PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
8143723-10	1994	(d) Heme-synthesis inhibitors, such as succinylacetone and isonicotinic acid hydrazide, which inhibit numerous aspects of erythroid differentiation, also inhibit TfR mRNA expression in induced MEL cells.	succinylacetone	39-54	transferrin receptor	Mus musculus	162-165
8037458-2	1994	We and others have previously observed that treatment of human myeloid leukemic cells with succinylacetone (SA), a potent inhibitor of 5-aminolevulinic acid dehydratase (ALA-D), and hence of heme biosynthesis, resulted in loss of MPO enzyme activity, inhibition of the appearance of mature MPO, and accumulation of enzymatically unreactive, but immunoreactive, MPO in the ER.	succinylacetone	91-106	aminolevulinate dehydratase	Homo sapiens	135-168
8037458-2	1994	We and others have previously observed that treatment of human myeloid leukemic cells with succinylacetone (SA), a potent inhibitor of 5-aminolevulinic acid dehydratase (ALA-D), and hence of heme biosynthesis, resulted in loss of MPO enzyme activity, inhibition of the appearance of mature MPO, and accumulation of enzymatically unreactive, but immunoreactive, MPO in the ER.	succinylacetone	91-106	aminolevulinate dehydratase	Homo sapiens	170-175
8037458-2	1994	We and others have previously observed that treatment of human myeloid leukemic cells with succinylacetone (SA), a potent inhibitor of 5-aminolevulinic acid dehydratase (ALA-D), and hence of heme biosynthesis, resulted in loss of MPO enzyme activity, inhibition of the appearance of mature MPO, and accumulation of enzymatically unreactive, but immunoreactive, MPO in the ER.	succinylacetone	91-106	myeloperoxidase	Homo sapiens	230-233
8037458-2	1994	We and others have previously observed that treatment of human myeloid leukemic cells with succinylacetone (SA), a potent inhibitor of 5-aminolevulinic acid dehydratase (ALA-D), and hence of heme biosynthesis, resulted in loss of MPO enzyme activity, inhibition of the appearance of mature MPO, and accumulation of enzymatically unreactive, but immunoreactive, MPO in the ER.	succinylacetone	91-106	myeloperoxidase	Homo sapiens	290-293
8037458-2	1994	We and others have previously observed that treatment of human myeloid leukemic cells with succinylacetone (SA), a potent inhibitor of 5-aminolevulinic acid dehydratase (ALA-D), and hence of heme biosynthesis, resulted in loss of MPO enzyme activity, inhibition of the appearance of mature MPO, and accumulation of enzymatically unreactive, but immunoreactive, MPO in the ER.	succinylacetone	91-106	myeloperoxidase	Homo sapiens	290-293
8037458-2	1994	We and others have previously observed that treatment of human myeloid leukemic cells with succinylacetone (SA), a potent inhibitor of 5-aminolevulinic acid dehydratase (ALA-D), and hence of heme biosynthesis, resulted in loss of MPO enzyme activity, inhibition of the appearance of mature MPO, and accumulation of enzymatically unreactive, but immunoreactive, MPO in the ER.	succinylacetone	108-110	aminolevulinate dehydratase	Homo sapiens	135-168
8037458-2	1994	We and others have previously observed that treatment of human myeloid leukemic cells with succinylacetone (SA), a potent inhibitor of 5-aminolevulinic acid dehydratase (ALA-D), and hence of heme biosynthesis, resulted in loss of MPO enzyme activity, inhibition of the appearance of mature MPO, and accumulation of enzymatically unreactive, but immunoreactive, MPO in the ER.	succinylacetone	108-110	aminolevulinate dehydratase	Homo sapiens	170-175
8037458-2	1994	We and others have previously observed that treatment of human myeloid leukemic cells with succinylacetone (SA), a potent inhibitor of 5-aminolevulinic acid dehydratase (ALA-D), and hence of heme biosynthesis, resulted in loss of MPO enzyme activity, inhibition of the appearance of mature MPO, and accumulation of enzymatically unreactive, but immunoreactive, MPO in the ER.	succinylacetone	108-110	myeloperoxidase	Homo sapiens	230-233
8037458-2	1994	We and others have previously observed that treatment of human myeloid leukemic cells with succinylacetone (SA), a potent inhibitor of 5-aminolevulinic acid dehydratase (ALA-D), and hence of heme biosynthesis, resulted in loss of MPO enzyme activity, inhibition of the appearance of mature MPO, and accumulation of enzymatically unreactive, but immunoreactive, MPO in the ER.	succinylacetone	108-110	myeloperoxidase	Homo sapiens	290-293
8037458-2	1994	We and others have previously observed that treatment of human myeloid leukemic cells with succinylacetone (SA), a potent inhibitor of 5-aminolevulinic acid dehydratase (ALA-D), and hence of heme biosynthesis, resulted in loss of MPO enzyme activity, inhibition of the appearance of mature MPO, and accumulation of enzymatically unreactive, but immunoreactive, MPO in the ER.	succinylacetone	108-110	myeloperoxidase	Homo sapiens	290-293
8037458-4	1994	Dose-response studies showed that SA (250 microM) did not affect cell viability or growth up to 72 h, but resulted in inhibition of ALA-D activity (> 93%) and decreased cellular levels of both heme and MPO (approximately 25% of control).	succinylacetone	34-36	aminolevulinate dehydratase	Homo sapiens	132-137
8037458-4	1994	Dose-response studies showed that SA (250 microM) did not affect cell viability or growth up to 72 h, but resulted in inhibition of ALA-D activity (> 93%) and decreased cellular levels of both heme and MPO (approximately 25% of control).	succinylacetone	34-36	myeloperoxidase	Homo sapiens	205-208
8037458-8	1994	The initial rate of disappearance of precursor MPO was identical for control and SA-treated cells and, after a lag of 2-3 h, there was a fourfold decrease in the rate of appearance of mature MPO in SA-treated cells.	succinylacetone	198-200	myeloperoxidase	Homo sapiens	191-194
8399368-9	1993	Porphyrin intermediates, heme oxygenase activity and cytochrome P-450 content evidenced varying responses to SA exposure which differed from tissue to tissue.	succinylacetone	109-111	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	53-69
8485055-2	1993	FeC mRNA increased within 12 h after DMSO or haemin treatment of MEL cells, and its level continued to increase for 48 h. Treatment of cells with succinylacetone (SA), a potent inhibitor of haem synthesis, suppressed a DMSO-mediated increase in FeC mRNA, and haemin treatment reversed a SA-mediated decrease in FeC mRNA.	succinylacetone	146-161	ferrochelatase	Mus musculus	0-3
8507877-4	1993	When succinylacetone is used to inhibit Belgrade heme synthesis, iron from diferric transferrin does not accumulate in the stromal fraction that contains mitochondria, nor does 59Fe accumulate in the nonheme cytosolic fraction.	succinylacetone	5-20	transferrin	Rattus norvegicus	84-95
8485055-2	1993	FeC mRNA increased within 12 h after DMSO or haemin treatment of MEL cells, and its level continued to increase for 48 h. Treatment of cells with succinylacetone (SA), a potent inhibitor of haem synthesis, suppressed a DMSO-mediated increase in FeC mRNA, and haemin treatment reversed a SA-mediated decrease in FeC mRNA.	succinylacetone	146-161	ferrochelatase	Mus musculus	245-248
8485055-2	1993	FeC mRNA increased within 12 h after DMSO or haemin treatment of MEL cells, and its level continued to increase for 48 h. Treatment of cells with succinylacetone (SA), a potent inhibitor of haem synthesis, suppressed a DMSO-mediated increase in FeC mRNA, and haemin treatment reversed a SA-mediated decrease in FeC mRNA.	succinylacetone	146-161	ferrochelatase	Mus musculus	245-248
8485055-2	1993	FeC mRNA increased within 12 h after DMSO or haemin treatment of MEL cells, and its level continued to increase for 48 h. Treatment of cells with succinylacetone (SA), a potent inhibitor of haem synthesis, suppressed a DMSO-mediated increase in FeC mRNA, and haemin treatment reversed a SA-mediated decrease in FeC mRNA.	succinylacetone	163-165	ferrochelatase	Mus musculus	0-3
8485055-2	1993	FeC mRNA increased within 12 h after DMSO or haemin treatment of MEL cells, and its level continued to increase for 48 h. Treatment of cells with succinylacetone (SA), a potent inhibitor of haem synthesis, suppressed a DMSO-mediated increase in FeC mRNA, and haemin treatment reversed a SA-mediated decrease in FeC mRNA.	succinylacetone	163-165	ferrochelatase	Mus musculus	245-248
8485055-2	1993	FeC mRNA increased within 12 h after DMSO or haemin treatment of MEL cells, and its level continued to increase for 48 h. Treatment of cells with succinylacetone (SA), a potent inhibitor of haem synthesis, suppressed a DMSO-mediated increase in FeC mRNA, and haemin treatment reversed a SA-mediated decrease in FeC mRNA.	succinylacetone	163-165	ferrochelatase	Mus musculus	245-248
8485055-2	1993	FeC mRNA increased within 12 h after DMSO or haemin treatment of MEL cells, and its level continued to increase for 48 h. Treatment of cells with succinylacetone (SA), a potent inhibitor of haem synthesis, suppressed a DMSO-mediated increase in FeC mRNA, and haemin treatment reversed a SA-mediated decrease in FeC mRNA.	succinylacetone	287-289	ferrochelatase	Mus musculus	0-3
8127053-2	1993	Owing to structural resemblance of SA to delta-aminolevulinic acid (ALA), SA inhibits the second enzyme in the pathway for haeme biosynthesis, porphobilinogen synthase, resulting in increased urinary ALA excretion.	succinylacetone	35-37	aminolevulinate dehydratase	Homo sapiens	143-167
