus norvegicus	57-60
10820188-2	2000	Bacterial lipopolysaccharides induced the GTP loading of p21(ras), and the expression of a dominant-negative mutant of p21(ras) (Deltap21(ras)) inhibited lipopolysaccharide-induced GTP loading in rat primary astrocytes.	Guanosine Triphosphate	181-184	KRAS proto-oncogene, GTPase	Rattus norvegicus	119-122
10664504-4	2000	METHODS: p21 messenger RNA (mRNA) levels in rat aortic smooth muscle cells (RASMCs) were determined by Northern blot analysis after treatment with S-nitroso-N-acetylpenicillamine (SNAP) or after adenoviral iNOS gene transfer.	S-Nitroso-N-Acetylpenicillamine	147-178	KRAS proto-oncogene, GTPase	Rattus norvegicus	9-12
10655059-6	2000	Furthermore, we identified common and distinct targets in cells transformed by mutant HRAS, KRAS and NRAS, as well as 61 putative target genes controlled by the RAF/MEK/ERK pathway in reverted cells treated with the MEK-specific inhibitor PD 98059.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	239-247	KRAS proto-oncogene, GTPase	Rattus norvegicus	92-96
10648615-4	2000	The lack of p21(WAF1/CIP1) expression appears to be the result of hypermethylation of the p21(WAF1/CIP1) promoter region, as p21(WAF1/CIP1) protein expression could be induced by growth of Rat-1 cells in the presence of 5-aza-2-deoxycytidine.	Decitabine	220-241	KRAS proto-oncogene, GTPase	Rattus norvegicus	90-93
10648615-4	2000	The lack of p21(WAF1/CIP1) expression appears to be the result of hypermethylation of the p21(WAF1/CIP1) promoter region, as p21(WAF1/CIP1) protein expression could be induced by growth of Rat-1 cells in the presence of 5-aza-2-deoxycytidine.	Decitabine	220-241	KRAS proto-oncogene, GTPase	Rattus norvegicus	90-93
10813127-1	2000	PURPOSE: The effect of pravastatin, an inhibitor of ras p21 isoprenylation, on the gross type of colon tumors induced by azoxymethane was investigated in Wistar rats.	Pravastatin	23-34	KRAS proto-oncogene, GTPase	Rattus norvegicus	56-59
10648615-5	2000	Furthermore, sequence analysis of bisulfite-treated DNA demonstrated extensive methylation of cytosine residues in CpG dinucleotides in a CpG-rich island in the promoter region of the p21(WAF1/CIP1) gene.	hydrogen sulfite	34-43	KRAS proto-oncogene, GTPase	Rattus norvegicus	184-187
10648615-5	2000	Furthermore, sequence analysis of bisulfite-treated DNA demonstrated extensive methylation of cytosine residues in CpG dinucleotides in a CpG-rich island in the promoter region of the p21(WAF1/CIP1) gene.	Cytosine	94-102	KRAS proto-oncogene, GTPase	Rattus norvegicus	184-187
10648615-5	2000	Furthermore, sequence analysis of bisulfite-treated DNA demonstrated extensive methylation of cytosine residues in CpG dinucleotides in a CpG-rich island in the promoter region of the p21(WAF1/CIP1) gene.	cytidylyl-3'-5'-guanosine	115-132	KRAS proto-oncogene, GTPase	Rattus norvegicus	184-187
10813127-6	2000	Administration of pravastatin at both dosages also significantly decreased the amounts of membrane-associated ras p21 in colon tumors.	Pravastatin	18-29	KRAS proto-oncogene, GTPase	Rattus norvegicus	114-117
10590233-9	1999	Since O(6)-methylguanine adducts can cause activating mutations in the K-ras and beta-catenin genes, we examined the effects of BG on these mutations.	O-(6)-methylguanine	6-24	KRAS proto-oncogene, GTPase	Rattus norvegicus	71-76
10601298-1	1999	p21(c-Ha-Ras) (Ras) can be activated by the guanine nucleotide exchange factor mSOS1 or by S-nitrosylation of cysteine 118 via nitric oxide (NO).	Cysteine	110-118	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-12
10601298-1	1999	p21(c-Ha-Ras) (Ras) can be activated by the guanine nucleotide exchange factor mSOS1 or by S-nitrosylation of cysteine 118 via nitric oxide (NO).	Nitric Oxide	127-139	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-12
10447521-11	1999	By suppressing cell proliferation and insulin biosynthesis, the p21 induction is likely to be implicated in the beta-cell glucose toxicity.	Glucose	122-129	KRAS proto-oncogene, GTPase	Rattus norvegicus	64-67
10597246-0	1999	2-acetaminofluorene blocks cell cycle progression after hepatectomy by p21 induction and lack of cyclin E expression.	2-Acetylaminofluorene	0-19	KRAS proto-oncogene, GTPase	Rattus norvegicus	71-74
10403787-3	1999	Consistently, the molar potency of accumulation of p21(ras)-GTP by aFGF was significantly higher in DBcAMP-treated AC than in quiescent AC.	Guanosine Triphosphate	60-63	KRAS proto-oncogene, GTPase	Rattus norvegicus	51-54
10403787-3	1999	Consistently, the molar potency of accumulation of p21(ras)-GTP by aFGF was significantly higher in DBcAMP-treated AC than in quiescent AC.	Bucladesine	100-106	KRAS proto-oncogene, GTPase	Rattus norvegicus	51-54
10220498-15	1999	Treatment with a DNA methylation inhibitor (azadeoxycytidine) resulted in reexpression of p16 in K-ras-transformed IEC-18 cells, suggesting that the expression of p16 was suppressed by DNA methylation.	azadeoxycytidine	44-60	KRAS proto-oncogene, GTPase	Rattus norvegicus	97-102
10374839-6	1999	In an in vivo rodent model systems using the aflatoxin B1-sensitive male F344 rat, previous studies have shown that hepatocarcinogenesis is accompanied by significant incidences of codon 12 mutations in K-ras and codon 13 mutations in N-ras genes, but in contrast to the human, apparently not by mutations in codon 243 of the p53 gene (which corresponds to codon 249 in the human gene).	Aflatoxin B1	45-57	KRAS proto-oncogene, GTPase	Rattus norvegicus	203-208
10544030-0	1999	Manumycin A, inhibitor of ras farnesyltransferase, inhibits proliferation and migration of rat vascular smooth muscle cells.	manumycin	0-11	KRAS proto-oncogene, GTPase	Rattus norvegicus	26-29
