PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
2426798-1	1986	Mammalian cells selected to resist N-(phosphonacetyl)-L-aspartate (PALA) contain amplified copies of the CAD gene.	sparfosic acid	35-65	aconitate decarboxylase 1	Homo sapiens	105-108
2563307-2	1989	The results indicate that treatment with these enzymes efficiently increases the frequency of clones resistant to N-phosphonacetyl-L-aspartate, indicating induction of CAD gene amplification.	sparfosic acid	114-142	CAD protein	Cricetulus griseus	168-171
3600632-1	1987	We analyzed the amplification of the CAD gene in independently isolated N-(phosphonacetyl)-L-aspartate-resistant clones derived from single parental clones in two mouse cell lines.	sparfosic acid	72-102	congenital cataract	Mus musculus	37-40
2481806-0	1989	Structural organization and expression of amplified chromosomal sequences, which include the rudimentary gene, in cultured Drosophila cells resistant to N-(phosphonacetyl)-L-aspartate.	sparfosic acid	153-183	rudimentary	Drosophila melanogaster	93-109
6896736-1	1982	Mutant Syrian hamster cell lines resistant to N-(phosphonacetyl)-L-aspartate, a potent and specific inhibitor of aspartate transcarbamylase, have amplified the gene coding for the multifunctional protein (CAD) that includes this activity.	sparfosic acid	46-76	CAD protein	Mesocricetus auratus	205-208
6656763-1	1983	Syrian hamster cell lines selected in multiple steps for resistance to high levels of N-(phosphonacetyl)-L-aspartate (PALA) contain many copies of the gene coding for the pyrimidine pathway enzyme CAD.	sparfosic acid	86-116	CAD protein	Mesocricetus auratus	197-200
323257-4	1977	If N-(phosphonacetyl)-L-aspartate is used to protect the active site, we find that phenylglyoxal causes destruction of the enzyme"s susceptibility to activation by ATP and inhibition by CTP.	sparfosic acid	3-33	solute carrier family 25 member 1	Homo sapiens	186-189
6160908-1	1981	The effect of N-phosphonacetyl-L-aspartate (PALA) pretreatment on the metabolism and cytotoxicity of 5-azacytidine (5-aza-Cyd) was studied in two murine leukemic cell lines.	sparfosic acid	44-48	cytochrome b-245, beta polypeptide	Mus musculus	122-125
381311-1	1979	Mutant Syrian hamster cells resistant to N-(phosphonacetyl)-L-aspartate (PALA), a transition state analog inhibitor of aspartate transcarbamylase, overproduce CAD, a multifunctional protein which catalyzes the first three reactions of de novo UMP biosynthesis.	sparfosic acid	41-71	CAD protein	Mesocricetus auratus	159-162
6180304-1	1982	Syrian hamster cells resistant to N-(phosphonacetyl)-L-aspartate (PALA), a specific inhibitor of the aspartate transcarbamylase activity of the multifunctional protein CAD, overproduce this protein as a result of amplification of the CAD gene.	sparfosic acid	34-64	CAD protein	Mesocricetus auratus	168-171
6180304-1	1982	Syrian hamster cells resistant to N-(phosphonacetyl)-L-aspartate (PALA), a specific inhibitor of the aspartate transcarbamylase activity of the multifunctional protein CAD, overproduce this protein as a result of amplification of the CAD gene.	sparfosic acid	34-64	CAD protein	Mesocricetus auratus	234-237
6180304-1	1982	Syrian hamster cells resistant to N-(phosphonacetyl)-L-aspartate (PALA), a specific inhibitor of the aspartate transcarbamylase activity of the multifunctional protein CAD, overproduce this protein as a result of amplification of the CAD gene.	sparfosic acid	66-70	CAD protein	Mesocricetus auratus	168-171
6180304-1	1982	Syrian hamster cells resistant to N-(phosphonacetyl)-L-aspartate (PALA), a specific inhibitor of the aspartate transcarbamylase activity of the multifunctional protein CAD, overproduce this protein as a result of amplification of the CAD gene.	sparfosic acid	66-70	CAD protein	Mesocricetus auratus	234-237
23189182-2	2012	Based on the signature changes at amino acid residue 487, EBNA1 is classified into five distinct subtypes: P-ala, P-thr, V-leu, V-val and V-pro.	sparfosic acid	107-112	EBNA-1	Human gammaherpesvirus 4	58-63