8127053-2	1993	Owing to structural resemblance of SA to delta-aminolevulinic acid (ALA), SA inhibits the second enzyme in the pathway for haeme biosynthesis, porphobilinogen synthase, resulting in increased urinary ALA excretion.	succinylacetone	74-76	aminolevulinate dehydratase	Homo sapiens	143-167
1288876-4	1992	Haem synthesis inhibitors (succinylacetone, isonicotinic acid hydrazide and penicillamine) caused a reduced gene expression for ferrochelatase in erythroleukaemic cells of mice induced with hexamethylenebisacetamide.	succinylacetone	27-42	ferrochelatase	Mus musculus	128-142
1330078-8	1992	Inhibition of heme synthesis with succinyl acetone (SA) reduced peroxidase activity and profoundly blocked processing of proMPO to mature MPO.	succinylacetone	34-50	myeloperoxidase	Homo sapiens	124-127
1330078-8	1992	Inhibition of heme synthesis with succinyl acetone (SA) reduced peroxidase activity and profoundly blocked processing of proMPO to mature MPO.	succinylacetone	52-54	myeloperoxidase	Homo sapiens	124-127
1397323-10	1992	In the presence of CoCl2 and/or SA, ornithine decarboxylase induction by insulin was not impaired; lactate dehydrogenase did not leak from the cells, which in electron microscopical inspections had normal cell structures.	succinylacetone	32-34	ornithine decarboxylase 1	Rattus norvegicus	36-59
1478852-7	1992	However, it appeared that SA may act selectively to inhibit expression of transferrin receptors (CD71), a T-cell activation antigen.	succinylacetone	26-28	transferrin receptor	Homo sapiens	97-101
1524874-0	1992	delta-Aminolevulinic acid dehydratase: effects of succinylacetone in rat liver and kidney in an in vivo model of the renal Fanconi syndrome.	succinylacetone	50-65	aminolevulinate dehydratase	Rattus norvegicus	0-37
1524874-2	1992	We have demonstrated previously the SA enhancement of delta-aminolevulinic acid dehydratase (ALAD) in renal tubules, while this enzyme is known to be impaired by SA in the liver.	succinylacetone	36-38	aminolevulinate dehydratase	Rattus norvegicus	54-91
1524874-2	1992	We have demonstrated previously the SA enhancement of delta-aminolevulinic acid dehydratase (ALAD) in renal tubules, while this enzyme is known to be impaired by SA in the liver.	succinylacetone	36-38	aminolevulinate dehydratase	Rattus norvegicus	93-97
1524874-3	1992	The present studies, based on in vivo treatment of animals with SA, show equivalent degree of inhibition of specific ALAD activity in liver and kidney.	succinylacetone	64-66	aminolevulinate dehydratase	Rattus norvegicus	117-121
1524874-5	1992	The discrepant in vitro and in vivo effect of SA on renal ALAD may be due to differences between a direct inhibitor-enzyme interaction and inhibitor actions in the living cell, respectively.	succinylacetone	46-48	aminolevulinate dehydratase	Rattus norvegicus	58-62
1912586-3	1991	In particular, SA induced: (1) a reduction of the level of alpha-globin mRNA; (2) a decreased number of exposed TfR molecules, without modification of their affinity for the ligand; (3) a reduced level of TfR RNA, without significant change of TfR gene transcription rate; and (4) a lower ferritin content.	succinylacetone	15-17	transferrin receptor	Homo sapiens	112-115
1321053-0	1992	Ultrastructural, immunochemical, and cytochemical study of myeloperoxidase in myeloid leukemia HL-60 cells following treatment with succinylacetone, an inhibitor of heme biosynthesis.	succinylacetone	132-147	myeloperoxidase	Homo sapiens	59-74
1734036-4	1992	Addition of 0.1 mM succinylacetone (SA) decreased cellular TfR to the level comparable with the uninduced cells.	succinylacetone	19-34	transferrin receptor	Mus musculus	59-62
1734036-4	1992	Addition of 0.1 mM succinylacetone (SA) decreased cellular TfR to the level comparable with the uninduced cells.	succinylacetone	36-38	transferrin receptor	Mus musculus	59-62
1734036-6	1992	In short-term (1-2 hours) incubation, SA inhibited 59Fe incorporation from transferrin into heme, whereas total cellular 59Fe uptake was increased.	succinylacetone	38-40	transferrin	Mus musculus	75-86
1734036-7	1992	A decrease in TfR mRNA synthesis was apparent after 2 hours of SA treatment.	succinylacetone	63-65	transferrin receptor	Mus musculus	14-17
1912586-3	1991	In particular, SA induced: (1) a reduction of the level of alpha-globin mRNA; (2) a decreased number of exposed TfR molecules, without modification of their affinity for the ligand; (3) a reduced level of TfR RNA, without significant change of TfR gene transcription rate; and (4) a lower ferritin content.	succinylacetone	15-17	transferrin receptor	Homo sapiens	205-208
1912586-3	1991	In particular, SA induced: (1) a reduction of the level of alpha-globin mRNA; (2) a decreased number of exposed TfR molecules, without modification of their affinity for the ligand; (3) a reduced level of TfR RNA, without significant change of TfR gene transcription rate; and (4) a lower ferritin content.	succinylacetone	15-17	transferrin receptor	Homo sapiens	205-208
2241158-6	1990	Lack of effect on the cytochrome P450 mRNAs was selective inasmuch as treatment with phenobarbital combined with succinyl acetone synergistically increased both ALA-S activity and ALA-S mRNA, presumably by blocking formation of heme, the feedback repressor of ALA-S.	succinylacetone	113-129	5'-aminolevulinate synthase 1	Rattus norvegicus	161-166
1764448-1	1991	Succinylacetone (SA), a metabolic end-product found in urine from individuals with hereditary tyrosinemia and associated renal Fanconi syndrome and a known inhibitor of hepatic 5-aminolevulinic acid dehydratase (ALAD), has been used to study heme metabolism in isolated rat renal tubules.	succinylacetone	0-15	aminolevulinate dehydratase	Rattus norvegicus	212-216
1764448-1	1991	Succinylacetone (SA), a metabolic end-product found in urine from individuals with hereditary tyrosinemia and associated renal Fanconi syndrome and a known inhibitor of hepatic 5-aminolevulinic acid dehydratase (ALAD), has been used to study heme metabolism in isolated rat renal tubules.	succinylacetone	17-19	aminolevulinate dehydratase	Rattus norvegicus	212-216
1898087-0	1991	Involvement of heme in the transcriptional activation of CYPIIB1/B2 gene by phenobarbitone in rat liver--studies with succinylacetone.	succinylacetone	118-133	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	57-64
1898087-3	1991	The present studies indicate that succinylacetone does inhibit the phenobarbitone-mediated increase in CYPIIB1/B2 mRNAs and their transcription in rat liver at early time points (45 min to 3 h), but the inhibition is not pronounced at later time points (16 h).	succinylacetone	34-49	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	103-110
2241158-6	1990	Lack of effect on the cytochrome P450 mRNAs was selective inasmuch as treatment with phenobarbital combined with succinyl acetone synergistically increased both ALA-S activity and ALA-S mRNA, presumably by blocking formation of heme, the feedback repressor of ALA-S.	succinylacetone	113-129	5'-aminolevulinate synthase 1	Rattus norvegicus	180-185
2241158-6	1990	Lack of effect on the cytochrome P450 mRNAs was selective inasmuch as treatment with phenobarbital combined with succinyl acetone synergistically increased both ALA-S activity and ALA-S mRNA, presumably by blocking formation of heme, the feedback repressor of ALA-S.	succinylacetone	113-129	5'-aminolevulinate synthase 1	Rattus norvegicus	180-185
2318295-3	1990	However reticulocytes, treated with succinylacetone or rotenone and taking up iron from transferrin, accumulated iron in nonhaem cytosolic proteins and in mitochondria and not in the low MW pool.	succinylacetone	36-51	transferrin	Homo sapiens	88-99
2359685-5	1990	These findings indicate that although succinylacetone, an abnormal metabolite produced in tyrosinemia, is a potent inhibitor of the activity of ALA dehydratase, it has a far less effect on the synthesis of the enzyme protein.	succinylacetone	38-53	aminolevulinate dehydratase	Homo sapiens	144-159
2361489-1	1990	Succinylacetone (SA) is known to be a potent inhibitor of delta-aminolevulinic acid dehydratase (ALAD) in the liver.	succinylacetone	0-15	aminolevulinate dehydratase	Rattus norvegicus	58-95
2361489-1	1990	Succinylacetone (SA) is known to be a potent inhibitor of delta-aminolevulinic acid dehydratase (ALAD) in the liver.	succinylacetone	0-15	aminolevulinate dehydratase	Rattus norvegicus	97-101
2361489-1	1990	Succinylacetone (SA) is known to be a potent inhibitor of delta-aminolevulinic acid dehydratase (ALAD) in the liver.	succinylacetone	17-19	aminolevulinate dehydratase	Rattus norvegicus	58-95
2361489-1	1990	Succinylacetone (SA) is known to be a potent inhibitor of delta-aminolevulinic acid dehydratase (ALAD) in the liver.	succinylacetone	17-19	aminolevulinate dehydratase	Rattus norvegicus	97-101
2361489-3	1990	While the temperature response of ALAD in both tissues was similar, addition of 4 mmol/l SA inhibited liver ALAD at 37 and 55 degrees C and enhanced renal ALAD activity 2- to 3-fold at each temperature.	succinylacetone	89-91	aminolevulinate dehydratase	Rattus norvegicus	108-112
2767184-6	1989	Epo nevertheless potentiated induction of ALA synthase in the presence of SA.	succinylacetone	74-76	erythropoietin	Homo sapiens	0-3
2361489-4	1990	This increase in renal ALAD was progressive with SA concentrations form 1 to 10 mmol/l.	succinylacetone	49-51	aminolevulinate dehydratase	Rattus norvegicus	23-27
7890722-5	1995	HL60 cells induced to differentiate in the presence of succinyl acetone (a inhibitor of heme synthesis) were unable to generate O2-., failed to express p22-phox but retained H+ channel activity.	succinylacetone	55-71	calcineurin like EF-hand protein 1	Homo sapiens	152-155