10544030-2	1999	A low dose (50 ng/ml) of manumycin A, an inhibitor of p21(ras) (ras) farnesylation, significantly inhibited proliferation of rat VSMCs stimulated by the platelet-derived growth factor (PDGF).	manumycin	25-36	KRAS proto-oncogene, GTPase	Rattus norvegicus	54-62
10544030-2	1999	A low dose (50 ng/ml) of manumycin A, an inhibitor of p21(ras) (ras) farnesylation, significantly inhibited proliferation of rat VSMCs stimulated by the platelet-derived growth factor (PDGF).	manumycin	25-36	KRAS proto-oncogene, GTPase	Rattus norvegicus	58-61
10544030-4	1999	Western blot analysis showed that manumycin A reduced the amount of functional ras localized at the cytoplasmic membrane and inhibited the phosphorylation of p42/44 mitogen-activated protein kinase (MAPK).	manumycin	34-45	KRAS proto-oncogene, GTPase	Rattus norvegicus	79-82
10544030-6	1999	These results indicate that the interruption of the ras/MAPK signal transduction pathway and the disorganization of alpha actin fibers are the main cause of manumycin A inhibition of VSMC proliferation and migration induced by PDGF.	manumycin	157-168	KRAS proto-oncogene, GTPase	Rattus norvegicus	52-55
10556660-5	1999	One rat with K-ras activation by G:C transversion (GGT-->GCT) at codon 12 was found among 26 rats of the CS groups in the three exposure periods.	Cesium	108-110	KRAS proto-oncogene, GTPase	Rattus norvegicus	13-18
10556660-6	1999	These results show that active oxygens introduced by passive smoking may contribute to K-ras activation as an initiator of a tumor model, possibly through the oxygen-induced DNA damage, and may also contribute to an initial activation and the subsequent down-regulation of PKC as a promoter.	Oxygen	31-38	KRAS proto-oncogene, GTPase	Rattus norvegicus	87-92
10556660-6	1999	These results show that active oxygens introduced by passive smoking may contribute to K-ras activation as an initiator of a tumor model, possibly through the oxygen-induced DNA damage, and may also contribute to an initial activation and the subsequent down-regulation of PKC as a promoter.	Oxygen	31-37	KRAS proto-oncogene, GTPase	Rattus norvegicus	87-92
10388522-8	1999	As shown by flow cytometric analysis, MPP+ induced a block in the G0/G1 to S phase transition that correlated with increased expression of the cyclin-dependent kinase inhibitor p21(WAF1/Cip1) and growth arrest.	mangion-purified polysaccharide (Candida albicans)	38-42	KRAS proto-oncogene, GTPase	Rattus norvegicus	177-180
10198335-1	1999	We evaluated intracellular pathways responsible for the activation of the small GTP-binding protein Rho p21 in rat pancreatic acini.	Guanosine Triphosphate	80-83	KRAS proto-oncogene, GTPase	Rattus norvegicus	104-107
10198335-13	1999	We concluded that the small GTP-binding protein RhoA p21 exists in pancreatic acini and appears to be involved in the mediation of pancreatic enzyme secretion evoked by CCK and carbachol.	Guanosine Triphosphate	28-31	KRAS proto-oncogene, GTPase	Rattus norvegicus	53-56
10198335-13	1999	We concluded that the small GTP-binding protein RhoA p21 exists in pancreatic acini and appears to be involved in the mediation of pancreatic enzyme secretion evoked by CCK and carbachol.	Carbachol	177-186	KRAS proto-oncogene, GTPase	Rattus norvegicus	53-56
9834277-5	1998	K-ras mutations in the neoplasms were determined by oligonucleotide hybridization and confirmed by primer mediated-restriction fragment length polymorphism.	Oligonucleotides	52-67	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-5
10069996-0	1999	Polyamine depletion arrests cell cycle and induces inhibitors p21(Waf1/Cip1), p27(Kip1), and p53 in IEC-6 cells.	Polyamines	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	62-65
10027563-3	1999	Exposure to RA caused an immediate up-regulation of NeuroD, increased p21 expression, and concurrent exit from cell cycle.	Tretinoin	12-14	KRAS proto-oncogene, GTPase	Rattus norvegicus	70-73
10200221-10	1999	Moreover, neurons of ages P14 or P21 showed a partial or complete recovery after reintroduction of oxygen and glucose, unlike mature neurons.	Oxygen	99-105	KRAS proto-oncogene, GTPase	Rattus norvegicus	33-36
10200221-10	1999	Moreover, neurons of ages P14 or P21 showed a partial or complete recovery after reintroduction of oxygen and glucose, unlike mature neurons.	Glucose	110-117	KRAS proto-oncogene, GTPase	Rattus norvegicus	33-36
10027851-4	1999	In forebrain the A2AR agonist-stimulated [35S]GTPgammaS binding increases rapidly after P7, reaching its highest levels at P21 and then declining slightly to adult levels.	Sulfur-35	42-45	KRAS proto-oncogene, GTPase	Rattus norvegicus	123-126
10390143-1	1999	The HMGCoA reductase inhibitor Lovastatin (LOV) has previously shown to abrogate p21ras farnesylation, which is associated with invasive and metastatic abilities in many tumor models.	Lovastatin	31-41	KRAS proto-oncogene, GTPase	Rattus norvegicus	81-84
10390143-1	1999	The HMGCoA reductase inhibitor Lovastatin (LOV) has previously shown to abrogate p21ras farnesylation, which is associated with invasive and metastatic abilities in many tumor models.	Lovastatin	43-46	KRAS proto-oncogene, GTPase	Rattus norvegicus	81-84
9792921-10	1998	Antisense oligonucleotides of C/EBPalpha repressed albumin secretion and the expression of p21, suggesting that the transcription factor, C/EBPalpha, may play a crucial role in the growth and differentiation of hepatocytes in spheroids.	Oligonucleotides	10-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	91-94