22430213-0	2013	N-(phosphonacetyl)-L-aspartate induces TAp73-dependent apoptosis by modulating multiple Bcl-2 proteins: potential for cancer therapy.	sparfosic acid	0-30	BCL2 apoptosis regulator	Homo sapiens	88-93
22430213-4	2013	In the complete absence of p53, cells treated with N-(phosphonacetyl)-L-aspartate (PALA) continue to synthesize DNA slowly and eventually progress through S-phase, suffering severe DNA damage that in turn triggers apoptosis, whereas cells with functional p53 undergo growth arrest.	sparfosic acid	51-81	tumor protein p53	Homo sapiens	255-258
30833451-8	2020	Inhibition studies using N-(phosphonoacetyl)-L-aspartic acid and fulvestrant, specific CAD and ESR1 inhibitors, respectively, uncovered their impact as antiviral targets.	sparfosic acid	25-60	estrogen receptor 1	Homo sapiens	95-99
18434539-3	2008	p53 is activated in normal cells starved for pyrimidine nucleotides by treatment with N-(phosphonacetyl)-l-aspartate (PALA).	sparfosic acid	86-116	tumor protein p53	Homo sapiens	0-3
19941915-1	2010	The Epstein-Barr virus (EBV) nuclear antigen 1 (EBNA1), the only viral protein consistently expressed in all EBV-associated tumors, is classified into five distinct subtypes: P-ala, P-thr, V-leu, V-val and V-pro based on the signature changes at amino acid residue 487.	sparfosic acid	175-180	EBNA-1	Human gammaherpesvirus 4	48-53
17050687-3	2006	In addition to its role in activating the G(1) and G(2) checkpoints, p53 also helps to protect cells in S phase when they are starved for DNA precursors by treatment with the specific aspartate transcarbamylase inhibitor N-phosphonacetyl-l-aspartate (PALA), which blocks the synthesis of pyrimidine nucleotides.	sparfosic acid	221-249	tumor protein p53	Homo sapiens	69-72
17050687-3	2006	In addition to its role in activating the G(1) and G(2) checkpoints, p53 also helps to protect cells in S phase when they are starved for DNA precursors by treatment with the specific aspartate transcarbamylase inhibitor N-phosphonacetyl-l-aspartate (PALA), which blocks the synthesis of pyrimidine nucleotides.	sparfosic acid	251-255	tumor protein p53	Homo sapiens	69-72
10618377-6	2000	Under the same dissociating conditions, incubating the altered CAD with the ATCase substrate carbamoyl phosphate or the bisubstrate analogue N-phosphonacetyl-L-aspartate unexpectedly leads to the reformation of hexamers.	sparfosic acid	141-169	aconitate decarboxylase 1	Homo sapiens	63-66
12860987-1	2003	Modification-specific antibodies were used to characterize the phosphorylation and acetylation of human p53 in response to genotoxic (UV, IR, and adriamycin) and non-genotoxic (PALA, taxol, nocodazole) stress in cultured human cells at 14 known modification sites.	sparfosic acid	177-181	tumor protein p53	Homo sapiens	104-107
11956089-11	2002	The reduced dependence of UPase knockout cells on the pyrimidine de novo synthesis is reflected in the apparent resistance to phosphonacetyl-L-aspartic acid, a specific inhibitor of pyrimidine pathway, with a 5-fold elevation in its IC(50) in UPase-nullified cells compared with WT.	sparfosic acid	126-156	uridine phosphorylase 1	Mus musculus	26-31
11956089-11	2002	The reduced dependence of UPase knockout cells on the pyrimidine de novo synthesis is reflected in the apparent resistance to phosphonacetyl-L-aspartic acid, a specific inhibitor of pyrimidine pathway, with a 5-fold elevation in its IC(50) in UPase-nullified cells compared with WT.	sparfosic acid	126-156	uridine phosphorylase 1	Mus musculus	243-248
9927185-3	1999	When treated with N-(phosphonacetyl)-L-aspartate (PALA), which inhibits pyrimidine nucleotide synthesis, leading to synthesis of damaged DNA from highly unbalanced dNTP pools, p53-null cells enter mitosis after they have completed DNA replication, but cells with wild-type p53 do not, revealing that p53 also mediates a checkpoint that monitors the quality of newly replicated DNA.	sparfosic acid	18-48	tumor protein p53	Homo sapiens	176-179
