PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
33204707-6	2020	This study is the first to report that the CAN1 and GAT1 genes have great influence on the generation of higher alcohols.	Alcohols	112-120	Gat1p	Saccharomyces cerevisiae S288C	52-56
29058647-5	2017	We found that Gat1 plays an important role in the induction of UGA4 transcription by GABA and that Gzf3 has an effect in cells grown in a poor nitrogen source such as proline and that this effect is positive on UGA4 expression.	gamma-Aminobutyric Acid	85-89	Gat1p	Saccharomyces cerevisiae S288C	14-18
31213504-5	2019	Two of TorC1"s many downstream targets are Gln3 and Gat1-GATA-family transcription activators-whose localization and function are Nitrogen Catabolite Repression- (NCR-) sensitive.	Nitrogen	130-138	Gat1p	Saccharomyces cerevisiae S288C	52-56
29564399-6	2018	For example, the core GATA activators GAT1 and GLN3 have a conserved role in nitrogen catabolite repression (NCR).	gata	22-26	Gat1p	Saccharomyces cerevisiae S288C	38-42
29564399-6	2018	For example, the core GATA activators GAT1 and GLN3 have a conserved role in nitrogen catabolite repression (NCR).	nitrogen catabolite	77-96	Gat1p	Saccharomyces cerevisiae S288C	38-42
25527290-0	2015	Nitrogen starvation and TorC1 inhibition differentially affect nuclear localization of the Gln3 and Gat1 transcription factors through the rare glutamine tRNACUG in Saccharomyces cerevisiae.	Nitrogen	0-8	Gat1p	Saccharomyces cerevisiae S288C	100-104
27908775-0	2017	Regulation of general amino acid permeases Gap1p, GATA transcription factors Gln3p and Gat1p on 2-phenylethanol biosynthesis via Ehrlich pathway.	Phenylethyl Alcohol	96-111	Gat1p	Saccharomyces cerevisiae S288C	87-92
27908775-2	2017	General amino acid permease Gap1p is response of aromatic amino acids transportation, and GATA transcription factors Gln3p and Gat1p regulate the transcription of permease gene and catabolic enzyme genes for nitrogen sources and aromatic amino acids utilization.	Amino Acids, Aromatic	49-69	Gat1p	Saccharomyces cerevisiae S288C	127-132
27908775-2	2017	General amino acid permease Gap1p is response of aromatic amino acids transportation, and GATA transcription factors Gln3p and Gat1p regulate the transcription of permease gene and catabolic enzyme genes for nitrogen sources and aromatic amino acids utilization.	Nitrogen	208-216	Gat1p	Saccharomyces cerevisiae S288C	127-132
27908775-2	2017	General amino acid permease Gap1p is response of aromatic amino acids transportation, and GATA transcription factors Gln3p and Gat1p regulate the transcription of permease gene and catabolic enzyme genes for nitrogen sources and aromatic amino acids utilization.	Amino Acids, Aromatic	229-249	Gat1p	Saccharomyces cerevisiae S288C	127-132
27908775-4	2017	The recombinant strains with over-expression of GAT1 gene from MT2 or YS58 also up-regulated Ehrlich pathway for 2-PE biosynthesis and increased 2-PE production.	2-pe	113-117	Gat1p	Saccharomyces cerevisiae S288C	48-52
27908775-4	2017	The recombinant strains with over-expression of GAT1 gene from MT2 or YS58 also up-regulated Ehrlich pathway for 2-PE biosynthesis and increased 2-PE production.	2-pe	145-149	Gat1p	Saccharomyces cerevisiae S288C	48-52
27920551-6	2016	Yeast expressing Gat1p and Lpt1p had phospholipids enriched with acyl chains that were unsaturated, 18 carbons long, and paired for length.	Phospholipids	37-50	Gat1p	Saccharomyces cerevisiae S288C	17-22
27920551-6	2016	Yeast expressing Gat1p and Lpt1p had phospholipids enriched with acyl chains that were unsaturated, 18 carbons long, and paired for length.	Carbon	103-110	Gat1p	Saccharomyces cerevisiae S288C	17-22
28007891-0	2017	General Amino Acid Control and 14-3-3 Proteins Bmh1/2 Are Required for Nitrogen Catabolite Repression-Sensitive Regulation of Gln3 and Gat1 Localization.	nitrogen catabolite	71-90	Gat1p	Saccharomyces cerevisiae S288C	135-139
28007891-1	2017	Nitrogen catabolite repression (NCR), the ability of Saccharomyces cerevisiae to use good nitrogen sources in preference to poor ones, derives from nitrogen-responsive regulation of the GATA family transcription activators Gln3 and Gat1 In nitrogen-replete conditions, the GATA factors are cytoplasmic and NCR-sensitive transcription minimal.	Nitrogen	0-8	Gat1p	Saccharomyces cerevisiae S288C	232-236
28007891-1	2017	Nitrogen catabolite repression (NCR), the ability of Saccharomyces cerevisiae to use good nitrogen sources in preference to poor ones, derives from nitrogen-responsive regulation of the GATA family transcription activators Gln3 and Gat1 In nitrogen-replete conditions, the GATA factors are cytoplasmic and NCR-sensitive transcription minimal.	Nitrogen	148-156	Gat1p	Saccharomyces cerevisiae S288C	232-236
28007891-1	2017	Nitrogen catabolite repression (NCR), the ability of Saccharomyces cerevisiae to use good nitrogen sources in preference to poor ones, derives from nitrogen-responsive regulation of the GATA family transcription activators Gln3 and Gat1 In nitrogen-replete conditions, the GATA factors are cytoplasmic and NCR-sensitive transcription minimal.	gata	186-190	Gat1p	Saccharomyces cerevisiae S288C	232-236
28007891-1	2017	Nitrogen catabolite repression (NCR), the ability of Saccharomyces cerevisiae to use good nitrogen sources in preference to poor ones, derives from nitrogen-responsive regulation of the GATA family transcription activators Gln3 and Gat1 In nitrogen-replete conditions, the GATA factors are cytoplasmic and NCR-sensitive transcription minimal.	Nitrogen	148-156	Gat1p	Saccharomyces cerevisiae S288C	232-236
28007891-1	2017	Nitrogen catabolite repression (NCR), the ability of Saccharomyces cerevisiae to use good nitrogen sources in preference to poor ones, derives from nitrogen-responsive regulation of the GATA family transcription activators Gln3 and Gat1 In nitrogen-replete conditions, the GATA factors are cytoplasmic and NCR-sensitive transcription minimal.	gata	273-277	Gat1p	Saccharomyces cerevisiae S288C	232-236
26899143-0	2016	The modification of Gat1p in nitrogen catabolite repression to enhance non-preferred nitrogen utilization in Saccharomyces cerevisiae.	Nitrogen	29-37	Gat1p	Saccharomyces cerevisiae S288C	20-25
26899143-0	2016	The modification of Gat1p in nitrogen catabolite repression to enhance non-preferred nitrogen utilization in Saccharomyces cerevisiae.	Nitrogen	85-93	Gat1p	Saccharomyces cerevisiae S288C	20-25
26899143-3	2016	Among these regulators, two positive regulators (Gln3p and Gat1p) could be phosphorylated and sequestered in the cytoplasm leading to the transcription of non-preferred nitrogen metabolic genes being repressed.	Nitrogen	169-177	Gat1p	Saccharomyces cerevisiae S288C	59-64