3170563-3	1988	Following 24 h of treatment with the iron chelator, desferrioxamine, or with succinylacetone, an inhibitor of heme synthesis, the number of TfR at the cell surface was increased severalfold, with no significant change in receptor affinity (KD) for transferrin.	succinylacetone	77-92	transferrin receptor	Rattus norvegicus	140-143
2788542-11	1989	The proposal that haem is required for the transcription of cytochrome P-450 IIB1/IIB2 and other cytochrome P-450 genes was investigated in rat liver using succinylacetone, a specific inhibitor of the haem biosynthetic pathway.	succinylacetone	156-171	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	97-113
3170563-3	1988	Following 24 h of treatment with the iron chelator, desferrioxamine, or with succinylacetone, an inhibitor of heme synthesis, the number of TfR at the cell surface was increased severalfold, with no significant change in receptor affinity (KD) for transferrin.	succinylacetone	77-92	transferrin	Rattus norvegicus	248-259
3170563-6	1988	Hemin decreased surface TfR expression and counteracted the enhancing effects of desferrioxamine or succinylacetone on TfR expression.	succinylacetone	100-115	transferrin receptor	Rattus norvegicus	119-122
3758232-6	1986	Nevertheless, Epo and hemin actions were not superimposable: in methylcellulose, Epo induced the appearance of large (greater than or equal to 32 cells) hemoglobinized colonies in 48 h, whereas hemin induced smaller and fewer colonies in only 24 h. Succinylacetone (SA, inhibitor of heme synthesis) mostly prevented the effects of Epo on cell proliferation and differentiation; SA inhibition was relieved by hemin.	succinylacetone	249-264	erythropoietin	Rattus norvegicus	81-84
3261670-1	1988	The effects of succinylacetone (SA) on the development of S-antigen-induced experimental autoimmune uveitis (EAU) in the rat were studied.	succinylacetone	32-34	S-antigen visual arrestin	Rattus norvegicus	58-67
3261670-7	1988	Succinylacetone inhibits the expression of EAU and significantly suppresses the immune response to S-antigen.	succinylacetone	0-15	S-antigen visual arrestin	Rattus norvegicus	99-108
3128295-5	1988	When succinylacetone, a potent inhibitor of delta-aminolevulinic acid dehydratase, was coadministered with Ox-DDC, phenobarbital, TCBP and nifedipine, UROG-D inhibition was not observed.	succinylacetone	5-20	aminolevulinate dehydratase	Gallus gallus	44-81
3128295-5	1988	When succinylacetone, a potent inhibitor of delta-aminolevulinic acid dehydratase, was coadministered with Ox-DDC, phenobarbital, TCBP and nifedipine, UROG-D inhibition was not observed.	succinylacetone	5-20	uroporphyrinogen decarboxylase	Gallus gallus	151-157
3546650-7	1987	All three patients continued to excrete higher than normal amounts of ALA, but the activity of ALA-D in red blood cells returned to normal after transplantation, indicating marked clearance of SA from the blood.	succinylacetone	193-195	aminolevulinate dehydratase	Homo sapiens	95-100
3758232-6	1986	Nevertheless, Epo and hemin actions were not superimposable: in methylcellulose, Epo induced the appearance of large (greater than or equal to 32 cells) hemoglobinized colonies in 48 h, whereas hemin induced smaller and fewer colonies in only 24 h. Succinylacetone (SA, inhibitor of heme synthesis) mostly prevented the effects of Epo on cell proliferation and differentiation; SA inhibition was relieved by hemin.	succinylacetone	249-264	erythropoietin	Rattus norvegicus	81-84
3758232-6	1986	Nevertheless, Epo and hemin actions were not superimposable: in methylcellulose, Epo induced the appearance of large (greater than or equal to 32 cells) hemoglobinized colonies in 48 h, whereas hemin induced smaller and fewer colonies in only 24 h. Succinylacetone (SA, inhibitor of heme synthesis) mostly prevented the effects of Epo on cell proliferation and differentiation; SA inhibition was relieved by hemin.	succinylacetone	266-268	erythropoietin	Rattus norvegicus	81-84
3758232-6	1986	Nevertheless, Epo and hemin actions were not superimposable: in methylcellulose, Epo induced the appearance of large (greater than or equal to 32 cells) hemoglobinized colonies in 48 h, whereas hemin induced smaller and fewer colonies in only 24 h. Succinylacetone (SA, inhibitor of heme synthesis) mostly prevented the effects of Epo on cell proliferation and differentiation; SA inhibition was relieved by hemin.	succinylacetone	266-268	erythropoietin	Rattus norvegicus	81-84
3722191-5	1986	Succinyl acetone, a heme synthesis inhibitor, reduced myoglobin levels by 40% while simultaneous treatment with hemin restored myoglobin levels to control values.	succinylacetone	0-16	myoglobin	Rattus norvegicus	54-63
6487660-3	1984	The heme synthesis inhibitors, isoniazid and succinylacetone, stimulated the rate of transferrin endocytosis by 15-30% and caused a proportional increase in the rate of iron uptake, possibly by reducing the intracellular free heme concentration.	succinylacetone	45-60	transferrin	Rattus norvegicus	85-96
3473612-7	1986	In two cases with deficient fumarylacetoacetase activity, succinylacetone was searched for but had not been found to be elevated when the enzyme defect was demonstrated.	succinylacetone	58-73	fumarylacetoacetate hydrolase	Homo sapiens	28-47
4064334-0	1985	Concentrations of succinylacetone after homogentisate and tyrosine loading in healthy individuals with low fumarylacetoacetase activity.	succinylacetone	18-33	fumarylacetoacetate hydrolase	Homo sapiens	107-126
3860503-9	1985	Heme depletion resulting from the presence of succinylacetone in the culture medium reduces the extent of the Me2SO-mediated accumulation of alpha- and beta-globin mRNAs, and this effect is reversed by the addition of 10 microM exogenous hemin.	succinylacetone	46-61	hemoglobin alpha, adult chain 1	Mus musculus	141-163
6617864-0	1983	Effect of succinylacetone on heme and cytochrome P450 synthesis in hepatocyte culture.	succinylacetone	10-25	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	38-53
6587918-8	1984	Succinylacetone, a potent inhibitor of ALA dehydratase, was shown to markedly inhibit the activity of the enzyme, but did not interfere with the synthesis of ALA dehydratase induced by Me2SO treatment.	succinylacetone	0-15	aminolevulinate, delta-, dehydratase	Mus musculus	39-54
6652907-1	1983	Experiments are described on the effects of succinylacetone and fumarylacetoacetate on delta-aminolevulinic acid dehydratase, methionine adenosyltransferase and p-OH-phenylpyruvate dioxygenase.	succinylacetone	44-59	aminolevulinate dehydratase	Homo sapiens	87-124
6652907-2	1983	delta-Aminolevulinic acid dehydratase from human erythrocytes is inhibited non-competitively by succinylacetone (Ki 0.03 mumol/l) and by fumarylacetoacetate (Ki 0.06 mumol/l).	succinylacetone	96-111	aminolevulinate dehydratase	Homo sapiens	0-37
6652907-6	1983	It is concluded that secondary enzyme deficiencies observed in hereditary tyrosinemia (delta-aminolevulinic acid dehydratase, methionine adenosyl transferase) are the result of inhibition by succinylacetone and fumarylacetoacetate, accumulating as a result of a primary deficiency of fumarylacetoacetase.	succinylacetone	191-206	aminolevulinate dehydratase	Homo sapiens	87-124
6652907-6	1983	It is concluded that secondary enzyme deficiencies observed in hereditary tyrosinemia (delta-aminolevulinic acid dehydratase, methionine adenosyl transferase) are the result of inhibition by succinylacetone and fumarylacetoacetate, accumulating as a result of a primary deficiency of fumarylacetoacetase.	succinylacetone	191-206	fumarylacetoacetate hydrolase	Homo sapiens	284-303
6617864-1	1983	The effects of succinylacetone, a tyrosine metabolite, on the hepatic biosynthesis of heme and cytochrome P450 were studied in primary culture of chick embryo hepatocytes.	succinylacetone	15-30	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	95-110
6617864-2	1983	Succinylacetone potentiated the phenobarbital-mediated induction of delta-aminolevulinate synthase, strongly inhibited porphobilinogen synthase activity, reduced cellular heme concentration and impaired induction of cytochrome P450.	succinylacetone	0-15	aminolevulinate dehydratase	Homo sapiens	119-143
6617864-2	1983	Succinylacetone potentiated the phenobarbital-mediated induction of delta-aminolevulinate synthase, strongly inhibited porphobilinogen synthase activity, reduced cellular heme concentration and impaired induction of cytochrome P450.	succinylacetone	0-15	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	216-231
6617864-3	1983	Enhanced induction of delta-aminolevulinate synthase and decreased cytochrome P450 induction may be explained by the succinylacetone-mediated inhibition of porphobilinogen synthase and the subsequent depletion of intracellular heme, since these effects of succinylacetone were reversed by addition of heme.	succinylacetone	117-132	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	67-82
6617864-3	1983	Enhanced induction of delta-aminolevulinate synthase and decreased cytochrome P450 induction may be explained by the succinylacetone-mediated inhibition of porphobilinogen synthase and the subsequent depletion of intracellular heme, since these effects of succinylacetone were reversed by addition of heme.	succinylacetone	117-132	aminolevulinate dehydratase	Homo sapiens	156-180
6826727-1	1983	Profound inhibition of delta-aminolevulinic acid dehydratase activity by succinylacetone.	succinylacetone	73-88	aminolevulinate dehydratase	Homo sapiens	23-60