9929613-6	1998	(ii) tritiated thymidine [3H]TdR autoradiographic birthdating studies show that the vast majority of 2A4(+) ORNs present at P21, when adult 2A4(+) ORN densities are first observed, were "born" postnatally, between P3 and P10.	Tritium	26-28	KRAS proto-oncogene, GTPase	Rattus norvegicus	124-127
9811854-0	1998	v-K-ras leads to preferential farnesylation of p21(ras) in FRTL-5 cells: multiple interference with the isoprenoid pathway.	Terpenes	104-114	KRAS proto-oncogene, GTPase	Rattus norvegicus	2-7
9811854-1	1998	The isoprenoid pathway in FRTL-5 thyroid cells was found to be deeply altered on transformation with v-K-ras.	Terpenes	4-14	KRAS proto-oncogene, GTPase	Rattus norvegicus	103-108
9811854-2	1998	A dramatic overall reduction of protein prenylation was found in v-K-ras-transformed cells in comparison with the parent FRTL-5 cells, as shown by labeling cells with [3H]mevalonic acid.	Tritium	168-170	KRAS proto-oncogene, GTPase	Rattus norvegicus	67-72
9811854-2	1998	A dramatic overall reduction of protein prenylation was found in v-K-ras-transformed cells in comparison with the parent FRTL-5 cells, as shown by labeling cells with [3H]mevalonic acid.	Mevalonic Acid	171-185	KRAS proto-oncogene, GTPase	Rattus norvegicus	67-72
9811854-6	1998	The K-ras oncogene activation also resulted in an overall decrease of [3H]-MVA incorporation into isopentenyl-tRNA together with an increase of unprocessed [3H]-MVA and no alteration in [3H]-MVA uptake.	Tritium	71-73	KRAS proto-oncogene, GTPase	Rattus norvegicus	4-9
9811854-6	1998	The K-ras oncogene activation also resulted in an overall decrease of [3H]-MVA incorporation into isopentenyl-tRNA together with an increase of unprocessed [3H]-MVA and no alteration in [3H]-MVA uptake.	isopentenyl-trna	98-114	KRAS proto-oncogene, GTPase	Rattus norvegicus	4-9
9811854-6	1998	The K-ras oncogene activation also resulted in an overall decrease of [3H]-MVA incorporation into isopentenyl-tRNA together with an increase of unprocessed [3H]-MVA and no alteration in [3H]-MVA uptake.	Tritium	157-159	KRAS proto-oncogene, GTPase	Rattus norvegicus	4-9
9811854-6	1998	The K-ras oncogene activation also resulted in an overall decrease of [3H]-MVA incorporation into isopentenyl-tRNA together with an increase of unprocessed [3H]-MVA and no alteration in [3H]-MVA uptake.	Tritium	157-159	KRAS proto-oncogene, GTPase	Rattus norvegicus	4-9
9811854-7	1998	The effects of v-K-ras on protein prenylation could be mimicked in FRTL-5 cells by lowering the concentration of exogenous [3H]-MVA whereas increasing the [3H]-MVA concentration did not revert the alterations observed in transformed cells.	Tritium	124-126	KRAS proto-oncogene, GTPase	Rattus norvegicus	17-22
9811854-10	1998	This study represents an example of how expression of the v-K-ras oncogene, through multiple interferences with the isoprenoid metabolic pathway, may result in the preferential farnesylation of the ras oncogene product p21(ras).	Terpenes	116-126	KRAS proto-oncogene, GTPase	Rattus norvegicus	60-65
9811854-10	1998	This study represents an example of how expression of the v-K-ras oncogene, through multiple interferences with the isoprenoid metabolic pathway, may result in the preferential farnesylation of the ras oncogene product p21(ras).	Terpenes	116-126	KRAS proto-oncogene, GTPase	Rattus norvegicus	219-222
9929613-6	1998	(ii) tritiated thymidine [3H]TdR autoradiographic birthdating studies show that the vast majority of 2A4(+) ORNs present at P21, when adult 2A4(+) ORN densities are first observed, were "born" postnatally, between P3 and P10.	Tritiated thymidine	5-24	KRAS proto-oncogene, GTPase	Rattus norvegicus	124-127
9693800-7	1998	C-fibre evoked dorsal horn neuronal responses recorded from anaesthetized rat pups were highly sensitive to spinal morphine at P21, (EC50 0.005 microgram), compared to the adult (EC50 0.9 microgram).	Morphine	115-123	KRAS proto-oncogene, GTPase	Rattus norvegicus	127-130
9671688-7	1998	Delaying the BDNF infusion until transplanted tissue was approximately P8-P21 greatly enhanced the effect on rotational behavior and doubled the area of dopamine fiber outgrowth from the transplants.	Dopamine	153-161	KRAS proto-oncogene, GTPase	Rattus norvegicus	74-77
9442036-0	1998	Glucocorticoids stimulate p21 gene expression by targeting multiple transcriptional elements within a steroid responsive region of the p21waf1/cip1 promoter in rat hepatoma cells.	Steroids	102-109	KRAS proto-oncogene, GTPase	Rattus norvegicus	26-29
9602029-4	1998	Kainate (0.03-0.3 nmol) was infused into the dorsal midbrain of postnatal day 7 (P7), P14 and P21 rat pups.	Kainic Acid	0-7	KRAS proto-oncogene, GTPase	Rattus norvegicus	94-97
9537650-0	1998	Alterations in the expression of alpha6beta4 integrin and p21/WAF1/Cip1 in N-nitrosomethylbenzylamine-induced rat esophageal tumorigenesis.	nitrosobenzylmethylamine	75-101	KRAS proto-oncogene, GTPase	Rattus norvegicus	58-61
9537650-10	1998	These findings suggest that alteration in alpha6beta4 integrin and p21/WAF1/Cip1 expression may be an important biomarker for tumor progression in NMBA-induced rat esophageal tumorigenesis.	nitrosobenzylmethylamine	147-151	KRAS proto-oncogene, GTPase	Rattus norvegicus	67-70
11601354-4	1998	RESULT: The extract of BR(500 mg/kg) has inhibitory effect on the formation of diethylnitrosamine-induced GST-P-positive foci in F344 rat and the expression of mutant p53 and p21 protein was lower than that of hepatic preneoplastic lesions, and the increasing gamma-glutamyltranspeptidase(gamma-GT) activity in rat liver treated with Solt-Farber protocol was decreased by the extract of BR.	Bromine	23-25	KRAS proto-oncogene, GTPase	Rattus norvegicus	175-178