26899143-7	2016	In addition, the modifications of Gat1p (mutations on the NLS and truncation on the NLRS) were attempted to enhance the transcription of non-preferred nitrogen metabolic genes.	Nitrogen	151-159	Gat1p	Saccharomyces cerevisiae S288C	34-39
26899143-10	2016	Based on these results, the genetic engineering on Gat1p has a great potential in enhancing non-preferred nitrogen metabolism in S. cerevisiae.	Nitrogen	106-114	Gat1p	Saccharomyces cerevisiae S288C	51-56
25527290-5	2015	In excess nitrogen, Gln3 and Gat1 are sequestered in the cytoplasm in a Ure2-dependent manner.	ure2	72-76	Gat1p	Saccharomyces cerevisiae S288C	29-33
25527290-8	2015	The sensitivity of Gln3 localization to glutamine and inhibition of glutamine synthesis prompted us to investigate the effects of a glutamine tRNA mutation (sup70-65) on nitrogen-responsive control of Gln3 and Gat1.	Nitrogen	170-178	Gat1p	Saccharomyces cerevisiae S288C	210-214
25527290-10	2015	However, nuclear Gat1 localization, which also exhibits a glutamine tRNACUG requirement for its response to short-term nitrogen starvation or growth in proline medium or a ure2Delta mutation, does not require tRNACUG for its response to rapamycin.	Glutamine	58-67	Gat1p	Saccharomyces cerevisiae S288C	17-21
25527290-10	2015	However, nuclear Gat1 localization, which also exhibits a glutamine tRNACUG requirement for its response to short-term nitrogen starvation or growth in proline medium or a ure2Delta mutation, does not require tRNACUG for its response to rapamycin.	Nitrogen	119-127	Gat1p	Saccharomyces cerevisiae S288C	17-21
25527290-10	2015	However, nuclear Gat1 localization, which also exhibits a glutamine tRNACUG requirement for its response to short-term nitrogen starvation or growth in proline medium or a ure2Delta mutation, does not require tRNACUG for its response to rapamycin.	Proline	152-159	Gat1p	Saccharomyces cerevisiae S288C	17-21
25527290-12	2015	These observations demonstrate the existence of a specific nitrogen-responsive component participating in the control of Gln3 and Gat1 localization and their downstream production of nitrogenous precursors.	Nitrogen	59-67	Gat1p	Saccharomyces cerevisiae S288C	130-134
25527290-14	2015	Our observations also demonstrate distinct mechanistic differences between the responses of Gln3 and Gat1 to rapamycin inhibition of TorC1 and nitrogen starvation.	Nitrogen	143-151	Gat1p	Saccharomyces cerevisiae S288C	101-105
23996237-7	2013	Moreover, the results indicated that the manner of urea metabolism regulation was different for two positive regulators involved in NCR; Gln3p can be retained in the cytoplasm by glutamine, while Gat1p can be retained by glutamine and glutamate.	Urea	51-55	Gat1p	Saccharomyces cerevisiae S288C	196-201
24644271-2	2014	Expression of NCR-sensitive genes is mediated by two transcription activators, Gln3 and Gat1, in response to provision of a poorly used nitrogen source or following treatment with the TORC1 inhibitor, rapamycin.	Nitrogen	136-144	Gat1p	Saccharomyces cerevisiae S288C	88-92
25512609-9	2015	The TORC1-controlled transcriptional activators Gln3p, Gat1p, Rtg1p, and Rtg3p, but not Msn2p and Msn4p, were required for full induction of LDs by rapamycin.	Sirolimus	148-157	Gat1p	Saccharomyces cerevisiae S288C	55-60
25512609-10	2015	Furthermore, we show that the deletion of Gln3p and Gat1p transcription factors, which are activated in response to nitrogen availability, led to abnormal LD dynamics.	Nitrogen	116-124	Gat1p	Saccharomyces cerevisiae S288C	52-57
26259534-0	2015	Premature termination of GAT1 transcription explains paradoxical negative correlation between nitrogen-responsive mRNA, but constitutive low-level protein production.	Nitrogen	94-102	Gat1p	Saccharomyces cerevisiae S288C	25-29
26259534-4	2015	In this paper, we show that the GAT1 gene, encoding a transcriptional activator of nitrogen-responsive catabolic genes, produces a variety of mRNAs differing in their 5" and 3" termini.	Nitrogen	83-91	Gat1p	Saccharomyces cerevisiae S288C	32-36
23996237-7	2013	Moreover, the results indicated that the manner of urea metabolism regulation was different for two positive regulators involved in NCR; Gln3p can be retained in the cytoplasm by glutamine, while Gat1p can be retained by glutamine and glutamate.	Glutamine	221-230	Gat1p	Saccharomyces cerevisiae S288C	196-201
23996237-7	2013	Moreover, the results indicated that the manner of urea metabolism regulation was different for two positive regulators involved in NCR; Gln3p can be retained in the cytoplasm by glutamine, while Gat1p can be retained by glutamine and glutamate.	Glutamic Acid	235-244	Gat1p	Saccharomyces cerevisiae S288C	196-201
23651256-5	2013	We show that Aro80 is absolutely required for Gat1 binding to the ARO9, ARO10 and ARO80 promoters upon rapamycin treatment.	Sirolimus	103-112	Gat1p	Saccharomyces cerevisiae S288C	46-50
20974806-8	2011	Finally, we demonstrate that a pph21Delta pph22Delta double mutant is epistatic to ure2Delta for nuclear Gat1 localization in untreated glutamine-grown cells, whereas for Gln3, just the opposite occurs: i.e., ure2Delta is epistatic to pph21Delta pph22Delta.	pph21delta pph22delta	31-52	Gat1p	Saccharomyces cerevisiae S288C	105-109
22267742-0	2012	Controlling lipid fluxes at glycerol-3-phosphate acyltransferase step in yeast: unique contribution of Gat1p to oleic acid-induced lipid particle formation.	Oleic Acid	112-122	Gat1p	Saccharomyces cerevisiae S288C	103-108
22267742-8	2012	Yeast lacking Gat1p (but not Gat2p) were sensitive to oleate and failed to accumulate LPs induced by this unsaturated fatty acid.	Fatty Acids, Unsaturated	106-128	Gat1p	Saccharomyces cerevisiae S288C	14-19
22267742-9	2012	It is shown that oleate induces dephosphorylation of Gat1p as well as an increment in its levels.	Oleic Acid	17-23	Gat1p	Saccharomyces cerevisiae S288C	53-58
22267742-10	2012	Most importantly, we identified novel Gat1p crescent structures that are formed in the presence of oleate.	Oleic Acid	99-105	Gat1p	Saccharomyces cerevisiae S288C	38-43
20974806-3	2011	Here, we demonstrate for the first time that binding of the nitrogen catabolite repression-responsive GATA transcription activators (Gln3 and Gat1) to the DAL5 promoter and DAL5 expression require Pph21/22-Tpd3-Cdc55/Rts1 in rapamycin-treated glutamine-grown cells.	Nitrogen	60-68	Gat1p	Saccharomyces cerevisiae S288C	142-146
20974806-8	2011	Finally, we demonstrate that a pph21Delta pph22Delta double mutant is epistatic to ure2Delta for nuclear Gat1 localization in untreated glutamine-grown cells, whereas for Gln3, just the opposite occurs: i.e., ure2Delta is epistatic to pph21Delta pph22Delta.	ure2delta	83-92	Gat1p	Saccharomyces cerevisiae S288C	105-109