6826727-2	1983	Succinylacetone (4,6-dioxoheptanoic acid) is an abnormal metabolite produced in patients with hereditary tyrosinemia as a consequence of an inherited deficiency of fumarylacetoacetate hydrolase.	succinylacetone	0-15	fumarylacetoacetate hydrolase	Homo sapiens	164-193
6826727-2	1983	Succinylacetone (4,6-dioxoheptanoic acid) is an abnormal metabolite produced in patients with hereditary tyrosinemia as a consequence of an inherited deficiency of fumarylacetoacetate hydrolase.	succinylacetone	17-40	fumarylacetoacetate hydrolase	Homo sapiens	164-193
6826727-7	1983	In cultured hepatocytes, succinylacetone also inhibited ALA dehydratase activity, decreased the cellular content of heme and cytochrome P-450, and greatly potentiated the induction response of ALA synthase to drugs such as phenobarbital, chemicals such as allylisopropylacetamide and 3,5-dicarbethoxy-1,4-dihydrocollidine, and natural steroids such as etiocholanolone.	succinylacetone	25-40	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	125-141
7116642-2	1982	It essentially involves the inhibition of delta-aminolevulinate dehydratase (EC 4.2.1.24) by succinylacetone.	succinylacetone	93-108	aminolevulinate dehydratase	Homo sapiens	42-75
289386-0	1979	Succinylacetone, a potent inhibitor of heme biosynthesis: effect on cell growth, heme content and delta-aminolevulinic acid dehydratase activity of malignant murine erythroleukemia cells.	succinylacetone	0-15	aminolevulinate, delta-, dehydratase	Mus musculus	98-135
7182986-0	1982	Succinylacetone inhibits delta-aminolevulinate dehydratase and potentiates the drug and steroid induction of delta-aminolevulinate synthase in liver.	succinylacetone	0-15	aminolevulinate dehydratase	Homo sapiens	25-58
7182986-1	1982	Succinylacetone, an abnormal metabolite of the tyrosine metabolic pathway, is produced in patients with hereditary tyrosinemia because of a genetic deficiency of fumarylacetoacetase.	succinylacetone	0-15	fumarylacetoacetate hydrolase	Homo sapiens	162-181
270706-5	1977	Succinylacetone and succinylacetoacetate presumably originate from maleylacetoacetate or fumarylacetoacetate, or both, and their accumulation indicates a block at the fumarylacetoacetase (EC 3.7.1.2) step in the degradation of tyrosine.	succinylacetone	0-15	fumarylacetoacetate hydrolase	Homo sapiens	167-186
31832512-2	2019	In the recent issue of the EMBO Journal, Yang and colleagues identified that succinylacetone (SA) could act as an oncometabolite and that accumulation of SA activates the NRF2/IGF1R axis in hepatocellular carcinoma (HCC) development.	succinylacetone	94-96	insulin like growth factor 1 receptor	Homo sapiens	176-181
33670179-2	2021	A deficiency in human FAH leads to hereditary tyrosinemia type I (HT1), an autosomal recessive disorder that results in the accumulation of toxic metabolites such as succinylacetone, maleylacetoacetate, and fumarylacetoacetate in the liver and kidney, among other tissues.	succinylacetone	166-181	fumarylacetoacetate hydrolase	Homo sapiens	22-25
31832512-2	2019	In the recent issue of the EMBO Journal, Yang and colleagues identified that succinylacetone (SA) could act as an oncometabolite and that accumulation of SA activates the NRF2/IGF1R axis in hepatocellular carcinoma (HCC) development.	succinylacetone	154-156	NFE2 like bZIP transcription factor 2	Homo sapiens	171-175
31832512-2	2019	In the recent issue of the EMBO Journal, Yang and colleagues identified that succinylacetone (SA) could act as an oncometabolite and that accumulation of SA activates the NRF2/IGF1R axis in hepatocellular carcinoma (HCC) development.	succinylacetone	154-156	insulin like growth factor 1 receptor	Homo sapiens	176-181
29326876-0	2018	Mildly elevated succinylacetone and normal liver function in compound heterozygotes with pathogenic and pseudodeficient FAH alleles.	succinylacetone	16-31	fumarylacetoacetate hydrolase	Homo sapiens	120-123
31026585-9	2019	A strong interplay between BACH1-mediated HO-1 expression and intracellular levels of labile heme was also confirmed in hMDMs with siRNA knockdown studies and following inhibition of de novo heme synthesis with succinylacetone.	succinylacetone	211-226	BTB and CNC homology 1, basic leucine zipper transcription factor 1	Mus musculus	27-32
31623369-6	2019	To understand SA-induced reduction in ATP production, we investigated the electron transfer chains (ETC) and pyruvate dehydrogenase kinase (PDK) activity, which prevents the transfer of acetyl-CoA to the TCA (tricarboxylic acid) cycle by inhibiting PDH (pyruvate dehydrogenase) activity.	succinylacetone	14-16	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	109-131
30666736-2	2019	The sscd1 mutant accumulates succinylacetone (SUAC), an abnormal metabolite caused by loss of FAH.	succinylacetone	29-44	fumarylacetoacetase	Arabidopsis thaliana	4-9
30666736-2	2019	The sscd1 mutant accumulates succinylacetone (SUAC), an abnormal metabolite caused by loss of FAH.	succinylacetone	29-44	fumarylacetoacetase	Arabidopsis thaliana	94-97
30666736-2	2019	The sscd1 mutant accumulates succinylacetone (SUAC), an abnormal metabolite caused by loss of FAH.	succinylacetone	46-50	fumarylacetoacetase	Arabidopsis thaliana	4-9
30666736-2	2019	The sscd1 mutant accumulates succinylacetone (SUAC), an abnormal metabolite caused by loss of FAH.	succinylacetone	46-50	fumarylacetoacetase	Arabidopsis thaliana	94-97
30666736-7	2019	In addition, Arabidopsis WT seedlings treated with SUAC mimic sscd1 in decline of ALAD activity and accumulation of Pchlide as well as cell death.	succinylacetone	51-55	fumarylacetoacetase	Arabidopsis thaliana	62-67
30666736-8	2019	These results demonstrate that increase in Pchlide causes cell death in sscd1 upon re-illumination and suggest that a decline in the Pchlide pool due to inhibition of ALAD activity by SUAC impairs the repression of ALA synthesis from the light-dark transition by feedback control, resulting in activation of the Chl biosynthesis pathway and accumulation of Pchlide in the dark.	succinylacetone	184-188	fumarylacetoacetase	Arabidopsis thaliana	72-77
29503615-8	2018	Overexpression of succinylacetone (4,6-dioxoheptanoic acid) suggests a novel inhibitory effect of Dex on hepatic fumarylacetoacetate hydrolase.	succinylacetone	18-33	fumarylacetoacetate hydrolase	Rattus norvegicus	113-142
29503615-8	2018	Overexpression of succinylacetone (4,6-dioxoheptanoic acid) suggests a novel inhibitory effect of Dex on hepatic fumarylacetoacetate hydrolase.	succinylacetone	35-58	fumarylacetoacetate hydrolase	Rattus norvegicus	113-142
28347842-5	2017	RESULTS: The blockade of heme biosynthesis by succinylacetone and N-methyl protoporphyrin, which are inhibitors of heme biosynthesis, markedly decreased the induction of HO-1.	succinylacetone	46-61	heme oxygenase 1	Homo sapiens	170-174
28808058-6	2017	Inhibition of 5-aminolevulinic acid dehydratase (EC 4.2.1.24) with succinylacetone resulted in both 5-aminolevulinic acid (ALA) accumulation in control and Abcb10-specific shRNA MEL cells, demonstrating that reductions in Abcb10 do not affect ALA export from mitochondria and indicating that Abcb10 does not transport ALA.	succinylacetone	67-82	ATP-binding cassette, sub-family B (MDR/TAP), member 10	Mus musculus	156-162
28808058-6	2017	Inhibition of 5-aminolevulinic acid dehydratase (EC 4.2.1.24) with succinylacetone resulted in both 5-aminolevulinic acid (ALA) accumulation in control and Abcb10-specific shRNA MEL cells, demonstrating that reductions in Abcb10 do not affect ALA export from mitochondria and indicating that Abcb10 does not transport ALA.	succinylacetone	67-82	ATP-binding cassette, sub-family B (MDR/TAP), member 10	Mus musculus	222-228
28808058-6	2017	Inhibition of 5-aminolevulinic acid dehydratase (EC 4.2.1.24) with succinylacetone resulted in both 5-aminolevulinic acid (ALA) accumulation in control and Abcb10-specific shRNA MEL cells, demonstrating that reductions in Abcb10 do not affect ALA export from mitochondria and indicating that Abcb10 does not transport ALA.	succinylacetone	67-82	ATP-binding cassette, sub-family B (MDR/TAP), member 10	Mus musculus	222-228
28053091-2	2017	Lack of FAH causes accumulation of toxic metabolites (fumarylacetoacetate and succinylacetone) in blood and tissues, ultimately resulting in severe liver and kidney damage with onset that ranges from infancy to adolescence.	succinylacetone	78-93	fumarylacetoacetase	Oryctolagus cuniculus	8-11
27876694-1	2017	BACKGROUND: A high level of succinylacetone (SA) in blood is a sensitive, specific newborn screening marker for hepatorenal tyrosinemia type 1 (HT1, MIM 276700) caused by deficiency of fumarylacetoacetate hydrolase (FAH).	succinylacetone	28-43	fumarylacetoacetate hydrolase	Homo sapiens	185-214
27876694-1	2017	BACKGROUND: A high level of succinylacetone (SA) in blood is a sensitive, specific newborn screening marker for hepatorenal tyrosinemia type 1 (HT1, MIM 276700) caused by deficiency of fumarylacetoacetate hydrolase (FAH).	succinylacetone	28-43	fumarylacetoacetate hydrolase	Homo sapiens	216-219
27876694-1	2017	BACKGROUND: A high level of succinylacetone (SA) in blood is a sensitive, specific newborn screening marker for hepatorenal tyrosinemia type 1 (HT1, MIM 276700) caused by deficiency of fumarylacetoacetate hydrolase (FAH).	succinylacetone	45-47	fumarylacetoacetate hydrolase	Homo sapiens	185-214
27876694-1	2017	BACKGROUND: A high level of succinylacetone (SA) in blood is a sensitive, specific newborn screening marker for hepatorenal tyrosinemia type 1 (HT1, MIM 276700) caused by deficiency of fumarylacetoacetate hydrolase (FAH).	succinylacetone	45-47	fumarylacetoacetate hydrolase	Homo sapiens	216-219