10097142-9	1999	Moreover, MYC could force normal human fibroblasts to transit G1 and S after treatment with N-(phosphonoacetyl)-L-aspartate (PALA) at concentrations that normally lead to arrest in S phase by checkpoint mechanisms.	sparfosic acid	92-123	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	10-13
9927185-3	1999	When treated with N-(phosphonacetyl)-L-aspartate (PALA), which inhibits pyrimidine nucleotide synthesis, leading to synthesis of damaged DNA from highly unbalanced dNTP pools, p53-null cells enter mitosis after they have completed DNA replication, but cells with wild-type p53 do not, revealing that p53 also mediates a checkpoint that monitors the quality of newly replicated DNA.	sparfosic acid	18-48	tumor protein p53	Homo sapiens	273-276
9927185-3	1999	When treated with N-(phosphonacetyl)-L-aspartate (PALA), which inhibits pyrimidine nucleotide synthesis, leading to synthesis of damaged DNA from highly unbalanced dNTP pools, p53-null cells enter mitosis after they have completed DNA replication, but cells with wild-type p53 do not, revealing that p53 also mediates a checkpoint that monitors the quality of newly replicated DNA.	sparfosic acid	18-48	tumor protein p53	Homo sapiens	273-276
9418900-0	1998	MYC abrogates p53-mediated cell cycle arrest in N-(phosphonacetyl)-L-aspartate-treated cells, permitting CAD gene amplification.	sparfosic acid	48-78	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	14-17
9566927-3	1998	However, this conclusion derives from studies employing the UMP synthesis inhibitor N-phosphonacetyl-L-aspartate (PALA), which, in addition to selecting for cells containing extra copies of the CAD locus, enables p53-deficient cells to enter S phase and acquire the DNA breaks that initiate the amplification process.	sparfosic acid	84-112	tumor protein p53	Homo sapiens	213-216
8868464-1	1996	Cells often acquire resistance to the antiproliferative agents methotrexate (MTX) or N-phosphonacetyl-L-aspartate (PALA) through amplification of genes encoding the target enzymes dihydrofolate reductase or carbamylphosphate synthetase/aspartate transcarbamylase/dihydroorotase (CAD), respectively.	sparfosic acid	85-113	CAD protein	Mesocricetus auratus	207-283
8706000-2	1996	We show here that keratinocyte cell lines from mice with a targeted deletion of the TGF-beta 1 gene have significantly increased frequencies of gene amplification in response to the drug N-phosphonoacetyl-L-aspartate (PALA) compared to TGF-beta 1-expressing control keratinocyte cell lines.	sparfosic acid	187-216	transforming growth factor, beta 1	Mus musculus	84-94
8706003-0	1996	Separate pathways for p53 induction by ionizing radiation and N-(phosphonoacetyl)-L-aspartate.	sparfosic acid	62-93	tumor protein p53	Homo sapiens	22-25
8706003-4	1996	Here, we demonstrate the existence of cell types in which the induction of p53 and associated G1 arrest by the antimetabolite, N-(phosphonoacetyl)-L-aspartate (PALA), is defective, whereas p53 induction and G1 arrest induced by ionizing radiation are intact.	sparfosic acid	127-158	tumor protein p53	Homo sapiens	75-78
8758262-1	1996	The aspartate transcarbamoylase inhibitor, N-(phosphonacetyl)-L-aspartate (PALA), synergistically enhanced the cytotoxicity of a combination of 5-fluorouracil (5-FU) and interferon-alpha (IFN) against human colon cancer cell lines in vitro.	sparfosic acid	43-73	interferon alpha 1	Homo sapiens	170-192
7623808-5	1995	DNA replication initiates within this region in the single-copy CAD gene in Syrian baby hamster kidney cells and in the large chromosomal amplicons that were generated after selection with N-phosphonacetyl-L-aspartate, a specific inhibitor of CAD.	sparfosic acid	189-217	CAD protein	Mesocricetus auratus	243-246
8554573-5	1995	Upon selection by N-(phosphonoacetyl)-L-aspartate (PALA), the cyclin D1-transfected NIH3T3 cells showed a higher ability to develop PALA-resistant colonies by amplifying the CAD gene, as compared to the parental NIH3T3 cells.	sparfosic acid	18-49	cyclin D1	Mus musculus	62-71