20974806-3	2011	Here, we demonstrate for the first time that binding of the nitrogen catabolite repression-responsive GATA transcription activators (Gln3 and Gat1) to the DAL5 promoter and DAL5 expression require Pph21/22-Tpd3-Cdc55/Rts1 in rapamycin-treated glutamine-grown cells.	Glutamine	243-252	Gat1p	Saccharomyces cerevisiae S288C	142-146
20378536-2	2010	TorC1 and intracellular nitrogen levels regulate the localization of Gln3 and Gat1, the activators of nitrogen catabolite repression (NCR)-sensitive genes whose products are required to utilize poor nitrogen sources.	Nitrogen	24-32	Gat1p	Saccharomyces cerevisiae S288C	78-82
20880842-10	2010	We conclude that HpUre2 is involved in salt tolerance and also in nitrate assimilation gene derepression via Ca(2+) homeostasis regulation and calcineurin activation, which control the levels of Gat1.	Nitrates	66-73	Gat1p	Saccharomyces cerevisiae S288C	195-199
20378536-11	2010	Furthermore, the extent to which Pph21/22-Tpd3-Cdc55 is required for the TorC1 pathway (Rap) to induce nuclear Gat1 localization is regulated in parallel with Pph21/22-Tpd3-Cdc55-dependent Gln3 dephosphorylation and NCR-sensitive transcription, being highest in limiting nitrogen and lowest when nitrogen is in excess.	Nitrogen	271-279	Gat1p	Saccharomyces cerevisiae S288C	111-115
20378536-2	2010	TorC1 and intracellular nitrogen levels regulate the localization of Gln3 and Gat1, the activators of nitrogen catabolite repression (NCR)-sensitive genes whose products are required to utilize poor nitrogen sources.	nitrogen catabolite	102-121	Gat1p	Saccharomyces cerevisiae S288C	78-82
20378536-11	2010	Furthermore, the extent to which Pph21/22-Tpd3-Cdc55 is required for the TorC1 pathway (Rap) to induce nuclear Gat1 localization is regulated in parallel with Pph21/22-Tpd3-Cdc55-dependent Gln3 dephosphorylation and NCR-sensitive transcription, being highest in limiting nitrogen and lowest when nitrogen is in excess.	Nitrogen	296-304	Gat1p	Saccharomyces cerevisiae S288C	111-115
20378536-2	2010	TorC1 and intracellular nitrogen levels regulate the localization of Gln3 and Gat1, the activators of nitrogen catabolite repression (NCR)-sensitive genes whose products are required to utilize poor nitrogen sources.	Nitrogen	102-110	Gat1p	Saccharomyces cerevisiae S288C	78-82
20378536-3	2010	In nitrogen excess, Gln3 and Gat1 are cytoplasmic, and NCR-sensitive transcription is repressed.	Nitrogen	3-11	Gat1p	Saccharomyces cerevisiae S288C	29-33
20378536-4	2010	During nitrogen limitation or Rap treatment, Gln3 and Gat1 are nuclear, and transcription is derepressed.	Nitrogen	7-15	Gat1p	Saccharomyces cerevisiae S288C	54-58
20378536-9	2010	In contrast, Gat1 localization predominantly responds to TorC1 regulation as reflected by its weaker NCR sensitivity, stronger response to Rap, and immunity to the effects of Msx.	Methionine Sulfoximine	175-178	Gat1p	Saccharomyces cerevisiae S288C	13-17
19777209-5	2009	It was suggested that the susceptibility of ure2Delta mutant to the exogenous hydrogen peroxide can result from increased GSH degradation due to the deregulated localization of the gamma-glutamyl transpeptidase activating factors Gln3/Gat1.	ure2delta	44-53	Gat1p	Saccharomyces cerevisiae S288C	235-239
19777209-5	2009	It was suggested that the susceptibility of ure2Delta mutant to the exogenous hydrogen peroxide can result from increased GSH degradation due to the deregulated localization of the gamma-glutamyl transpeptidase activating factors Gln3/Gat1.	Hydrogen Peroxide	78-95	Gat1p	Saccharomyces cerevisiae S288C	235-239
19777209-5	2009	It was suggested that the susceptibility of ure2Delta mutant to the exogenous hydrogen peroxide can result from increased GSH degradation due to the deregulated localization of the gamma-glutamyl transpeptidase activating factors Gln3/Gat1.	Glutathione	122-125	Gat1p	Saccharomyces cerevisiae S288C	235-239
19525420-5	2009	Metabolic analysis of yeast lacking either GAT1 or GAT2 indicated partitioning of the two main branches of phospholipid synthesis at the initial and rate-limiting GPAT step.	Phospholipids	107-119	Gat1p	Saccharomyces cerevisiae S288C	43-47
19574222-6	2009	The proline-independent activation of the PUT genes requires both Put3p and the positively acting GATA factors, Gln3p and Gat1p.	Proline	4-11	Gat1p	Saccharomyces cerevisiae S288C	122-127
19574222-8	2009	Here, we find that the mutation of Put3p at amino acid Tyr-788 modulates the proline-independent activation of PUT1 through Gat1p.	Tyrosine	55-58	Gat1p	Saccharomyces cerevisiae S288C	124-129
19574222-8	2009	Here, we find that the mutation of Put3p at amino acid Tyr-788 modulates the proline-independent activation of PUT1 through Gat1p.	Proline	77-84	Gat1p	Saccharomyces cerevisiae S288C	124-129
19380492-0	2009	The yeast GATA factor Gat1 occupies a central position in nitrogen catabolite repression-sensitive gene activation.	Nitrogen	58-66	Gat1p	Saccharomyces cerevisiae S288C	22-26
19273591-4	2009	This could explain the observed decrease in both the basal and rapamycin-induced expression of several genes subjected to nitrogen catabolite repression (GAT1, MEP1, and GLN1) and stress response element (STRE)-driven promoters.	Nitrogen	122-130	Gat1p	Saccharomyces cerevisiae S288C	154-158
18245087-0	2008	Tor pathway control of the nitrogen-responsive DAL5 gene bifurcates at the level of Gln3 and Gat1 regulation in Saccharomyces cerevisiae.	Toremifene	0-3	Gat1p	Saccharomyces cerevisiae S288C	93-97
19054131-2	2008	It is especially useful for low abundance proteins, for example the GATA-factors (Gln3, Gat1) which activate nitrogen catabolite repression (NCR)-sensitive transcription.	Nitrogen	109-117	Gat1p	Saccharomyces cerevisiae S288C	88-92
19054131-6	2008	With low formalin (0.8% or 1.6%), Gat1-Myc(13) became more nuclear, and with higher concentrations (5.6%), it became more cytoplasmic.	Formaldehyde	9-17	Gat1p	Saccharomyces cerevisiae S288C	34-38
19054131-8	2008	Interestingly, the high concentration of formalin had no demonstrable effect when the GATA factors were completely nuclear, i.e. after rapamycin (Gat1-Myc(13)) or Msx (Gln3-Myc(13)) treatment.	Formaldehyde	41-49	Gat1p	Saccharomyces cerevisiae S288C	146-150
18245087-0	2008	Tor pathway control of the nitrogen-responsive DAL5 gene bifurcates at the level of Gln3 and Gat1 regulation in Saccharomyces cerevisiae.	Nitrogen	27-35	Gat1p	Saccharomyces cerevisiae S288C	93-97
18245087-1	2008	The Tor1,2 protein kinases globally influence many cellular processes including nitrogen-responsive gene expression that correlates with intracellular localization of GATA transcription activators Gln3 and Gat1/Nil1.	Nitrogen	80-88	Gat1p	Saccharomyces cerevisiae S288C	206-210