28868498-8	2016	We describe an improved, non-derivatized DBS extraction and MS/MS analytical method (AAAC-GAMT) which incorporates quantitation of CRE and GAA into routine analysis of amino acids, acylcarnitines, and succinylacetone.	succinylacetone	201-216	guanidinoacetate N-methyltransferase	Homo sapiens	90-94
27097641-7	2016	In addition, a high concentration of sugar attenuated cell death of Arabidopsis wild-type seedlings caused by treatment with exogenous succinylacetone, an abnormal metabolite resulting from the loss of FAH in the Tyr degradation pathway.	succinylacetone	135-150	fumarylacetoacetase	Arabidopsis thaliana	202-205
27097641-8	2016	These results indicated that (1) sugar could suppress cell death in sscd1, which might be because sugar supply enhances the resistance of Arabidopsis seedlings to toxic effects of succinylacetone and reduces the accumulation of Tyr degradation intermediates, resulting in suppression of cell death; and (2) sucrose-processing genes cell-wall invertase 1 and alkaline/neutral invertase G might be involved in the cell death in sscd1.	succinylacetone	180-195	fumarylacetoacetase	Arabidopsis thaliana	68-73
19862332-4	2009	Increasing intracellular heme synthesis through the addition of aminolevulinic acid, protoporphyrin IX, or transferrin-bound iron increased the cytotoxicity of dihydroartemisinin, while decreasing heme synthesis through the addition of succinyl acetone decreased its cytotoxic activity.	succinylacetone	236-252	transferrin	Homo sapiens	107-118
20071481-4	2010	Because NOS and sGC are important regulators of cardiovascular function, we hypothesized that inhibition of heme supply to these enzymes by SA would result in the induction of a measurable hypertensive response.	succinylacetone	140-142	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	16-19
20071481-7	2010	After SA treatment, systemic nitrite/nitrate excretion was reduced by 72% (P < 0.001), and renal NOS and sGC activities were decreased by 32 (P < 0.05) and 38% (P < 0.01), respectively.	succinylacetone	6-8	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	108-111
20003495-11	2009	The patient, currently aged 12 years, shows a normal physical and psychomotor development.This is the first report of mild tyrosinemia type I disease caused by an Ala35Thr mutation in the FAH gene, presenting atypically without increase of the diagnostically important toxic metabolites succinylacetone and succinylacetoacetate.	succinylacetone	287-302	fumarylacetoacetate hydrolase	Homo sapiens	188-191
25982796-7	2015	Succinylacetone decreased the Nrf2a-mediated hmox1a induction, whereas pre-treatment with hemin caused ectopic induction of hmox1a in nonliver tissues, implying that the high heme levels in the liver may release the repressive activity of Bach1.	succinylacetone	0-15	nfe2 like bZIP transcription factor 2a	Danio rerio	30-35
25982796-7	2015	Succinylacetone decreased the Nrf2a-mediated hmox1a induction, whereas pre-treatment with hemin caused ectopic induction of hmox1a in nonliver tissues, implying that the high heme levels in the liver may release the repressive activity of Bach1.	succinylacetone	0-15	heme oxygenase 1a	Danio rerio	45-51
25982796-7	2015	Succinylacetone decreased the Nrf2a-mediated hmox1a induction, whereas pre-treatment with hemin caused ectopic induction of hmox1a in nonliver tissues, implying that the high heme levels in the liver may release the repressive activity of Bach1.	succinylacetone	0-15	BTB and CNC homology 1, basic leucine zipper transcription factor 1 b	Danio rerio	239-244
23895425-1	2014	Hereditary tyrosinemia type I (HT1) is a rare disease caused by a deficiency of fumarylacetoacetate hydrolase (FAH) in the tyrosine catabolic pathway, resulting mainly in hepatic alterations due to accumulation of the toxic metabolites fumarylacetoacetate, maleylacetoacetate and succinylacetone.	succinylacetone	280-295	fumarylacetoacetate hydrolase	Homo sapiens	80-109
23895425-1	2014	Hereditary tyrosinemia type I (HT1) is a rare disease caused by a deficiency of fumarylacetoacetate hydrolase (FAH) in the tyrosine catabolic pathway, resulting mainly in hepatic alterations due to accumulation of the toxic metabolites fumarylacetoacetate, maleylacetoacetate and succinylacetone.	succinylacetone	280-295	fumarylacetoacetate hydrolase	Homo sapiens	111-114
23743712-7	2013	Furthermore, treatment of Arabidopsis wild-type seedlings with succinylacetone, an abnormal metabolite caused by loss of FAH in the Tyr degradation pathway, mimicked the sscd1 cell death phenotype.	succinylacetone	63-78	fumarylacetoacetase	Arabidopsis thaliana	121-124
23743712-7	2013	Furthermore, treatment of Arabidopsis wild-type seedlings with succinylacetone, an abnormal metabolite caused by loss of FAH in the Tyr degradation pathway, mimicked the sscd1 cell death phenotype.	succinylacetone	63-78	fumarylacetoacetase	Arabidopsis thaliana	170-175
23840483-7	2013	In fact, the inhibition of the heme synthesis by succinylacetone rather than heme catabolism by HO-1, led to a confinement of the Nox4/p22(phox) heterodimer in the endoplasmic reticulum with an absence of redox differential spectrum highlighting an incomplete maturation.	succinylacetone	49-64	NADPH oxidase 4	Homo sapiens	130-134
23840483-7	2013	In fact, the inhibition of the heme synthesis by succinylacetone rather than heme catabolism by HO-1, led to a confinement of the Nox4/p22(phox) heterodimer in the endoplasmic reticulum with an absence of redox differential spectrum highlighting an incomplete maturation.	succinylacetone	49-64	calcineurin like EF-hand protein 1	Homo sapiens	135-138
22859313-6	2012	CYP2A5 was intensively and HMOX1 moderately elevated in heme synthesis blockades by succinylacetone and N-methyl protoporphyrin IX, and Nrf2 partially mediated the induction of CYP2A5.	succinylacetone	84-99	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	0-6
22859313-6	2012	CYP2A5 was intensively and HMOX1 moderately elevated in heme synthesis blockades by succinylacetone and N-methyl protoporphyrin IX, and Nrf2 partially mediated the induction of CYP2A5.	succinylacetone	84-99	heme oxygenase 1	Mus musculus	27-32
16841962-12	2006	More importantly, the formation of the glutathione adduct was significantly suppressed by the pretreatment of HL60 cells with the heme synthesis inhibitor succinylacetone (p < 0.001), which resulted in a decreased level and activity of MPO.	succinylacetone	155-170	myeloperoxidase	Homo sapiens	239-242
19597542-10	2009	In vitro enzyme assays revealed a approximately 600-fold difference in drug sensitivities to succinyl acetone (SA) between Wolbachia and human 5"-aminolevulinic acid dehydratase (ALAD, the second step).	succinylacetone	93-109	aminolevulinate dehydratase	Homo sapiens	143-177
18651177-8	2009	Succinyl acetone was estimated indirectly through the inhibition of porphobilinogen synthase activity (PBGS assay).	succinylacetone	0-16	aminolevulinate dehydratase	Homo sapiens	68-92
18651177-8	2009	Succinyl acetone was estimated indirectly through the inhibition of porphobilinogen synthase activity (PBGS assay).	succinylacetone	0-16	aminolevulinate dehydratase	Homo sapiens	103-107
18758510-2	2008	The goal of this study was to examine the vascular effects of a short-term depletion of heme achieved through administration of the heme-synthesis inhibitor succinylacetone (SA), an irreversible inhibitor of aminolevulinic acid dehydratase (ALAD).	succinylacetone	157-172	aminolevulinate dehydratase	Homo sapiens	208-239
18758510-2	2008	The goal of this study was to examine the vascular effects of a short-term depletion of heme achieved through administration of the heme-synthesis inhibitor succinylacetone (SA), an irreversible inhibitor of aminolevulinic acid dehydratase (ALAD).	succinylacetone	157-172	aminolevulinate dehydratase	Homo sapiens	241-245
18758510-2	2008	The goal of this study was to examine the vascular effects of a short-term depletion of heme achieved through administration of the heme-synthesis inhibitor succinylacetone (SA), an irreversible inhibitor of aminolevulinic acid dehydratase (ALAD).	succinylacetone	174-176	aminolevulinate dehydratase	Homo sapiens	208-239
18758510-2	2008	The goal of this study was to examine the vascular effects of a short-term depletion of heme achieved through administration of the heme-synthesis inhibitor succinylacetone (SA), an irreversible inhibitor of aminolevulinic acid dehydratase (ALAD).	succinylacetone	174-176	aminolevulinate dehydratase	Homo sapiens	241-245
17875773-6	2007	Preincubation of myeloid leukemic cells with the MPO-specific inhibitor, 4-aminobenzoic acid hydrazide, and the heme biosynthesis inhibitor, succinylacetone, resulted in inhibition of the intracellular MPO activity, ROS production, and induction of apoptosis following addition of EGCG.	succinylacetone	141-156	myeloperoxidase	Homo sapiens	49-52
17875773-6	2007	Preincubation of myeloid leukemic cells with the MPO-specific inhibitor, 4-aminobenzoic acid hydrazide, and the heme biosynthesis inhibitor, succinylacetone, resulted in inhibition of the intracellular MPO activity, ROS production, and induction of apoptosis following addition of EGCG.	succinylacetone	141-156	myeloperoxidase	Homo sapiens	202-205
17435269-9	2006	Lead toxicity, succinylacetone, and zinc deficiency are known to depress ALA-D, but these conditions were not present.	succinylacetone	15-30	aminolevulinate dehydratase	Homo sapiens	73-78