11601354-4	1998	RESULT: The extract of BR(500 mg/kg) has inhibitory effect on the formation of diethylnitrosamine-induced GST-P-positive foci in F344 rat and the expression of mutant p53 and p21 protein was lower than that of hepatic preneoplastic lesions, and the increasing gamma-glutamyltranspeptidase(gamma-GT) activity in rat liver treated with Solt-Farber protocol was decreased by the extract of BR.	Diethylnitrosamine	79-97	KRAS proto-oncogene, GTPase	Rattus norvegicus	175-178
9494119-12	1998	Ethanol and NGF co-treatment increased expression of p21(Cip-1/WAF1) and p16(INK4a) cdk inhibitor proteins and decreased hepatocyte DNA synthesis.	Ethanol	0-7	KRAS proto-oncogene, GTPase	Rattus norvegicus	53-56
9484833-3	1998	Induction of p21 led to permanent growth arrest, as evidenced by cell counts, FACS analysis, and thymidine incorporation.	Thymidine	97-106	KRAS proto-oncogene, GTPase	Rattus norvegicus	13-16
9484833-5	1998	Northern analysis revealed that endogenous p21 mRNA increased following IPTG removal, which may be responsible for the continued growth arrest despite the decrease in ectopic p21 expression.	Isopropyl Thiogalactoside	72-76	KRAS proto-oncogene, GTPase	Rattus norvegicus	43-46
9484833-5	1998	Northern analysis revealed that endogenous p21 mRNA increased following IPTG removal, which may be responsible for the continued growth arrest despite the decrease in ectopic p21 expression.	Isopropyl Thiogalactoside	72-76	KRAS proto-oncogene, GTPase	Rattus norvegicus	175-178
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
9442037-5	1998	The stimulation of p21 protein levels and promoter activity, as well as inhibition of CDK2-mediated retinoblastoma protein phosphorylation, by the synthetic glucocorticoid, dexamethasone, required the expression of C/EBP alpha.	Dexamethasone	173-186	KRAS proto-oncogene, GTPase	Rattus norvegicus	19-22
9442037-6	1998	Overexpression of C/EBP alpha in as4 cells rescued the dexamethasone responsiveness of the p21 promoter.	Dexamethasone	55-68	KRAS proto-oncogene, GTPase	Rattus norvegicus	91-94
9442037-7	1998	Site-directed mutagenesis of the p21 promoter revealed that dexamethasone stimulation of p21 promoter activity required the C/EBP consensus DNA-binding site.	Dexamethasone	60-73	KRAS proto-oncogene, GTPase	Rattus norvegicus	33-36
9442037-7	1998	Site-directed mutagenesis of the p21 promoter revealed that dexamethasone stimulation of p21 promoter activity required the C/EBP consensus DNA-binding site.	Dexamethasone	60-73	KRAS proto-oncogene, GTPase	Rattus norvegicus	89-92
9442037-9	1998	Our results have established a functional link between the glucocorticoid receptor signaling pathway that mediates a G1 cell cycle arrest of rat hepatoma cells and the transcriptional control of p21 by a cascade that requires the steroid induction of C/EBP alpha gene expression.	Steroids	230-237	KRAS proto-oncogene, GTPase	Rattus norvegicus	195-198
9405068-19	1997	The ras-related small GTP-binding protein rho p21 is at least partially involved in mediating NMB-induced tyrosine phosphorylation of p125(FAK).	Tyrosine	106-114	KRAS proto-oncogene, GTPase	Rattus norvegicus	46-49
9422737-3	1998	Radicicol, an antifungal antibiotic, was found to inhibit the K-ras signaling pathway reconstituted in yeast.	monorden	0-9	KRAS proto-oncogene, GTPase	Rattus norvegicus	62-67
9422737-4	1998	In K-ras-transformed, rat epithelial, and K-ras-activated, human pancreatic carcinoma cell lines, radicicol inhibited K-Ras-induced hyperphosphorylation of Erk2.	monorden	98-107	KRAS proto-oncogene, GTPase	Rattus norvegicus	3-8
9422737-4	1998	In K-ras-transformed, rat epithelial, and K-ras-activated, human pancreatic carcinoma cell lines, radicicol inhibited K-Ras-induced hyperphosphorylation of Erk2.	monorden	98-107	KRAS proto-oncogene, GTPase	Rattus norvegicus	42-47
9511172-5	1998	Beginning on P21, capsaicin-treated rats under both conditions showed transient skin ulcers distributed throughout the head and neck regions.	Capsaicin	18-27	KRAS proto-oncogene, GTPase	Rattus norvegicus	13-16
9405068-15	1997	Pretreatment with Clostridium botulinum C3 exoenzyme which inactivates the small GTP-binding protein rho p21, also inhibited tyrosine phosphorylation of p125(FAK) by 55%.	Guanosine Triphosphate	81-84	KRAS proto-oncogene, GTPase	Rattus norvegicus	105-108
9405068-19	1997	The ras-related small GTP-binding protein rho p21 is at least partially involved in mediating NMB-induced tyrosine phosphorylation of p125(FAK).	Guanosine Triphosphate	22-25	KRAS proto-oncogene, GTPase	Rattus norvegicus	46-49
9406920-1	1997	Pentylenetetrazol (PTZ)-induced status epilepticus (SE) leads to acute and long-term metabolic decreases in specific brain regions of rats at 10 (P10) or 21 days after birth (P21).	Pentylenetetrazole	0-17	KRAS proto-oncogene, GTPase	Rattus norvegicus	175-178
9394728-1	1997	BACKGROUND & AIMS: Mutations of c-K-ras occur commonly in colonic neoplasms.	Adenosine Monophosphate	12-15	KRAS proto-oncogene, GTPase	Rattus norvegicus	36-43
9394728-2	1997	The aim of this study was to determine how c-K-ras mutations alter the responses to the chemopreventive agent sulindac.	Sulindac	110-118	KRAS proto-oncogene, GTPase	Rattus norvegicus	43-50
9394728-3	1997	METHODS: The parental rat intestinal cell line IEC-18 and c-K-ras-transformed derivatives were treated with sulindac sulfide.	sulindac sulfide	108-124	KRAS proto-oncogene, GTPase	Rattus norvegicus	58-65