18245087-1	2008	The Tor1,2 protein kinases globally influence many cellular processes including nitrogen-responsive gene expression that correlates with intracellular localization of GATA transcription activators Gln3 and Gat1/Nil1.	Nitrogen	80-88	Gat1p	Saccharomyces cerevisiae S288C	211-215
18245087-2	2008	Gln3-Myc(13) and Gat1-Myc(13) are restricted to the cytoplasm of cells provided with good nitrogen sources, e.g. glutamine.	Nitrogen	90-98	Gat1p	Saccharomyces cerevisiae S288C	17-21
18245087-2	2008	Gln3-Myc(13) and Gat1-Myc(13) are restricted to the cytoplasm of cells provided with good nitrogen sources, e.g. glutamine.	Glutamine	113-122	Gat1p	Saccharomyces cerevisiae S288C	17-21
15806612-4	2005	This complex formation correlates with Gln3 being sequestered in the cytoplasm under conditions of excess nitrogen, where Gln3/Gat1-mediated transcription is minimal.	Nitrogen	106-114	Gat1p	Saccharomyces cerevisiae S288C	127-131
16253991-9	2005	Gat1p is translocated to the nucleus only upon TOR inhibition by rapamycin.	Sirolimus	65-74	Gat1p	Saccharomyces cerevisiae S288C	0-5
16487345-0	2006	Differing responses of Gat1 and Gln3 phosphorylation and localization to rapamycin and methionine sulfoximine treatment in Saccharomyces cerevisiae.	Sirolimus	73-82	Gat1p	Saccharomyces cerevisiae S288C	23-27
16487345-0	2006	Differing responses of Gat1 and Gln3 phosphorylation and localization to rapamycin and methionine sulfoximine treatment in Saccharomyces cerevisiae.	Methionine Sulfoximine	87-109	Gat1p	Saccharomyces cerevisiae S288C	23-27
16487345-1	2006	Gln3 and Gat1/Nil1 are GATA-family transcription factors responsible for transcription of nitrogen-catabolic genes in Saccharomyces cerevisiae.	Nitrogen	90-98	Gat1p	Saccharomyces cerevisiae S288C	9-13
16487345-1	2006	Gln3 and Gat1/Nil1 are GATA-family transcription factors responsible for transcription of nitrogen-catabolic genes in Saccharomyces cerevisiae.	Nitrogen	90-98	Gat1p	Saccharomyces cerevisiae S288C	14-18
16487345-5	2006	Gat1 and Gln3 localization are similar during steady-state growth, being cytoplasmic and nuclear with good and poor nitrogen sources, respectively.	Nitrogen	116-124	Gat1p	Saccharomyces cerevisiae S288C	0-4
16487345-7	2006	In contrast, three characteristics of Gat1 and Gln3 differ significantly: (i) the kinetics of their localization in response to nutritional transitions and rapamycin-treatment; (ii) their opposite responses to MSX-treatment, i.e. that cytoplasmic Gln3 becomes nuclear following MSX addition, whereas nuclear Gat1 becomes cytoplasmic; and (iii) their phosphorylation levels in the above situations.	msx	210-213	Gat1p	Saccharomyces cerevisiae S288C	38-42
16487345-7	2006	In contrast, three characteristics of Gat1 and Gln3 differ significantly: (i) the kinetics of their localization in response to nutritional transitions and rapamycin-treatment; (ii) their opposite responses to MSX-treatment, i.e. that cytoplasmic Gln3 becomes nuclear following MSX addition, whereas nuclear Gat1 becomes cytoplasmic; and (iii) their phosphorylation levels in the above situations.	msx	278-281	Gat1p	Saccharomyces cerevisiae S288C	38-42
16487345-9	2006	The only exception was following carbon starvation, where Gat1, like Gln3, is hyperphosphorylated in a Snf1-dependent manner.	Carbon	33-39	Gat1p	Saccharomyces cerevisiae S288C	58-62
12828642-5	2003	Arg82p and Kcs1p are required for activation of NCR-regulated genes in response to nitrogen availability, mainly through Nil1p, and for repression of PHO genes by phosphate.	Nitrogen	83-91	Gat1p	Saccharomyces cerevisiae S288C	121-126
15780659-2	2005	One such system, the target of rapamycin (Tor) proteins, senses nutrients and uses the GATA activators Gln3p and Nil1p to regulate translation in response to low-quality carbon and nitrogen.	gata	87-91	Gat1p	Saccharomyces cerevisiae S288C	113-118
15780659-2	2005	One such system, the target of rapamycin (Tor) proteins, senses nutrients and uses the GATA activators Gln3p and Nil1p to regulate translation in response to low-quality carbon and nitrogen.	Carbon	170-176	Gat1p	Saccharomyces cerevisiae S288C	113-118
15780659-2	2005	One such system, the target of rapamycin (Tor) proteins, senses nutrients and uses the GATA activators Gln3p and Nil1p to regulate translation in response to low-quality carbon and nitrogen.	Nitrogen	181-189	Gat1p	Saccharomyces cerevisiae S288C	113-118
15780659-4	2005	When carbon and nitrogen are abundant, the phosphorylated Ure2p anchors the also phosphorylated Gln3p and Nil1p in the cytoplasm.	Carbon	5-11	Gat1p	Saccharomyces cerevisiae S288C	106-111
15780659-4	2005	When carbon and nitrogen are abundant, the phosphorylated Ure2p anchors the also phosphorylated Gln3p and Nil1p in the cytoplasm.	Nitrogen	16-24	Gat1p	Saccharomyces cerevisiae S288C	106-111
15780659-5	2005	Upon a shift from high- to low-quality nitrogen or treatment with rapamycin all three proteins are dephosphorylated, causing Gln3p and Nil1p to enter the nucleus and promote transcription.	Nitrogen	39-47	Gat1p	Saccharomyces cerevisiae S288C	135-140
15247235-1	2004	The GATA transcription factors GLN3 and GAT1 activate nitrogen-regulated genes in Saccharomyces cerevisiae.	Nitrogen	54-62	Gat1p	Saccharomyces cerevisiae S288C	40-44
14559239-1	2003	It has been considered that three key elements participate in nitrogen catabolite repression (NCR) of Saccharomyces cerevisiae: the GLN3 and GAT1/NIL1-encoded transcriptional activators and their negative regulator Ure2.	Nitrogen	62-70	Gat1p	Saccharomyces cerevisiae S288C	141-145
14559239-1	2003	It has been considered that three key elements participate in nitrogen catabolite repression (NCR) of Saccharomyces cerevisiae: the GLN3 and GAT1/NIL1-encoded transcriptional activators and their negative regulator Ure2.	Nitrogen	62-70	Gat1p	Saccharomyces cerevisiae S288C	146-150
12796300-2	2003	Among other effects, rapamycin treatment results in the nuclear localization of the global nitrogen activators Gln3p and Nil1p/Gat1p, which leads to expression of nitrogen assimilation genes.	Nitrogen	91-99	Gat1p	Saccharomyces cerevisiae S288C	121-126
12796300-9	2003	Rapamycin treatment and nitrogen derepression may share some, but not all, regulatory elements, since Gln3p and Nil1p do not participate identically in both processes and are not required for hyperphosphorylation.	Nitrogen	24-32	Gat1p	Saccharomyces cerevisiae S288C	112-117
12796300-2	2003	Among other effects, rapamycin treatment results in the nuclear localization of the global nitrogen activators Gln3p and Nil1p/Gat1p, which leads to expression of nitrogen assimilation genes.	Nitrogen	91-99	Gat1p	Saccharomyces cerevisiae S288C	127-132