19597542-10	2009	In vitro enzyme assays revealed a approximately 600-fold difference in drug sensitivities to succinyl acetone (SA) between Wolbachia and human 5"-aminolevulinic acid dehydratase (ALAD, the second step).	succinylacetone	93-109	aminolevulinate dehydratase	Homo sapiens	179-183
19597542-10	2009	In vitro enzyme assays revealed a approximately 600-fold difference in drug sensitivities to succinyl acetone (SA) between Wolbachia and human 5"-aminolevulinic acid dehydratase (ALAD, the second step).	succinylacetone	111-113	aminolevulinate dehydratase	Homo sapiens	143-177
19597542-10	2009	In vitro enzyme assays revealed a approximately 600-fold difference in drug sensitivities to succinyl acetone (SA) between Wolbachia and human 5"-aminolevulinic acid dehydratase (ALAD, the second step).	succinylacetone	111-113	aminolevulinate dehydratase	Homo sapiens	179-183
18384829-2	2008	CD1 mice were treated with either an inhibitor (succinyl acetone (SA)) or stimulator (2-allyl-2-isopropylacetamide (AIA)) of haem biosynthesis.	succinylacetone	48-64	CD1 antigen complex	Mus musculus	0-3
18384829-2	2008	CD1 mice were treated with either an inhibitor (succinyl acetone (SA)) or stimulator (2-allyl-2-isopropylacetamide (AIA)) of haem biosynthesis.	succinylacetone	66-68	CD1 antigen complex	Mus musculus	0-3
17877375-3	2007	In this study, a heme biosynthesis inhibitor, succinylacetone (SA), was found to inhibit cellular TrpRS activity in IFN-gamma-activated cells without affecting TrpRS protein expression.	succinylacetone	46-61	tryptophanyl-tRNA synthetase 1	Homo sapiens	98-103
17877375-3	2007	In this study, a heme biosynthesis inhibitor, succinylacetone (SA), was found to inhibit cellular TrpRS activity in IFN-gamma-activated cells without affecting TrpRS protein expression.	succinylacetone	46-61	interferon gamma	Homo sapiens	116-125
17877375-3	2007	In this study, a heme biosynthesis inhibitor, succinylacetone (SA), was found to inhibit cellular TrpRS activity in IFN-gamma-activated cells without affecting TrpRS protein expression.	succinylacetone	63-65	tryptophanyl-tRNA synthetase 1	Homo sapiens	98-103
17877375-3	2007	In this study, a heme biosynthesis inhibitor, succinylacetone (SA), was found to inhibit cellular TrpRS activity in IFN-gamma-activated cells without affecting TrpRS protein expression.	succinylacetone	63-65	interferon gamma	Homo sapiens	116-125
17877375-3	2007	In this study, a heme biosynthesis inhibitor, succinylacetone (SA), was found to inhibit cellular TrpRS activity in IFN-gamma-activated cells without affecting TrpRS protein expression.	succinylacetone	63-65	tryptophanyl-tRNA synthetase 1	Homo sapiens	160-165
17877375-4	2007	In addition, supplementation of lysates from the SA-treated cells with hemin fully restored TrpRS activity to control levels.	succinylacetone	49-51	tryptophanyl-tRNA synthetase 1	Homo sapiens	92-97
17682061-4	2007	In contrast, succinylacetone, an inhibitor of heme synthesis, caused accumulation of Bach1 in murine embryonic fibroblasts, indicating that physiological levels of heme regulated the Bach1 turnover.	succinylacetone	13-28	BTB and CNC homology 1, basic leucine zipper transcription factor 1	Mus musculus	85-90
17682061-4	2007	In contrast, succinylacetone, an inhibitor of heme synthesis, caused accumulation of Bach1 in murine embryonic fibroblasts, indicating that physiological levels of heme regulated the Bach1 turnover.	succinylacetone	13-28	BTB and CNC homology 1, basic leucine zipper transcription factor 1	Mus musculus	183-188
16838078-0	2006	Increased mutant frequencies in the HPRT gene locus of leukemia HL-60 cells treated with succinylacetone.	succinylacetone	89-104	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	36-40
16838078-2	2006	SA has been used to downregulate the activity of myeloperoxidase (MPO) through its specific inhibition of heme biosynthesis and to investigate the biological properties of MPO in the human myeloid leukemic (HL-60) cell line.	succinylacetone	0-2	myeloperoxidase	Homo sapiens	49-64
16838078-2	2006	SA has been used to downregulate the activity of myeloperoxidase (MPO) through its specific inhibition of heme biosynthesis and to investigate the biological properties of MPO in the human myeloid leukemic (HL-60) cell line.	succinylacetone	0-2	myeloperoxidase	Homo sapiens	66-69
16838078-2	2006	SA has been used to downregulate the activity of myeloperoxidase (MPO) through its specific inhibition of heme biosynthesis and to investigate the biological properties of MPO in the human myeloid leukemic (HL-60) cell line.	succinylacetone	0-2	myeloperoxidase	Homo sapiens	172-175
16838078-3	2006	The goal of this study is to evaluate the mutagenic potential of SA by determining the frequencies of somatic mutations in the hypoxanthine-guanine phosphoribosyl transferase (HPRT) reporter gene in HL-60 cells following treatment with the chemical.	succinylacetone	65-67	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	127-174
16838078-3	2006	The goal of this study is to evaluate the mutagenic potential of SA by determining the frequencies of somatic mutations in the hypoxanthine-guanine phosphoribosyl transferase (HPRT) reporter gene in HL-60 cells following treatment with the chemical.	succinylacetone	65-67	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	176-180
16838078-4	2006	Treatments of HL-60 cells with 500 micromol/L SA for 72 h, a condition generally used to inhibit the MPO activity, resulted in a significantly increased HPRT mutant frequency (HPRT-Mf), compared with the control of untreated cells (47.25 x 10(-6) versus 7.5 x 10(-6), respectively, p <0.01).	succinylacetone	46-48	myeloperoxidase	Homo sapiens	101-104
16838078-4	2006	Treatments of HL-60 cells with 500 micromol/L SA for 72 h, a condition generally used to inhibit the MPO activity, resulted in a significantly increased HPRT mutant frequency (HPRT-Mf), compared with the control of untreated cells (47.25 x 10(-6) versus 7.5 x 10(-6), respectively, p <0.01).	succinylacetone	46-48	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	153-157
16838078-4	2006	Treatments of HL-60 cells with 500 micromol/L SA for 72 h, a condition generally used to inhibit the MPO activity, resulted in a significantly increased HPRT mutant frequency (HPRT-Mf), compared with the control of untreated cells (47.25 x 10(-6) versus 7.5 x 10(-6), respectively, p <0.01).	succinylacetone	46-48	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	176-180
16838078-5	2006	Treatment of the cells with lower doses of SA also led to an increase in HPRT-Mf but this was significant only with 200 micromol/L (28.67 x 10(-6), p<0.05) and not with doses lower than 100 micromol/L (p0.05), compared with the control of untreated cells (7.5 x 10(-6)).	succinylacetone	43-45	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	73-77
16838078-6	2006	These data show a dose-response increase in HPRT-Mf in HL-60 cells treated with SA, suggesting that this chemical causes mutations in the HPRT locus in these cells either directly or indirectly through its inhibition of the MPO activity.	succinylacetone	80-82	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	44-48
16838078-6	2006	These data show a dose-response increase in HPRT-Mf in HL-60 cells treated with SA, suggesting that this chemical causes mutations in the HPRT locus in these cells either directly or indirectly through its inhibition of the MPO activity.	succinylacetone	80-82	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	138-142
16838078-6	2006	These data show a dose-response increase in HPRT-Mf in HL-60 cells treated with SA, suggesting that this chemical causes mutations in the HPRT locus in these cells either directly or indirectly through its inhibition of the MPO activity.	succinylacetone	80-82	myeloperoxidase	Homo sapiens	224-227
15464985-3	2004	A decrease of alpha-globin mRNA was observed in SA-treated cells, which was restored by the addition of hemin.	succinylacetone	48-50	hemoglobin subunit alpha 2	Homo sapiens	14-26
16479012-7	2006	Actinomycin D, cycloheximide, succinylacetone, and dimethyl-oxalylglycine antagonize IRP2 degradation in response to both FAC and SNP, suggesting a common mechanistic basis.	succinylacetone	30-45	iron responsive element binding protein 2	Homo sapiens	85-89
16278372-1	2006	Glutathione S-transferase (GST) zeta (GSTZ1-1) plays a significant role in the catabolism of phenylalanine and tyrosine, and a deficiency of GSTZ1-1 results in the accumulation of maleylacetoacetate and its derivatives maleylacetone (MA) and succinylacetone.	succinylacetone	242-257	glutathione transferase zeta 1 (maleylacetoacetate isomerase)	Mus musculus	38-45
16033334-5	2005	A 9.1 kb cALAS-1 (chicken ALAS-1) promoter-luciferase-reporter construct, was poorly induced by Glut and not by DHA alone, but was synergistically induced by the combination.	succinylacetone	112-115	5'-aminolevulinate synthase 1	Gallus gallus	10-16
16306232-6	2006	Inhibition of heme synthesis (by 70-80%) at different enzymic steps by succinyl acetone and N-methylprotoporphyrin IX resulted in the earlier lowered expression of NMDAzeta1 and -epsilon2 and NF-L.	succinylacetone	71-87	neurofilament, light polypeptide	Mus musculus	192-196
16414314-2	2006	SA is pathognonomic for tyrosinemia type I, a genetic disorder caused by a reduced activity of fumarylacetoacetate hydrolase (FAH).	succinylacetone	0-2	fumarylacetoacetate hydrolase	Homo sapiens	95-124
16414314-2	2006	SA is pathognonomic for tyrosinemia type I, a genetic disorder caused by a reduced activity of fumarylacetoacetate hydrolase (FAH).	succinylacetone	0-2	fumarylacetoacetate hydrolase	Homo sapiens	126-129