9394728-10	1997	CONCLUSIONS: c-K-ras-transformed enterocytes are relatively resistant to sulindac sulfide-induced growth inhibition and apoptosis, which may result from specific reduction of bak expression.	sulindac sulfide	73-89	KRAS proto-oncogene, GTPase	Rattus norvegicus	13-20
9427485-3	1997	The most rapid decline in dye coupling was observed between P14 and P21, the beginning of the most active period of synaptogenesis in the dentate molecular layer.	dentate	138-145	KRAS proto-oncogene, GTPase	Rattus norvegicus	68-71
9333187-6	1997	Chronic treatment with PCP resulted in greater behavioral ratings of seizure activity after NMDA administration, observed 1 (P21), 5 (P26), and 15 (P36) days after the last injection of PCP, indicating increased sensitivity of the NMDA receptor/channel complex during this period after withdrawal from developmental NMDA antagonism.	Phencyclidine	23-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	125-128
9359417-3	1997	The present study was aimed at examining whether protein kinase C (PKC) activation, calcium mobilization, cytoskeletal organization and small G-protein p21(rho) activation play a role in mediating the stimulation of tyrosine phosphorylation by CCK-8 in acini.	Tyrosine	216-224	KRAS proto-oncogene, GTPase	Rattus norvegicus	152-155
9359417-14	1997	For this tyrosine phosphorylation to occur, the integrity of the actin, but not the microtubule, cytoskeleton is essential as well as the activation of p21(rho).	Tyrosine	9-17	KRAS proto-oncogene, GTPase	Rattus norvegicus	152-155
9406920-1	1997	Pentylenetetrazol (PTZ)-induced status epilepticus (SE) leads to acute and long-term metabolic decreases in specific brain regions of rats at 10 (P10) or 21 days after birth (P21).	Pentylenetetrazole	19-22	KRAS proto-oncogene, GTPase	Rattus norvegicus	175-178
9211935-6	1997	In contrast, signaling was blocked by preventing p21(ras) from associating with the plasma membrane or mutating Cys118 on p21(ras) to Ser.	Serine	134-137	KRAS proto-oncogene, GTPase	Rattus norvegicus	49-52
9295352-4	1997	The resulting nitric oxide (NO) acts as a second messenger, activating the p21(WAF1) promoter and inducing expression of p21(WAF1) cyclin-dependent kinase inhibitor.	Nitric Oxide	14-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	75-78
9295352-4	1997	The resulting nitric oxide (NO) acts as a second messenger, activating the p21(WAF1) promoter and inducing expression of p21(WAF1) cyclin-dependent kinase inhibitor.	Nitric Oxide	14-26	KRAS proto-oncogene, GTPase	Rattus norvegicus	121-124
9295352-8	1997	Blocking NOS with an inhibitor decreases neurite extension, but induction of p21(WAF1) with isopropyl-1-thio-beta-D-galactopyranoside restored this response.	Isopropyl Thiogalactoside	92-133	KRAS proto-oncogene, GTPase	Rattus norvegicus	77-80
9295352-9	1997	Levels of p21(WAF1) induced by isopropyl-1-thio-beta-D-galactopyranoside were similar to those induced by NGF.	Isopropyl Thiogalactoside	31-72	KRAS proto-oncogene, GTPase	Rattus norvegicus	10-13
9211935-6	1997	In contrast, signaling was blocked by preventing p21(ras) from associating with the plasma membrane or mutating Cys118 on p21(ras) to Ser.	Serine	134-137	KRAS proto-oncogene, GTPase	Rattus norvegicus	122-125
9215709-4	1997	Neutralization of endogenous p21-ras by microinjection of p21-ras antibody (Y13-259) reduced the maximum peak barium current, I(max), whereas microinjection of oncogenic p21-K-ras increased the current.	Barium	110-116	KRAS proto-oncogene, GTPase	Rattus norvegicus	29-32
9224717-4	1997	The gax-induced growth inhibition correlated with a p53-independent up-regulation of the cyclin-dependent kinase inhibitor p21.	1-{3-[(4-Pyridin-2-Ylpiperazin-1-Yl)sulfonyl]phenyl}-3-(1,3-Thiazol-2-Yl)urea	4-7	KRAS proto-oncogene, GTPase	Rattus norvegicus	123-126
9224717-5	1997	Gax overexpression also led to an association of p21 with cdk2 complexes and a decrease in cdk2 activity.	1-{3-[(4-Pyridin-2-Ylpiperazin-1-Yl)sulfonyl]phenyl}-3-(1,3-Thiazol-2-Yl)urea	0-3	KRAS proto-oncogene, GTPase	Rattus norvegicus	49-52
9224717-8	1997	These data indicate that gax overexpression can inhibit cell proliferation in a p21-dependent manner and can modulate injury-induced changes in vessel wall morphology that result from excessive cellular proliferation.	1-{3-[(4-Pyridin-2-Ylpiperazin-1-Yl)sulfonyl]phenyl}-3-(1,3-Thiazol-2-Yl)urea	25-28	KRAS proto-oncogene, GTPase	Rattus norvegicus	80-83
9223123-10	1997	After RA dosing, cyclin protein inhibitors (p16, p21, p27) revealed robust labeling with their respective antibodies in Y/AL and O/DR rats as analyzed by Western blotting.	Tretinoin	6-8	KRAS proto-oncogene, GTPase	Rattus norvegicus	49-52
9215709-4	1997	Neutralization of endogenous p21-ras by microinjection of p21-ras antibody (Y13-259) reduced the maximum peak barium current, I(max), whereas microinjection of oncogenic p21-K-ras increased the current.	Barium	110-116	KRAS proto-oncogene, GTPase	Rattus norvegicus	58-61
9215709-4	1997	Neutralization of endogenous p21-ras by microinjection of p21-ras antibody (Y13-259) reduced the maximum peak barium current, I(max), whereas microinjection of oncogenic p21-K-ras increased the current.	Barium	110-116	KRAS proto-oncogene, GTPase	Rattus norvegicus	58-61
9215709-5	1997	Thus, endogenous p21-ras is involved in the tonic regulation of calcium currents in these cells.	Calcium	64-71	KRAS proto-oncogene, GTPase	Rattus norvegicus	17-20
9215709-13	1997	However, co-microinjection of pp60c-src with Y13-259 antibody prevented the increase in I(max), implying that pp60c-src can also regulate calcium currents via the activation of endogenous p21-ras.	Calcium	138-145	KRAS proto-oncogene, GTPase	Rattus norvegicus	188-191