12796300-2	2003	Among other effects, rapamycin treatment results in the nuclear localization of the global nitrogen activators Gln3p and Nil1p/Gat1p, which leads to expression of nitrogen assimilation genes.	Nitrogen	163-171	Gat1p	Saccharomyces cerevisiae S288C	121-126
12796300-2	2003	Among other effects, rapamycin treatment results in the nuclear localization of the global nitrogen activators Gln3p and Nil1p/Gat1p, which leads to expression of nitrogen assimilation genes.	Nitrogen	163-171	Gat1p	Saccharomyces cerevisiae S288C	127-132
12796300-5	2003	Treatment with rapamycin resulted in the hyperphosphorylation of Put3p, which was independent of Gln3p, Nil1p, and Ure2p.	Sirolimus	15-24	Gat1p	Saccharomyces cerevisiae S288C	104-109
12489124-1	2003	The role of Gln3p, Nil1p, Dal80p and Ure2p in the nitrogen regulation of ASP3, which codes for the periplasmic Saccharomyces cerevisiae asparaginase II, was investigated.	Nitrogen	50-58	Gat1p	Saccharomyces cerevisiae S288C	19-24
12529169-0	2003	Nitrogen-source regulation of yeast gamma-glutamyl transpeptidase synthesis involves the regulatory network including the GATA zinc-finger factors Gln3, Nil1/Gat1 and Gzf3.	Nitrogen	0-8	Gat1p	Saccharomyces cerevisiae S288C	153-157
12529169-0	2003	Nitrogen-source regulation of yeast gamma-glutamyl transpeptidase synthesis involves the regulatory network including the GATA zinc-finger factors Gln3, Nil1/Gat1 and Gzf3.	Nitrogen	0-8	Gat1p	Saccharomyces cerevisiae S288C	158-162
12529169-9	2003	Furthermore, rapamycin causes similar CIS2 activation, indicating that the target of rapamycin signalling pathway controls CIS2 expression via Gln3 and Nil1 in nitrogen-starved cells.	Nitrogen	160-168	Gat1p	Saccharomyces cerevisiae S288C	152-156
11356843-1	2001	The GATA family proteins Gln3p and Gat1p mediate nitrogen catabolite repression (NCR)-sensitive transcription in Saccharomyces cerevisiae.	nitrogen catabolite	49-68	Gat1p	Saccharomyces cerevisiae S288C	35-40
12167660-3	2002	Metabolic analyses of gat1 and gat2 yeast detected that the major differences were: (i) a 50% increase in the rate of triacylglycerol synthesis in gat1 yeast and a corresponding 50% decrease in gat2 yeast, and (ii) a 5-fold increase in glycerophosphocholine production through deacylation of phosphatidylcholine synthesized through the CDP-choline pathway in gat1 yeast, whereas gat2 yeast displayed a 10-fold decrease.	Triglycerides	118-133	Gat1p	Saccharomyces cerevisiae S288C	22-26
12167660-3	2002	Metabolic analyses of gat1 and gat2 yeast detected that the major differences were: (i) a 50% increase in the rate of triacylglycerol synthesis in gat1 yeast and a corresponding 50% decrease in gat2 yeast, and (ii) a 5-fold increase in glycerophosphocholine production through deacylation of phosphatidylcholine synthesized through the CDP-choline pathway in gat1 yeast, whereas gat2 yeast displayed a 10-fold decrease.	Triglycerides	118-133	Gat1p	Saccharomyces cerevisiae S288C	147-151
12167660-3	2002	Metabolic analyses of gat1 and gat2 yeast detected that the major differences were: (i) a 50% increase in the rate of triacylglycerol synthesis in gat1 yeast and a corresponding 50% decrease in gat2 yeast, and (ii) a 5-fold increase in glycerophosphocholine production through deacylation of phosphatidylcholine synthesized through the CDP-choline pathway in gat1 yeast, whereas gat2 yeast displayed a 10-fold decrease.	Triglycerides	118-133	Gat1p	Saccharomyces cerevisiae S288C	147-151
12167660-4	2002	To address why we observed alterations in phospholipid turnover specific to phosphatidylcholine produced through the CDP-choline pathway in gat1 and gat2 yeast we tested their sensitivity to various cytotoxic lysolipids and observed that gat2 cells were more sensitive to lysophosphatidylcholine, but not other lysolipids.	Phospholipids	42-54	Gat1p	Saccharomyces cerevisiae S288C	140-144
12167660-4	2002	To address why we observed alterations in phospholipid turnover specific to phosphatidylcholine produced through the CDP-choline pathway in gat1 and gat2 yeast we tested their sensitivity to various cytotoxic lysolipids and observed that gat2 cells were more sensitive to lysophosphatidylcholine, but not other lysolipids.	Phosphatidylcholines	76-95	Gat1p	Saccharomyces cerevisiae S288C	140-144
12167660-4	2002	To address why we observed alterations in phospholipid turnover specific to phosphatidylcholine produced through the CDP-choline pathway in gat1 and gat2 yeast we tested their sensitivity to various cytotoxic lysolipids and observed that gat2 cells were more sensitive to lysophosphatidylcholine, but not other lysolipids.	Cytidine Diphosphate	117-120	Gat1p	Saccharomyces cerevisiae S288C	140-144
12167660-4	2002	To address why we observed alterations in phospholipid turnover specific to phosphatidylcholine produced through the CDP-choline pathway in gat1 and gat2 yeast we tested their sensitivity to various cytotoxic lysolipids and observed that gat2 cells were more sensitive to lysophosphatidylcholine, but not other lysolipids.	Choline	88-95	Gat1p	Saccharomyces cerevisiae S288C	140-144
12165425-2	2002	Under nitrogen-rich conditions, the GATA family transcriptional activators, Gln3 and Gat1, form complexes with Ure2, and are localized to the cytoplasm, which decreases NCR-sensitive expression.	Nitrogen	6-14	Gat1p	Saccharomyces cerevisiae S288C	85-89
12165425-3	2002	Under nitrogen-limiting conditions, Gln3 and Gat1 are dephosphorylated, move from the cytoplasm to the nucleus, in wild-type but not rna1 and srp1 mutants, and increase expression of NCR-sensitive genes.	Nitrogen	6-14	Gat1p	Saccharomyces cerevisiae S288C	45-49
11923302-1	2002	The Tor1/2p signal transduction pathway regulates nitrogen catabolite repression (NCR)-sensitive (GAP1, GAT1, DAL5) and retrograde (CIT2, DLD3, IDH1/2) gene expression by controlling intracellular localization of the transcription activators, Gln3p and Gat1p, and Rtg1p and Rtg3p, respectively.	Nitrogen	50-58	Gat1p	Saccharomyces cerevisiae S288C	104-108
11923302-1	2002	The Tor1/2p signal transduction pathway regulates nitrogen catabolite repression (NCR)-sensitive (GAP1, GAT1, DAL5) and retrograde (CIT2, DLD3, IDH1/2) gene expression by controlling intracellular localization of the transcription activators, Gln3p and Gat1p, and Rtg1p and Rtg3p, respectively.	Nitrogen	50-58	Gat1p	Saccharomyces cerevisiae S288C	253-258
11544256-8	2001	Furthermore, biochemical results are presented to show that both Gat1p and Gat2p(Sct1p) are G-3-P/dihydroxyacetone phosphate dual substrate-specific sn-1 acyltransferases.	alpha-glycerophosphoric acid	92-97	Gat1p	Saccharomyces cerevisiae S288C	65-70