15950757-6	2005	Further, we found that in succinyl acetone-treated, NGF-induced cells, the pro-survival Ras-ERK1/2 signaling pathway was inactivated and the pro-apoptotic JNK signaling pathway was activated.	succinylacetone	26-42	mitogen activated protein kinase 3	Rattus norvegicus	92-98
15464985-4	2004	The heme-dependent expression of alpha-globin occurred at the transcriptional level since the expression of human alpha-globin gene promoter-reporter gene containing hypersensitive site-40 (HS-40) was decreased when K562 cells were cultured with SA.	succinylacetone	246-248	hemoglobin subunit alpha 2	Homo sapiens	33-45
15464985-4	2004	The heme-dependent expression of alpha-globin occurred at the transcriptional level since the expression of human alpha-globin gene promoter-reporter gene containing hypersensitive site-40 (HS-40) was decreased when K562 cells were cultured with SA.	succinylacetone	246-248	hemoglobin subunit alpha 2	Homo sapiens	114-126
15464985-7	2004	The NA site-binding activity of Bach1 in K562 increased upon SA-treatment, and the increase was diminished by the addition of hemin.	succinylacetone	61-63	BTB domain and CNC homolog 1	Homo sapiens	32-37
15464985-10	2004	Interestingly, nuclear localization of Bach1 increased when cells were treated with SA, while hemin induced the nuclear export of Bach1.	succinylacetone	84-86	BTB domain and CNC homolog 1	Homo sapiens	39-44
14975735-4	2004	Our data show that succinyl acetone-induced heme deficiency increases the protein levels of the tumor suppressor gene product p53 and CDK inhibitor p21, and decreases the protein levels of Cdk4, Cdc2, and cyclin D2.	succinylacetone	19-35	tumor protein p53	Homo sapiens	126-129
15498530-7	2004	A comparison of SA analysis of this MS/MS method with an established enzyme assay indirectly quantitating SA by inhibition of delta-aminolevulinic acid dehydratase demonstrated a strong correlation.	succinylacetone	16-18	aminolevulinate dehydratase	Homo sapiens	126-163
15039448-7	2004	A thiol-blocking reagent, N-ethylmaleimide, as well as myeloperoxidase inhibitors (succinyl acetone and azide), blocked formation of fluorescent acridine-piperidine.	succinylacetone	83-99	myeloperoxidase	Homo sapiens	55-70
15144216-4	2004	In this context, oxidation of SA by peroxynitrite or cytochrome c yielding reactive intermediates and products was investigated here.	succinylacetone	30-32	cytochrome c, somatic	Homo sapiens	53-65
15144216-5	2004	Both peroxynitrite and cytochrome c were able to initiate oxygen consumption by SA, which was followed by polarimetric and chemiluminescence measurements.	succinylacetone	80-82	cytochrome c, somatic	Homo sapiens	23-35
14975735-4	2004	Our data show that succinyl acetone-induced heme deficiency increases the protein levels of the tumor suppressor gene product p53 and CDK inhibitor p21, and decreases the protein levels of Cdk4, Cdc2, and cyclin D2.	succinylacetone	19-35	cyclin dependent kinase inhibitor 1A	Homo sapiens	148-151
14975735-4	2004	Our data show that succinyl acetone-induced heme deficiency increases the protein levels of the tumor suppressor gene product p53 and CDK inhibitor p21, and decreases the protein levels of Cdk4, Cdc2, and cyclin D2.	succinylacetone	19-35	cyclin dependent kinase 4	Homo sapiens	189-193
14975735-4	2004	Our data show that succinyl acetone-induced heme deficiency increases the protein levels of the tumor suppressor gene product p53 and CDK inhibitor p21, and decreases the protein levels of Cdk4, Cdc2, and cyclin D2.	succinylacetone	19-35	cyclin dependent kinase 1	Homo sapiens	195-199
14975735-4	2004	Our data show that succinyl acetone-induced heme deficiency increases the protein levels of the tumor suppressor gene product p53 and CDK inhibitor p21, and decreases the protein levels of Cdk4, Cdc2, and cyclin D2.	succinylacetone	19-35	cyclin D2	Homo sapiens	205-214
14597854-8	2003	As for LPS and TNFalpha, eNOS monomer decreased already after a 72-h treatment and further at 144 h, whereas the down-regulation of the dimer was slower, peaking at 144 h. Succinylacetone and desferrioxamine were effective only at 144 h. The mRNA levels were increasingly reduced after incubation, more markedly by LPS and TNFalpha together, whereas succinylacetone and desferrioxamine had no effect on transcription.	succinylacetone	172-187	tumor necrosis factor	Homo sapiens	323-331
14599561-9	2003	DCA-nai;ve MAAI-KO mice accumulate very high levels of the tyrosine catabolites maleylacetone and succinylacetone, and DCA exposure did not significantly increase the levels of these compounds.	succinylacetone	98-113	glutathione transferase zeta 1 (maleylacetoacetate isomerase)	Mus musculus	11-15
14660636-9	2004	The MARE binding activity of Bach1 in K562 and MEL cells increased upon SA treatment, and the increase was diminished by the treatment with hemin.	succinylacetone	72-74	BTB domain and CNC homolog 1	Homo sapiens	29-34
14660636-12	2004	Furthermore, chromatin immunoprecipitation experiments revealed that Bach1 bound to the MARE of HS2 increased by the treatment of MEL cells with SA, and this was cancelled by hemin.	succinylacetone	145-147	BTB domain and CNC homolog 1	Homo sapiens	69-74
14660636-12	2004	Furthermore, chromatin immunoprecipitation experiments revealed that Bach1 bound to the MARE of HS2 increased by the treatment of MEL cells with SA, and this was cancelled by hemin.	succinylacetone	145-147	spectrin beta, erythrocytic	Homo sapiens	96-99
12469218-4	2003	Treatment of HLE/2E1 cells with succinylacetone (SA), a potent inhibitor of delta-aminolevulinate dehydratase and thereby heme synthesis, resulted in a further increase in ALAS-N mRNA but a decrease in HO-1 mRNA levels.	succinylacetone	32-47	aminolevulinate dehydratase	Homo sapiens	76-109
12972033-11	2003	Inhibition of endogenous heme synthesis with succinylacetone significantly inhibited iron- dependent degradation of IRP2.	succinylacetone	45-60	iron responsive element binding protein 2	Homo sapiens	116-120
12469218-4	2003	Treatment of HLE/2E1 cells with succinylacetone (SA), a potent inhibitor of delta-aminolevulinate dehydratase and thereby heme synthesis, resulted in a further increase in ALAS-N mRNA but a decrease in HO-1 mRNA levels.	succinylacetone	32-47	heme oxygenase 1	Homo sapiens	202-206
12469218-4	2003	Treatment of HLE/2E1 cells with succinylacetone (SA), a potent inhibitor of delta-aminolevulinate dehydratase and thereby heme synthesis, resulted in a further increase in ALAS-N mRNA but a decrease in HO-1 mRNA levels.	succinylacetone	49-51	aminolevulinate dehydratase	Homo sapiens	76-109
12469218-4	2003	Treatment of HLE/2E1 cells with succinylacetone (SA), a potent inhibitor of delta-aminolevulinate dehydratase and thereby heme synthesis, resulted in a further increase in ALAS-N mRNA but a decrease in HO-1 mRNA levels.	succinylacetone	49-51	heme oxygenase 1	Homo sapiens	202-206
12391268-5	2002	Succinylacetone, an inhibitor of heme biosynthesis, increased the ratio of cytosolic to microsomal EROD activity of transiently expressed CYP1A1 in COS-1 cells from 1:1 to nearly 6:1.	succinylacetone	0-15	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	138-144
9933639-7	1999	The heme synthesis inhibitor, succinyl acetone, reduced the abundance of mature gp91(phox) and p22(phox) but had little or no impact on p65.	succinylacetone	30-46	calcineurin like EF-hand protein 1	Homo sapiens	95-98
11545591-1	2001	The structures of 5-aminolaevulinic acid dehydratase (ALAD) complexed with substrate (5-aminolaevulinic acid) and three inhibitors: laevulinic acid, succinylacetone and 4-keto-5-aminolaevulinic acid, have been solved at high resolution.	succinylacetone	149-164	aminolevulinate dehydratase	Homo sapiens	54-58
11545591-5	2001	Succinylacetone appears to be unique by inducing a number of conformational changes in loops covering the active site, which may be important for understanding the co-operative properties of ALAD enzymes.	succinylacetone	0-15	aminolevulinate dehydratase	Homo sapiens	191-195
11545591-6	2001	Succinylacetone is produced in large amounts by patients suffering from the hereditary disease type I tyrosinaemia and its potent inhibition of ALAD also has implications for the pathology of this disease.	succinylacetone	0-15	aminolevulinate dehydratase	Homo sapiens	144-148
11468232-2	2001	We developed a semiquantitative assay based on inhibition of delta-aminolevulinate dehydratase (ALA-D) by succinylacetone.	succinylacetone	106-121	aminolevulinate dehydratase	Homo sapiens	61-94
11468232-2	2001	We developed a semiquantitative assay based on inhibition of delta-aminolevulinate dehydratase (ALA-D) by succinylacetone.	succinylacetone	106-121	aminolevulinate dehydratase	Homo sapiens	96-101
11342657-6	2001	Similar to PDTC, the heme biosynthesis inhibitor succinylacetone (SA) and the iron-chelator pyridoxal isonicotinoyl hydrazone inhibited cellular IDO activity without affecting protein expression, whereas addition of hemin or the heme precursor delta-aminolevulinic acid increased IDO activity.	succinylacetone	49-64	indoleamine 2,3-dioxygenase 1	Homo sapiens	145-148
11342657-6	2001	Similar to PDTC, the heme biosynthesis inhibitor succinylacetone (SA) and the iron-chelator pyridoxal isonicotinoyl hydrazone inhibited cellular IDO activity without affecting protein expression, whereas addition of hemin or the heme precursor delta-aminolevulinic acid increased IDO activity.	succinylacetone	49-64	indoleamine 2,3-dioxygenase 1	Homo sapiens	280-283