9210960-0	1997	Assessment of mutations in Ki-ras and p53 in colon cancers from azoxymethane- and dimethylhydrazine-treated rats.	Azoxymethane	64-76	KRAS proto-oncogene, GTPase	Rattus norvegicus	27-33
9210960-0	1997	Assessment of mutations in Ki-ras and p53 in colon cancers from azoxymethane- and dimethylhydrazine-treated rats.	Dimethylhydrazines	82-99	KRAS proto-oncogene, GTPase	Rattus norvegicus	27-33
9210960-8	1997	These data confirm that Ki-ras was mutated in most colon cancers in AOM- or DMH-treated rats but indicate that molecular alterations in the p53 gene, if they occur in this animal model, are different from most p53 mutations in human colon cancers.	Dimethylhydrazines	76-79	KRAS proto-oncogene, GTPase	Rattus norvegicus	24-30
9070894-0	1997	Geranylgeranyl as well as farnesyl moiety is transferred to Ras p21 overproduced in adrenocortical cells transformed by c-Ha-rasEJ oncogene.	geranylgeranyl	0-14	KRAS proto-oncogene, GTPase	Rattus norvegicus	64-67
9163674-10	1997	The G-->T transversions observed in this study contrast with the most frequent aflatoxin B1 in vivo induced mutations, G-->A transitions in the rat Ki-ras gene.	Aflatoxin B1	82-94	KRAS proto-oncogene, GTPase	Rattus norvegicus	154-160
9070894-0	1997	Geranylgeranyl as well as farnesyl moiety is transferred to Ras p21 overproduced in adrenocortical cells transformed by c-Ha-rasEJ oncogene.	FARNESYL	26-34	KRAS proto-oncogene, GTPase	Rattus norvegicus	64-67
9070894-4	1997	Radioactivity derived from [14C]mevalonolactone was strongly incorporated into Ras p21 overproduced in RTAC cells.	[14c]mevalonolactone	27-47	KRAS proto-oncogene, GTPase	Rattus norvegicus	83-86
9070894-5	1997	RTAC cells pretreated with lovastatin and labeled with either [3H]geranylgeranyl-pyrophosphate or [3H]farnesyl-pyrophosphate incorporated also radioactivity into Ras p21.	Lovastatin	27-37	KRAS proto-oncogene, GTPase	Rattus norvegicus	166-169
8640740-0	1996	Low expression of the WAF1/CIP1 gene product, p21, in enzyme-altered foci induced in rat liver by diethylnitrosamine or phenobarbital.	Diethylnitrosamine	98-116	KRAS proto-oncogene, GTPase	Rattus norvegicus	46-49
9006098-0	1996	Variant mutational activation of the K-ras oncogene in renal mesenchymal tumors induced in newborn F344 rats by methyl(methoxymethyl)nitrosamine.	Methoxymethyl-methylnitrosamine	112-144	KRAS proto-oncogene, GTPase	Rattus norvegicus	37-42
8761421-0	1996	Hepatocyte expression of tumor associated aldehyde dehydrogenase (ALDH-3) and p21 Ras following diethylnitrosamine (DEN) initiation and chronic exposure to di(2-ethylhexyl)phthalate (DHEP).	Diethylnitrosamine	96-114	KRAS proto-oncogene, GTPase	Rattus norvegicus	78-81
8761421-6	1996	We found that ALDH-3 and p21 expression were significantly enhanced in rats receiving PB after DEN initiation at 26 weeks and that the incidence of hepatocellular carcinomas was likewise increased compared to control or DEN only treated animals.	Phenobarbital	86-88	KRAS proto-oncogene, GTPase	Rattus norvegicus	25-28
8761421-6	1996	We found that ALDH-3 and p21 expression were significantly enhanced in rats receiving PB after DEN initiation at 26 weeks and that the incidence of hepatocellular carcinomas was likewise increased compared to control or DEN only treated animals.	Diethylnitrosamine	95-98	KRAS proto-oncogene, GTPase	Rattus norvegicus	25-28
8663173-2	1996	In this study, we investigated the influence of the protein kinase C (PKC)-dependent system upon the ability of insulin to stimulate p21(ras).GTP loading in 3T3-L1 adipocytes.	Guanosine Triphosphate	142-145	KRAS proto-oncogene, GTPase	Rattus norvegicus	133-136
8663173-3	1996	Activation of PKC by 12-0-tetradecanoylphorbol-13-acetate (TPA) did not affect the basal amount of p21(ras).GTP but significantly reduced insulin-induced increases in p21(ras).GTP.	Tetradecanoylphorbol Acetate	59-62	KRAS proto-oncogene, GTPase	Rattus norvegicus	167-170
8663173-3	1996	Activation of PKC by 12-0-tetradecanoylphorbol-13-acetate (TPA) did not affect the basal amount of p21(ras).GTP but significantly reduced insulin-induced increases in p21(ras).GTP.	Guanosine Triphosphate	108-111	KRAS proto-oncogene, GTPase	Rattus norvegicus	167-170
8663173-5	1996	Depletion of PKC by an 18-h incubation with TPA or inhibition by bisindolylmaleimide resulted in profound inhibition of the insulin-induced p21(ras).GTP loading.	Tetradecanoylphorbol Acetate	44-47	KRAS proto-oncogene, GTPase	Rattus norvegicus	140-143
8663173-5	1996	Depletion of PKC by an 18-h incubation with TPA or inhibition by bisindolylmaleimide resulted in profound inhibition of the insulin-induced p21(ras).GTP loading.	bisindolylmaleimide	65-84	KRAS proto-oncogene, GTPase	Rattus norvegicus	140-143
8663173-5	1996	Depletion of PKC by an 18-h incubation with TPA or inhibition by bisindolylmaleimide resulted in profound inhibition of the insulin-induced p21(ras).GTP loading.	Guanosine Triphosphate	149-152	KRAS proto-oncogene, GTPase	Rattus norvegicus	140-143
8663173-9	1996	Removal of this inhibitory influence activates GAP and reduces insulin-stimulated p21(ras).GTP loading.	Guanosine Triphosphate	91-94	KRAS proto-oncogene, GTPase	Rattus norvegicus	82-85
9119740-10	1997	These results indicate firstly that specific Ki-ras, Ha-ras and p53 gene mutations in MNU-induced lesions are related to particular alkylation sites (G:C to A:T transitions) and secondly, although not essential, Ki-ras, Ha-ras or p53 gene mutations may be involved in the progression stage of forestomach, intestine and soft tissue neoplasms induced by MNU.	Methylnitrosourea	86-89	KRAS proto-oncogene, GTPase	Rattus norvegicus	45-51