11544256-8	2001	Furthermore, biochemical results are presented to show that both Gat1p and Gat2p(Sct1p) are G-3-P/dihydroxyacetone phosphate dual substrate-specific sn-1 acyltransferases.	Dihydroxyacetone Phosphate	98-124	Gat1p	Saccharomyces cerevisiae S288C	65-70
11408486-2	2001	When nitrogen is limiting, Gln3p and Gat1p are concentrated in the nucleus where they bind GATA sequences upstream of nitrogen catabolite repression (NCR)-sensitive genes and activate their transcription.	Nitrogen	5-13	Gat1p	Saccharomyces cerevisiae S288C	37-42
11408486-2	2001	When nitrogen is limiting, Gln3p and Gat1p are concentrated in the nucleus where they bind GATA sequences upstream of nitrogen catabolite repression (NCR)-sensitive genes and activate their transcription.	gata	91-95	Gat1p	Saccharomyces cerevisiae S288C	37-42
11408486-2	2001	When nitrogen is limiting, Gln3p and Gat1p are concentrated in the nucleus where they bind GATA sequences upstream of nitrogen catabolite repression (NCR)-sensitive genes and activate their transcription.	Nitrogen	118-126	Gat1p	Saccharomyces cerevisiae S288C	37-42
11356843-2	2001	When cells are cultured with a good nitrogen source (glutamine, ammonia), Gln3p and Gat1p are restricted to the cytoplasm, whereas with a poor nitrogen source (proline), they localize to the nucleus, bind to the GATA sequences of NCR-sensitive gene promoters, and activate transcription.	gata	212-216	Gat1p	Saccharomyces cerevisiae S288C	84-89
11356843-4	2001	Rapamycin, a Tor protein inhibitor, like growth with a poor nitrogen source, promotes nuclear localization of Gln3p and Gat1p.	Sirolimus	0-9	Gat1p	Saccharomyces cerevisiae S288C	120-125
12167660-6	2002	Our data showed that gat1 and gat2 yeast were resistant and sensitive to lysoplatelet activating factor, platelet activating factor, and the anti-tumor lipid edelfosine, respectively, indicating that their sensitivity to these compounds was not because of differences in rates of phosphatidylcholine deacylation.	edelfosine	158-168	Gat1p	Saccharomyces cerevisiae S288C	21-25
12167660-6	2002	Our data showed that gat1 and gat2 yeast were resistant and sensitive to lysoplatelet activating factor, platelet activating factor, and the anti-tumor lipid edelfosine, respectively, indicating that their sensitivity to these compounds was not because of differences in rates of phosphatidylcholine deacylation.	Phosphatidylcholines	280-299	Gat1p	Saccharomyces cerevisiae S288C	21-25
11679080-8	2001	Additionally, the proper transcription of several nitrogen-regulated genes, including NIL1 and DAL80, encoding well-studied GATA transcription factors, is dependent upon Ssy1p.	Nitrogen	50-58	Gat1p	Saccharomyces cerevisiae S288C	86-90
11457832-0	2001	The GATA transcription factors GLN3 and GAT1 link TOR to salt stress in Saccharomyces cerevisiae.	Salts	57-61	Gat1p	Saccharomyces cerevisiae S288C	40-44
11457832-4	2001	Second, the absence of the TOR-controlled GATA transcription factors GLN3 and GAT1 results in reduced basal and salt-induced expression of ENA1.	Salts	112-116	Gat1p	Saccharomyces cerevisiae S288C	78-82
11457832-5	2001	Third, a gln3 gat1 mutant displays a pronounced sensitivity to high concentrations of lithium and sodium.	Lithium	86-93	Gat1p	Saccharomyces cerevisiae S288C	14-18
11457832-5	2001	Third, a gln3 gat1 mutant displays a pronounced sensitivity to high concentrations of lithium and sodium.	Sodium	98-104	Gat1p	Saccharomyces cerevisiae S288C	14-18
11457832-7	2001	In summary, our results suggest that TOR plays a role in the general response to saline stress by regulating the transcription of ENA1 via GLN3 and GAT1.	Toremifene	37-40	Gat1p	Saccharomyces cerevisiae S288C	148-152
11457832-7	2001	In summary, our results suggest that TOR plays a role in the general response to saline stress by regulating the transcription of ENA1 via GLN3 and GAT1.	Sodium Chloride	81-87	Gat1p	Saccharomyces cerevisiae S288C	148-152
11356843-2	2001	When cells are cultured with a good nitrogen source (glutamine, ammonia), Gln3p and Gat1p are restricted to the cytoplasm, whereas with a poor nitrogen source (proline), they localize to the nucleus, bind to the GATA sequences of NCR-sensitive gene promoters, and activate transcription.	Nitrogen	36-44	Gat1p	Saccharomyces cerevisiae S288C	84-89
11073899-1	2000	Nitrogen-catabolic gene expression in Saccharomyces cerevisiae is regulated by the action of four GATA family transcription factors: Gln3p and Gat1p/Nil1p are transcriptional activators, and Dal80 and Deh1p/Gzf3p are repressors.	Nitrogen	0-8	Gat1p	Saccharomyces cerevisiae S288C	143-148
11073899-1	2000	Nitrogen-catabolic gene expression in Saccharomyces cerevisiae is regulated by the action of four GATA family transcription factors: Gln3p and Gat1p/Nil1p are transcriptional activators, and Dal80 and Deh1p/Gzf3p are repressors.	Nitrogen	0-8	Gat1p	Saccharomyces cerevisiae S288C	149-154
11073899-2	2000	In addition to the GATA sequences situated upstream of all nitrogen catabolite repression-sensitive genes that encode enzyme and transport proteins, the promoters of the GAT1, DAL80, and DEH1 genes all contain multiple GATA sequences as well.	gata	219-223	Gat1p	Saccharomyces cerevisiae S288C	170-174
11073899-4	2000	Here we show, using DAL80 fused to the carbon-regulated GAL1,10 or copper-regulated CUP1 promoter, that GAT1 expression is inversely regulated by the level of DAL80 expression, i.e., as DAL80 expression increases, GAT1 expression decreases.	Carbon	39-45	Gat1p	Saccharomyces cerevisiae S288C	104-108
11073899-4	2000	Here we show, using DAL80 fused to the carbon-regulated GAL1,10 or copper-regulated CUP1 promoter, that GAT1 expression is inversely regulated by the level of DAL80 expression, i.e., as DAL80 expression increases, GAT1 expression decreases.	Carbon	39-45	Gat1p	Saccharomyces cerevisiae S288C	214-218
11073899-4	2000	Here we show, using DAL80 fused to the carbon-regulated GAL1,10 or copper-regulated CUP1 promoter, that GAT1 expression is inversely regulated by the level of DAL80 expression, i.e., as DAL80 expression increases, GAT1 expression decreases.	Copper	67-73	Gat1p	Saccharomyces cerevisiae S288C	104-108
10554772-1	1999	In Saccharomyces cerevisiae the expression of all known nitrogen catabolite pathways are regulated by four regulators known as Gln3, Gat1, Dal80, and Deh1.	nitrogen catabolite	56-75	Gat1p	Saccharomyces cerevisiae S288C	133-137
10559172-1	1999	Dal82p binds to the UIS(ALL) sites of allophanate-induced genes of the allantoin-degradative pathway and functions synergistically with the GATA family Gln3p and Gat1p transcriptional activators that are responsible for nitrogen catabolite repression-sensitive gene expression.	Nitrogen	220-228	Gat1p	Saccharomyces cerevisiae S288C	162-167