11342657-6	2001	Similar to PDTC, the heme biosynthesis inhibitor succinylacetone (SA) and the iron-chelator pyridoxal isonicotinoyl hydrazone inhibited cellular IDO activity without affecting protein expression, whereas addition of hemin or the heme precursor delta-aminolevulinic acid increased IDO activity.	succinylacetone	66-68	indoleamine 2,3-dioxygenase 1	Homo sapiens	145-148
11342657-6	2001	Similar to PDTC, the heme biosynthesis inhibitor succinylacetone (SA) and the iron-chelator pyridoxal isonicotinoyl hydrazone inhibited cellular IDO activity without affecting protein expression, whereas addition of hemin or the heme precursor delta-aminolevulinic acid increased IDO activity.	succinylacetone	66-68	indoleamine 2,3-dioxygenase 1	Homo sapiens	280-283
11342657-8	2001	Furthermore, supplementation of lysates from PDTC- or SA-treated hMDM with hemin fully restored IDO activity to control levels, and hemin also reversed the inhibitory action of SA but not PDTC in intact cells.	succinylacetone	54-56	indoleamine 2,3-dioxygenase 1	Homo sapiens	96-99
11209059-6	2001	Increased levels of the diagnostic metabolite succinylacetone in the urine of the Fah(6287SB) and Fah(5961SB) mutants indicate that these mutations cause a decrease in Fah enzymatic activity.	succinylacetone	46-61	fumarylacetoacetate hydrolase	Homo sapiens	82-85
11209059-6	2001	Increased levels of the diagnostic metabolite succinylacetone in the urine of the Fah(6287SB) and Fah(5961SB) mutants indicate that these mutations cause a decrease in Fah enzymatic activity.	succinylacetone	46-61	fumarylacetoacetate hydrolase	Homo sapiens	98-101
11209059-6	2001	Increased levels of the diagnostic metabolite succinylacetone in the urine of the Fah(6287SB) and Fah(5961SB) mutants indicate that these mutations cause a decrease in Fah enzymatic activity.	succinylacetone	46-61	fumarylacetoacetate hydrolase	Homo sapiens	98-101
10923223-8	2000	Such findings do not seem directly related to tyrosinaemia type 1 where succinylacetone inhibits delta-aminolevulinic acid (delta-ALA) dehydratase and where the accumulation of delta-ALA results in neurotoxicity without photosensitivity.	succinylacetone	72-87	aminolevulinate dehydratase	Homo sapiens	97-146
10788525-7	2000	In succinyl acetone-treated cells, p22(phox) and gp65 were degraded completely by 8 h of chase, a process mediated by the cytosolic proteasome.	succinylacetone	3-19	calcineurin like EF-hand protein 1	Homo sapiens	35-38
10788525-7	2000	In succinyl acetone-treated cells, p22(phox) and gp65 were degraded completely by 8 h of chase, a process mediated by the cytosolic proteasome.	succinylacetone	3-19	neuroplastin	Homo sapiens	49-53
10542064-1	1999	The in vivo effects of heme biosynthesis inhibitors, succinylacetone and CoCl2 on the cytochrome c oxidase (COX) gene expression and enzyme activity in different mouse tissues were investigated.	succinylacetone	53-68	cytochrome c oxidase subunit 4I1	Mus musculus	108-111
10187846-4	1999	Peroxidase activity at the cell surface and cell surface expression of hTPO were decreased by approximately 30 and approximately 80%, respectively, with succinyl acetone, an inhibitor of heme biosynthesis, and were increased by 20% with holotransferrin and aminolevulinic acid, precursors of heme biosynthesis.	succinylacetone	153-169	thyroid peroxidase	Homo sapiens	71-75
12052898-5	2002	MAAI-deficient mice accumulated FAA and succinylacetone in urine but appeared otherwise healthy.	succinylacetone	40-55	glutathione transferase zeta 1 (maleylacetoacetate isomerase)	Mus musculus	0-4
12042072-4	2002	Further, by microarray expression analysis, we found that inhibition of heme synthesis by succinyl acetone in NGF-induced PC12 cells drastically altered the expression of several groups of important neuronal genes, including the structural genes encoding neurofilament proteins and synaptic vesicle proteins, regulatory genes encoding signaling components beta-arrestin and p38 MAPK, and stress-response genes encoding hsp70.	succinylacetone	90-106	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	419-424
10772954-3	2000	In HL-60 cells pretreated with succinylacetone, an inhibitor of heme synthesis, a greater than 4-fold decrease in myeloperoxidase activity resulted in a dramatically decreased steady-state concentrations of PMC phenoxyl radicals hardly detectable in EPR spectra.	succinylacetone	31-46	myeloperoxidase	Homo sapiens	114-129
10699462-5	2000	Epo mRNA expression was inhibited only at higher concentrations of DHA (2, 4 mM) which also inhibited cell viability.	succinylacetone	67-70	erythropoietin	Homo sapiens	0-3
10665936-9	2000	In the homogentisate-treated Fah-/- Hpd-/- mice, massive amounts of succinylacetone were excreted into the urine, regardless of treatment with inhibitors.	succinylacetone	68-83	fumarylacetoacetate hydrolase	Mus musculus	29-32
10665936-9	2000	In the homogentisate-treated Fah-/- Hpd-/- mice, massive amounts of succinylacetone were excreted into the urine, regardless of treatment with inhibitors.	succinylacetone	68-83	4-hydroxyphenylpyruvic acid dioxygenase	Mus musculus	36-39
8645006-7	1996	Hb synthesis was inhibited 50% after addition of succinylacetone (SA), a potent inhibitor of delta-aminolevulinate dehydratase.	succinylacetone	49-64	aminolevulinate dehydratase	Homo sapiens	93-126
8605367-1	1996	Succinylacetone (SA) is an inhibitor of heme synthesis that acts on the enzyme delta-aminolevulinic acid dehydratase.	succinylacetone	0-15	delta-aminolevulinic acid dehydratase	Oryctolagus cuniculus	79-116
8605367-1	1996	Succinylacetone (SA) is an inhibitor of heme synthesis that acts on the enzyme delta-aminolevulinic acid dehydratase.	succinylacetone	17-19	delta-aminolevulinic acid dehydratase	Oryctolagus cuniculus	79-116
8605367-2	1996	When reticulocytes are incubated with 59Fe-transferrin (59Fe-Tf) in the presence of SA, there is an accumulation of 59Fe in the mitochondrion and in a cytosolic non-heme intermediate that has been described as a putative Fe transporter (Adams et al, Biochim Biophys Acta 1012:243, 1989).	succinylacetone	84-86	serotransferrin	Oryctolagus cuniculus	43-54
9575215-6	1998	Studies have shown that the degradation of IRP1 that is induced by iron can be inhibited by either desferrioxamine mesylate (an iron chelator) or succinyl acetone (an inhibitor of heme synthesis), whereas the degradation induced by heme cannot.	succinylacetone	146-162	cytoplasmic aconitate hydratase	Oryctolagus cuniculus	43-47
9575215-11	1998	However, as shown earlier with IRP1, both desferrioxamine mesylate and succinyl acetone will inhibit the degradation of IRP2 induced by iron but not that induced by heme.	succinylacetone	71-87	cytoplasmic aconitate hydratase	Oryctolagus cuniculus	31-35
9341176-4	1997	Succinyl acetone markedly reduced expression of p22(phox) and the mature 91-kDa form of gp91(phox) but not its 65-kDa high mannose precursor, in association with a profound reduction in NADPH oxidase activity.	succinylacetone	0-16	dynein cytoplasmic 1 heavy chain 1	Mus musculus	48-51
9341176-4	1997	Succinyl acetone markedly reduced expression of p22(phox) and the mature 91-kDa form of gp91(phox) but not its 65-kDa high mannose precursor, in association with a profound reduction in NADPH oxidase activity.	succinylacetone	0-16	paired Ig-like receptor B	Mus musculus	88-92
9341176-6	1997	The reduction in cytochrome b558 expression and NADPH oxidase activity was prevented by adding exogenous heme and was reversible upon removal of succinyl acetone.	succinylacetone	145-161	cytochrome b, mitochondrial	Mus musculus	17-29
9305902-9	1997	These results suggest that accumulation of fumarylacetoacetate, maleylacetoacetate, or succinylacetone seems to trigger the endogenous process of apoptosis in hepatocytes that lack fumarylacetoacetate hydrolase activity.	succinylacetone	87-102	fumarylacetoacetate hydrolase	Mus musculus	181-210
8645006-7	1996	Hb synthesis was inhibited 50% after addition of succinylacetone (SA), a potent inhibitor of delta-aminolevulinate dehydratase.	succinylacetone	66-68	aminolevulinate dehydratase	Homo sapiens	93-126
7568087-3	1995	We report here that fahA, the gene encoding Fah in the fungus Aspergillus nidulans, encodes a polypeptide showing 47.1% identity to its human homologue, fahA disruption results in secretion of succinylacetone (a diagnostic compound for human type I tyrosinaemia) and phenylalanine toxicity.	succinylacetone	193-208	fumarylacetoacetate hydrolase	Homo sapiens	44-47
7616655-2	1995	ALAD deficiency is well known to develop signs and symptoms of typical hepatic porphyria, and classified into three categories as follows: (i) ALAD porphyria, a genetic defect of the enzyme, (ii) tyrosinemia type I, a genetic defect of fumarylacetoacetase in the tyrosine catabolic pathway, producing succinylacetone (a potent inhibitor of ALAD), and (iii) ALAD inhibition by environmental hazards, such as lead, trichloroethylene, and styrene.	succinylacetone	301-316	aminolevulinate dehydratase	Homo sapiens	0-4
7945268-7	1994	Inhibition of haem synthesis in the transformed E. coli cells expressing cytochrome b5, by the use of gabaculin or succinylacetone, prevented the assembly of the cytochrome b5 holoprotein but had little effect on the accumulation of cytochrome apoprotein.	succinylacetone	115-130	cytochrome b5 type A	Homo sapiens	73-86
7614006-7	1995	The cobalt-induced increase in DOR expression was blocked by the heme synthesis inhibitor, 4,6-dioxoheptanoic acid.	succinylacetone	91-114	opioid receptor, delta 1	Mus musculus	31-34