9119740-10	1997	These results indicate firstly that specific Ki-ras, Ha-ras and p53 gene mutations in MNU-induced lesions are related to particular alkylation sites (G:C to A:T transitions) and secondly, although not essential, Ki-ras, Ha-ras or p53 gene mutations may be involved in the progression stage of forestomach, intestine and soft tissue neoplasms induced by MNU.	Methylnitrosourea	86-89	KRAS proto-oncogene, GTPase	Rattus norvegicus	212-218
9119740-10	1997	These results indicate firstly that specific Ki-ras, Ha-ras and p53 gene mutations in MNU-induced lesions are related to particular alkylation sites (G:C to A:T transitions) and secondly, although not essential, Ki-ras, Ha-ras or p53 gene mutations may be involved in the progression stage of forestomach, intestine and soft tissue neoplasms induced by MNU.	Methylnitrosourea	353-356	KRAS proto-oncogene, GTPase	Rattus norvegicus	45-51
9029163-0	1997	p53 mutation and absence of mdm2 amplification and Ki-ras mutation in 4-hydroxyamino quinoline 1-oxide induced transplantable osteosarcomas in rats.	4-Hydroxyaminoquinoline-1-oxide	70-102	KRAS proto-oncogene, GTPase	Rattus norvegicus	51-57
9020896-0	1996	K-ras codon 12 and 61 point mutations in bromodeoxyuridine- and N-nitrosomethylurea-induced rat renal mesenchymal tumors.	Bromodeoxyuridine	41-58	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-5
9020896-0	1996	K-ras codon 12 and 61 point mutations in bromodeoxyuridine- and N-nitrosomethylurea-induced rat renal mesenchymal tumors.	Methylnitrosourea	64-83	KRAS proto-oncogene, GTPase	Rattus norvegicus	0-5
9020896-7	1996	The base sequence of codons 12-13 and 59-63 of K-ras was determined by the dideoxynucleotide method.	Dideoxynucleotides	75-92	KRAS proto-oncogene, GTPase	Rattus norvegicus	47-52
8950220-1	1996	Mutations of Ki-ras and p53 genes in hepatocellular carcinomas (HCCs) induced by the choline deficient L-amino acid defined (CDAA) diet in rats were investigated by polymerase chain reaction (PCR), single strand conformation polymorphism (SSCP) analysis followed by direct sequencing.	Choline	85-92	KRAS proto-oncogene, GTPase	Rattus norvegicus	13-19
8950220-1	1996	Mutations of Ki-ras and p53 genes in hepatocellular carcinomas (HCCs) induced by the choline deficient L-amino acid defined (CDAA) diet in rats were investigated by polymerase chain reaction (PCR), single strand conformation polymorphism (SSCP) analysis followed by direct sequencing.	Amino Acids	103-115	KRAS proto-oncogene, GTPase	Rattus norvegicus	13-19
8950220-1	1996	Mutations of Ki-ras and p53 genes in hepatocellular carcinomas (HCCs) induced by the choline deficient L-amino acid defined (CDAA) diet in rats were investigated by polymerase chain reaction (PCR), single strand conformation polymorphism (SSCP) analysis followed by direct sequencing.	CDAA	125-129	KRAS proto-oncogene, GTPase	Rattus norvegicus	13-19
8913708-0	1996	Increases in Ki-ras and ornithine decarboxylase gene expression in rat pancreas after caerulein-induced pancreatitis.	Ceruletide	86-95	KRAS proto-oncogene, GTPase	Rattus norvegicus	13-19
8913708-9	1996	During that period, maximal increases in ODC activity and Ki-ras mRNA expression occurred after 1 day of caerulein treatment; ODC mRNA expression was also significantly increased after 3 and 5 days in the pancreatitis animals with no effect of caerulein treatment.	Ceruletide	105-114	KRAS proto-oncogene, GTPase	Rattus norvegicus	58-64
8634091-1	1996	In this study, human and rat cancer cells were used to investigate the expression of p53 and p21/WAF1/CIP1 and their association with apoptosis after exposure to nitric oxide (NO).	Nitric Oxide	162-174	KRAS proto-oncogene, GTPase	Rattus norvegicus	93-96
8634086-1	1996	Point mutations of the Ki-ras and p53 genes in rat lung lesions induced by N-nitrosobis(2-hydroxypropyl)amine (BHP) were investigated by polymerase chain reaction-single strand conformation polymorphism analysis followed by direct sequencing using paraffin-embedded tissues.	diisopropanolnitrosamine	75-109	KRAS proto-oncogene, GTPase	Rattus norvegicus	23-29
8634086-1	1996	Point mutations of the Ki-ras and p53 genes in rat lung lesions induced by N-nitrosobis(2-hydroxypropyl)amine (BHP) were investigated by polymerase chain reaction-single strand conformation polymorphism analysis followed by direct sequencing using paraffin-embedded tissues.	bhp	111-114	KRAS proto-oncogene, GTPase	Rattus norvegicus	23-29
8634086-1	1996	Point mutations of the Ki-ras and p53 genes in rat lung lesions induced by N-nitrosobis(2-hydroxypropyl)amine (BHP) were investigated by polymerase chain reaction-single strand conformation polymorphism analysis followed by direct sequencing using paraffin-embedded tissues.	Paraffin	248-256	KRAS proto-oncogene, GTPase	Rattus norvegicus	23-29
8662912-6	1996	Ang II caused a rapid increase in the binding of GTP to p21(ras), and this was inhibited by genistein, TMB-8, and calmidazolium but not by pertussis toxin or GF109203X.	Guanosine Triphosphate	49-52	KRAS proto-oncogene, GTPase	Rattus norvegicus	56-59
8662912-6	1996	Ang II caused a rapid increase in the binding of GTP to p21(ras), and this was inhibited by genistein, TMB-8, and calmidazolium but not by pertussis toxin or GF109203X.	Genistein	92-101	KRAS proto-oncogene, GTPase	Rattus norvegicus	56-59
8662912-6	1996	Ang II caused a rapid increase in the binding of GTP to p21(ras), and this was inhibited by genistein, TMB-8, and calmidazolium but not by pertussis toxin or GF109203X.	8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate	103-108	KRAS proto-oncogene, GTPase	Rattus norvegicus	56-59