10906145-1	2000	Allophanate/oxalurate-induced gene expression in Saccharomyces cerevisiae requires at least five transcription factors, four of which act positively (Gln3p, Gat1p, Dal81p, and Dal82p) and one negatively (Dal80p).	allophanic acid	0-11	Gat1p	Saccharomyces cerevisiae S288C	157-162
10906145-1	2000	Allophanate/oxalurate-induced gene expression in Saccharomyces cerevisiae requires at least five transcription factors, four of which act positively (Gln3p, Gat1p, Dal81p, and Dal82p) and one negatively (Dal80p).	oxaluric acid	12-21	Gat1p	Saccharomyces cerevisiae S288C	157-162
10799523-0	2000	Nitrogen catabolite repression of DAL80 expression depends on the relative levels of Gat1p and Ure2p production in Saccharomyces cerevisiae.	Nitrogen	0-8	Gat1p	Saccharomyces cerevisiae S288C	85-90
10799523-1	2000	GATA family activators (Gln3p and Gat1p) and repressors (Dal80p and Deh1p) regulate nitrogen catabolite repression (NCR)-sensitive transcription in Saccharomyces cerevisiae presumably via their competitive binding to the GATA sequences upstream of NCR-sensitive genes.	gata	0-4	Gat1p	Saccharomyces cerevisiae S288C	34-39
10799523-1	2000	GATA family activators (Gln3p and Gat1p) and repressors (Dal80p and Deh1p) regulate nitrogen catabolite repression (NCR)-sensitive transcription in Saccharomyces cerevisiae presumably via their competitive binding to the GATA sequences upstream of NCR-sensitive genes.	Nitrogen	84-92	Gat1p	Saccharomyces cerevisiae S288C	34-39
10799523-1	2000	GATA family activators (Gln3p and Gat1p) and repressors (Dal80p and Deh1p) regulate nitrogen catabolite repression (NCR)-sensitive transcription in Saccharomyces cerevisiae presumably via their competitive binding to the GATA sequences upstream of NCR-sensitive genes.	gata	221-225	Gat1p	Saccharomyces cerevisiae S288C	34-39
10799523-2	2000	Ure2p, which is not a GATA family member, inhibits Gln3p/Gat1p from functioning in the presence of good nitrogen sources.	Nitrogen	104-112	Gat1p	Saccharomyces cerevisiae S288C	57-62
10799523-4	2000	NCR, normally observed with ammonia or glutamine, is severely diminished when Gat1p is overproduced, and this inhibition is overcome by simultaneously increasing URE2 expression.	Ammonia	28-35	Gat1p	Saccharomyces cerevisiae S288C	78-83
10799523-4	2000	NCR, normally observed with ammonia or glutamine, is severely diminished when Gat1p is overproduced, and this inhibition is overcome by simultaneously increasing URE2 expression.	Glutamine	39-48	Gat1p	Saccharomyces cerevisiae S288C	78-83
10554772-8	1999	Another group of genes whose expression is also regulated by Gln3, Gat1, Dal80, and Deh1 are some proteases, CPS1, PRB1, LAP1, and PEP4, responsible for the degradation of proteins into amino acids thereby providing a nitrogen source to the cell.	Nitrogen	218-226	Gat1p	Saccharomyces cerevisiae S288C	67-71
10048020-1	1999	In Saccharomyces cerevisiae, the transcription factors Gln3p and Nil1p of the GATA family play a determinant role in expression of genes that are subject to nitrogen catabolite repression.	Nitrogen	157-165	Gat1p	Saccharomyces cerevisiae S288C	65-70
10049376-1	1999	In the yeast Saccharomyces cerevisiae lipid particles harbor two acyltransferases, Gat1p and Slc1p, which catalyze subsequent steps of acylation required for the formation of phosphatidic acid.	Phosphatidic Acids	175-192	Gat1p	Saccharomyces cerevisiae S288C	83-88
10049376-4	1999	Using the gat1 mutant strain TTA1, we show here that Gat1p present in both subcellular fractions accepts glycerol-3-phosphate and dihydroxyacetone phosphate as a substrate.	alpha-glycerophosphoric acid	105-125	Gat1p	Saccharomyces cerevisiae S288C	10-14
10049376-4	1999	Using the gat1 mutant strain TTA1, we show here that Gat1p present in both subcellular fractions accepts glycerol-3-phosphate and dihydroxyacetone phosphate as a substrate.	alpha-glycerophosphoric acid	105-125	Gat1p	Saccharomyces cerevisiae S288C	53-58
10049376-4	1999	Using the gat1 mutant strain TTA1, we show here that Gat1p present in both subcellular fractions accepts glycerol-3-phosphate and dihydroxyacetone phosphate as a substrate.	Dihydroxyacetone Phosphate	130-156	Gat1p	Saccharomyces cerevisiae S288C	10-14
10049376-4	1999	Using the gat1 mutant strain TTA1, we show here that Gat1p present in both subcellular fractions accepts glycerol-3-phosphate and dihydroxyacetone phosphate as a substrate.	Dihydroxyacetone Phosphate	130-156	Gat1p	Saccharomyces cerevisiae S288C	53-58
10049376-9	1999	In the gat1 mutant and the 1-acylglycerol-3-phosphate acyltransferase slc1 mutant, the dihydroxyacetone phosphate pathway of phosphatidic acid biosynthesis is slightly preferred as compared to the wild type.	Dihydroxyacetone Phosphate	87-113	Gat1p	Saccharomyces cerevisiae S288C	7-11
10049376-9	1999	In the gat1 mutant and the 1-acylglycerol-3-phosphate acyltransferase slc1 mutant, the dihydroxyacetone phosphate pathway of phosphatidic acid biosynthesis is slightly preferred as compared to the wild type.	Phosphatidic Acids	125-142	Gat1p	Saccharomyces cerevisiae S288C	7-11
10049376-10	1999	Thus, mutations of the major acyltransferases Gat1p and Slc1p lead to an increased contribution of mitochondrial acyltransferase(s) to glycerolipid synthesis due to their substrate preference for dihydroxyacetone phosphate.	glycerolipid	135-147	Gat1p	Saccharomyces cerevisiae S288C	46-51
10049376-10	1999	Thus, mutations of the major acyltransferases Gat1p and Slc1p lead to an increased contribution of mitochondrial acyltransferase(s) to glycerolipid synthesis due to their substrate preference for dihydroxyacetone phosphate.	Dihydroxyacetone Phosphate	196-222	Gat1p	Saccharomyces cerevisiae S288C	46-51
10048020-10	1999	Ada1/Gan1p thus represents the first reported case of an accessory protein (a co-activator) linking the GATA-binding proteins Gln3p and Nil1p, mediating nitrogen-regulated transcription, to the basal transcription machinery.	Nitrogen	153-161	Gat1p	Saccharomyces cerevisiae S288C	136-141
9171383-1	1997	Nitrogen catabolic gene expression in Saccharomyces cerevisiae has been reported to be regulated by three GATA family proteins, the positive regulators Gln3p and Gat1p/Nil1p and the negative regulator Dal80p/Uga43p.	Nitrogen	0-8	Gat1p	Saccharomyces cerevisiae S288C	162-167
9401016-10	1997	These results indicate that two distinct enzymes are necessary for phosphatidic acid synthesis in lipid particles: the first step, acylation of glycerol-3-phosphate, is catalyzed by a putative Gat1p; the second step, acylation of lysophosphatidic acid, requires S1c1p.	Phosphatidic Acids	67-84	Gat1p	Saccharomyces cerevisiae S288C	193-198