8554573-5	1995	Upon selection by N-(phosphonoacetyl)-L-aspartate (PALA), the cyclin D1-transfected NIH3T3 cells showed a higher ability to develop PALA-resistant colonies by amplifying the CAD gene, as compared to the parental NIH3T3 cells.	sparfosic acid	51-55	cyclin D1	Mus musculus	62-71
8554573-5	1995	Upon selection by N-(phosphonoacetyl)-L-aspartate (PALA), the cyclin D1-transfected NIH3T3 cells showed a higher ability to develop PALA-resistant colonies by amplifying the CAD gene, as compared to the parental NIH3T3 cells.	sparfosic acid	132-136	cyclin D1	Mus musculus	62-71
7623808-6	1995	DNA synthesis also initiates within this OBR in autonomously replicating extrachromosomal amplicons (CAD episomes) located in an N-phosphonacetyl-L-aspartate-resistant clone (5P20) of CHOK1 cells.	sparfosic acid	129-157	CAD protein	Mesocricetus auratus	101-104
7712485-2	1995	We show that a TGF-beta 1-overexpressing mouse 10T1/2 cell line transfected with a TGF-beta 1 sequence that allows the synthesis of bioactive growth factor exhibits reduced sensitivity to the cytotoxic effects of the drug N-(phosphonacetyl)-L-aspartate (PALA) in colony-forming experiments.	sparfosic acid	222-252	transforming growth factor, beta 1	Mus musculus	15-25
7712485-2	1995	We show that a TGF-beta 1-overexpressing mouse 10T1/2 cell line transfected with a TGF-beta 1 sequence that allows the synthesis of bioactive growth factor exhibits reduced sensitivity to the cytotoxic effects of the drug N-(phosphonacetyl)-L-aspartate (PALA) in colony-forming experiments.	sparfosic acid	222-252	transforming growth factor, beta 1	Mus musculus	83-93
7904743-2	1994	Resistance to methotrexate, N-(phosphonacetyl)-L-aspartate and hydroxyurea was observed with K-fgf transfectants, due to amplification of dihydrofolate reductase, CAD or ribonucleotide reductase R2 genes, respectively.	sparfosic acid	28-58	fibroblast growth factor 4	Mus musculus	93-98
8162600-9	1994	The increased capacity to amplify DNA in response to mutant Ha-ras induction was not locus specific since cells also displayed an increased frequency of resistance to N-(phosphonacetyl)-L-aspartic acid in the presence of ITPG.	sparfosic acid	167-201	Harvey rat sarcoma virus oncogene	Mus musculus	60-66
8050490-2	1994	Colony-forming experiments and fluctuation analyses showed that the frequency and rate of resistance to N-(phosphonacetyl)-L-aspartate (PALA) was dramatically elevated in cells transfected with either the normal bFGF coding sequence that lacks a known signal for secretion or a chimeric bFGF sequence that targets the growth factor to the secretory pathway.	sparfosic acid	104-134	fibroblast growth factor 2	Homo sapiens	212-216
8050490-2	1994	Colony-forming experiments and fluctuation analyses showed that the frequency and rate of resistance to N-(phosphonacetyl)-L-aspartate (PALA) was dramatically elevated in cells transfected with either the normal bFGF coding sequence that lacks a known signal for secretion or a chimeric bFGF sequence that targets the growth factor to the secretory pathway.	sparfosic acid	104-134	fibroblast growth factor 2	Homo sapiens	287-291
8114714-6	1994	Furthermore, treatment of cells with the antimetabolite N(phosphonoacetyl)-L-aspartate (PALA) did not cause rapid p53 protein increases but resulted in delayed increases in p53 protein levels temporally correlated with the appearance of DNA strand breaks.	sparfosic acid	56-86	tumor protein p53	Homo sapiens	173-176
7904743-3	1994	In keeping with the increase in gene amplification frequency, cells transfected with the K-fgf gene also exhibited a marked increase in CAD gene amplification rate, as determined by fluctuation analysis in the presence of N-(phosphonacetyl)-L-aspartate.	sparfosic acid	222-252	fibroblast growth factor 4	Mus musculus	89-94
7904743-4	1994	Cells transfected with bFGF encoding cDNA also exhibited a significant elevation in N-(phosphonacetyl)-L-aspartate resistance, and CAD gene amplification.	sparfosic acid	84-114	fibroblast growth factor 2	Mus musculus	23-27