8662912-6	1996	Ang II caused a rapid increase in the binding of GTP to p21(ras), and this was inhibited by genistein, TMB-8, and calmidazolium but not by pertussis toxin or GF109203X.	calmidazolium	114-127	KRAS proto-oncogene, GTPase	Rattus norvegicus	56-59
8804697-6	1996	The progressive decrease in the effect of NMDA with brain development was also indicated by a decrease in the volume of tissue in which the changes in ADC occurred (50 mm3 at P4 and 8 mm3 at P21).	N-Methylaspartate	42-46	KRAS proto-oncogene, GTPase	Rattus norvegicus	191-194
8651753-8	1996	Cyclin D1, Cdk4, and p21 protein complex formation was analyzed by immunoprecipitating the complexes from cell lysates with an antibody to one of the constituents, followed by SDS polyacrylamide gel electrophoresis (SDS-PAGE) and Western blot analysis of the precipitated complexes using antibodies to the other proteins.	Sodium Dodecyl Sulfate	176-179	KRAS proto-oncogene, GTPase	Rattus norvegicus	21-24
8651753-8	1996	Cyclin D1, Cdk4, and p21 protein complex formation was analyzed by immunoprecipitating the complexes from cell lysates with an antibody to one of the constituents, followed by SDS polyacrylamide gel electrophoresis (SDS-PAGE) and Western blot analysis of the precipitated complexes using antibodies to the other proteins.	polyacrylamide	180-194	KRAS proto-oncogene, GTPase	Rattus norvegicus	21-24
8651753-8	1996	Cyclin D1, Cdk4, and p21 protein complex formation was analyzed by immunoprecipitating the complexes from cell lysates with an antibody to one of the constituents, followed by SDS polyacrylamide gel electrophoresis (SDS-PAGE) and Western blot analysis of the precipitated complexes using antibodies to the other proteins.	Sodium Dodecyl Sulfate	216-219	KRAS proto-oncogene, GTPase	Rattus norvegicus	21-24
8640740-0	1996	Low expression of the WAF1/CIP1 gene product, p21, in enzyme-altered foci induced in rat liver by diethylnitrosamine or phenobarbital.	Phenobarbital	120-133	KRAS proto-oncogene, GTPase	Rattus norvegicus	46-49
8640740-1	1996	The expression of the WAF1/CIP1 gene product, p21, in enzyme-altered foci (EAF) induced by diethylnitrosamine (DEN) and phenobarbital (PB) was examined.	Diethylnitrosamine	91-109	KRAS proto-oncogene, GTPase	Rattus norvegicus	46-49
8640740-1	1996	The expression of the WAF1/CIP1 gene product, p21, in enzyme-altered foci (EAF) induced by diethylnitrosamine (DEN) and phenobarbital (PB) was examined.	Diethylnitrosamine	111-114	KRAS proto-oncogene, GTPase	Rattus norvegicus	46-49
8640740-1	1996	The expression of the WAF1/CIP1 gene product, p21, in enzyme-altered foci (EAF) induced by diethylnitrosamine (DEN) and phenobarbital (PB) was examined.	Phenobarbital	120-133	KRAS proto-oncogene, GTPase	Rattus norvegicus	46-49
8640740-1	1996	The expression of the WAF1/CIP1 gene product, p21, in enzyme-altered foci (EAF) induced by diethylnitrosamine (DEN) and phenobarbital (PB) was examined.	Phenobarbital	135-137	KRAS proto-oncogene, GTPase	Rattus norvegicus	46-49
8620454-9	1996	These results indicate that, in the ras family, DHPN induces Ki-ras gene activation preferentially and that p53 mutation may be infrequent in thyroid carcinogenesis in rats, our data thus corresponding well with the previous reports that an inactivated p53 gene only plays a major role in human undifferentiated thyroid carcinomas.	diisopropanolnitrosamine	48-52	KRAS proto-oncogene, GTPase	Rattus norvegicus	61-67
8598314-7	1996	Protein tyrosine phosphorylation and invasion by MM1 cells induced by LPA are largely regulated by rho p21, because both were inhibited by Clostridium botulinum C3 exo-enzyme, which is known to specifically inactivate rho p21.	Tyrosine	8-16	KRAS proto-oncogene, GTPase	Rattus norvegicus	103-106
8598314-7	1996	Protein tyrosine phosphorylation and invasion by MM1 cells induced by LPA are largely regulated by rho p21, because both were inhibited by Clostridium botulinum C3 exo-enzyme, which is known to specifically inactivate rho p21.	Tyrosine	8-16	KRAS proto-oncogene, GTPase	Rattus norvegicus	222-225
21153293-6	1996	TPA, an activator of protein kinase C, enhanced p21( ras ) and MAP-kinase activity in Nb2-11C cells but failed to induce proliferation.	Tetradecanoylphorbol Acetate	0-3	KRAS proto-oncogene, GTPase	Rattus norvegicus	48-51
21153293-7	1996	The mechanism of activation of p21( ras ) in Nb2-11C cells by lactogenic hormones involves both an increased binding of guanine nucleotides to p21( ras ) as well as an increase in GTP/GDP+GTP ratio.	Guanine Nucleotides	120-139	KRAS proto-oncogene, GTPase	Rattus norvegicus	31-34
21153293-7	1996	The mechanism of activation of p21( ras ) in Nb2-11C cells by lactogenic hormones involves both an increased binding of guanine nucleotides to p21( ras ) as well as an increase in GTP/GDP+GTP ratio.	Guanine Nucleotides	120-139	KRAS proto-oncogene, GTPase	Rattus norvegicus	143-146
21153293-7	1996	The mechanism of activation of p21( ras ) in Nb2-11C cells by lactogenic hormones involves both an increased binding of guanine nucleotides to p21( ras ) as well as an increase in GTP/GDP+GTP ratio.	Guanosine Triphosphate	180-183	KRAS proto-oncogene, GTPase	Rattus norvegicus	31-34
21153293-7	1996	The mechanism of activation of p21( ras ) in Nb2-11C cells by lactogenic hormones involves both an increased binding of guanine nucleotides to p21( ras ) as well as an increase in GTP/GDP+GTP ratio.	gdp+gtp	184-191	KRAS proto-oncogene, GTPase	Rattus norvegicus	31-34