9401016-10	1997	These results indicate that two distinct enzymes are necessary for phosphatidic acid synthesis in lipid particles: the first step, acylation of glycerol-3-phosphate, is catalyzed by a putative Gat1p; the second step, acylation of lysophosphatidic acid, requires S1c1p.	alpha-glycerophosphoric acid	144-164	Gat1p	Saccharomyces cerevisiae S288C	193-198
9401016-10	1997	These results indicate that two distinct enzymes are necessary for phosphatidic acid synthesis in lipid particles: the first step, acylation of glycerol-3-phosphate, is catalyzed by a putative Gat1p; the second step, acylation of lysophosphatidic acid, requires S1c1p.	lysophosphatidic acid	230-251	Gat1p	Saccharomyces cerevisiae S288C	193-198
9401021-1	1997	Regulated nitrogen catabolic gene transcription in Saccharomyces cerevisiae is mediated by four positive (Gln3p and Gat1p/Nil1p) and negative (Dal80p/Uga43p and Deh1p/Nil2p/GZF3p) regulators which function in opposition to one another.	Nitrogen	10-18	Gat1p	Saccharomyces cerevisiae S288C	116-121
9401021-1	1997	Regulated nitrogen catabolic gene transcription in Saccharomyces cerevisiae is mediated by four positive (Gln3p and Gat1p/Nil1p) and negative (Dal80p/Uga43p and Deh1p/Nil2p/GZF3p) regulators which function in opposition to one another.	Nitrogen	10-18	Gat1p	Saccharomyces cerevisiae S288C	122-127
9791119-1	1998	GATA family proteins Gln3p, Gat1p, Dal80p, and Deh1p mediate the regulation of nitrogen catabolite repression (NCR)-sensitive gene expression in Saccharomyces cerevisiae.	Nitrogen	79-87	Gat1p	Saccharomyces cerevisiae S288C	28-33
9287023-5	1997	Here we show that the expression of some (CPS1, PEP4, PRB1, and LAP4) but not all (PRC1) vacuolar protease genes is nitrogen catabolite repression sensitive and is regulated by the GATA-family proteins Gln3p, Gat1p, and Dal80p.	nitrogen catabolite	116-135	Gat1p	Saccharomyces cerevisiae S288C	209-214
9234685-11	1997	High-level MEP2 transcription requires at least one of the two GATA family factors Gln3p and Nil1p, which are involved in transcriptional activation of many other nitrogen-regulated genes.	Nitrogen	163-171	Gat1p	Saccharomyces cerevisiae S288C	93-98
9171383-1	1997	Nitrogen catabolic gene expression in Saccharomyces cerevisiae has been reported to be regulated by three GATA family proteins, the positive regulators Gln3p and Gat1p/Nil1p and the negative regulator Dal80p/Uga43p.	Nitrogen	0-8	Gat1p	Saccharomyces cerevisiae S288C	168-173
9171427-2	1997	The expression of many nitrogen-regulated genes of Saccharomyces cerevisiae requires activation by GATA factor Gln3p or Nil1p and is prevented by the presence of glutamine in the growth medium.	Nitrogen	23-31	Gat1p	Saccharomyces cerevisiae S288C	120-125
9171427-2	1997	The expression of many nitrogen-regulated genes of Saccharomyces cerevisiae requires activation by GATA factor Gln3p or Nil1p and is prevented by the presence of glutamine in the growth medium.	Glutamine	162-171	Gat1p	Saccharomyces cerevisiae S288C	120-125
9171427-3	1997	Disruption of NIL2 results in a great increase in the expression of NIL1 and of GAP1, the structural gene for the general amino acid permease, in glutamine-grown cells in response to activation by Nil1p.	Glutamine	146-155	Gat1p	Saccharomyces cerevisiae S288C	68-72
9171427-3	1997	Disruption of NIL2 results in a great increase in the expression of NIL1 and of GAP1, the structural gene for the general amino acid permease, in glutamine-grown cells in response to activation by Nil1p.	Glutamine	146-155	Gat1p	Saccharomyces cerevisiae S288C	197-202
9106207-1	1997	In Saccharomyces cerevisiae, two positive transcription factors of the GATA family, Gln3p and Nil1p/Gat1p, upregulate the expression of multiple nitrogen pathway genes via upstream 5"-GATA-3" sequences.	Nitrogen	145-153	Gat1p	Saccharomyces cerevisiae S288C	94-99
9106207-1	1997	In Saccharomyces cerevisiae, two positive transcription factors of the GATA family, Gln3p and Nil1p/Gat1p, upregulate the expression of multiple nitrogen pathway genes via upstream 5"-GATA-3" sequences.	Nitrogen	145-153	Gat1p	Saccharomyces cerevisiae S288C	100-105
7798155-1	1995	The cellular level and activity of the general amino acid permease, the product of the GAP1 gene of Saccharomyces cerevisiae, are regulated at the level of transcription by two systems, the products of URE2/GLN3 and NIL1 in response to the nitrogen sources of the growth medium and inactivation in response to the presence of glutamine or glutamate.	Nitrogen	240-248	Gat1p	Saccharomyces cerevisiae S288C	216-220
8636059-2	1996	This gene is not expressed in media containing glutamine, and its transcription is activated in response to Gln3p in cells using glutamate as the source of nitrogen and by Nil1p in cells using urea as the source of nitrogen.	Glutamine	47-56	Gat1p	Saccharomyces cerevisiae S288C	172-177
8636059-2	1996	This gene is not expressed in media containing glutamine, and its transcription is activated in response to Gln3p in cells using glutamate as the source of nitrogen and by Nil1p in cells using urea as the source of nitrogen.	Glutamic Acid	129-138	Gat1p	Saccharomyces cerevisiae S288C	172-177
8636059-2	1996	This gene is not expressed in media containing glutamine, and its transcription is activated in response to Gln3p in cells using glutamate as the source of nitrogen and by Nil1p in cells using urea as the source of nitrogen.	Nitrogen	156-164	Gat1p	Saccharomyces cerevisiae S288C	172-177
8636059-2	1996	This gene is not expressed in media containing glutamine, and its transcription is activated in response to Gln3p in cells using glutamate as the source of nitrogen and by Nil1p in cells using urea as the source of nitrogen.	Urea	193-197	Gat1p	Saccharomyces cerevisiae S288C	172-177
8636059-2	1996	This gene is not expressed in media containing glutamine, and its transcription is activated in response to Gln3p in cells using glutamate as the source of nitrogen and by Nil1p in cells using urea as the source of nitrogen.	Nitrogen	215-223	Gat1p	Saccharomyces cerevisiae S288C	172-177
8622686-0	1996	Gat1p, a GATA family protein whose production is sensitive to nitrogen catabolite repression, participates in transcriptional activation of nitrogen-catabolic genes in Saccharomyces cerevisiae.	nitrogen catabolite	62-81	Gat1p	Saccharomyces cerevisiae S288C	0-5
8622686-0	1996	Gat1p, a GATA family protein whose production is sensitive to nitrogen catabolite repression, participates in transcriptional activation of nitrogen-catabolic genes in Saccharomyces cerevisiae.	Nitrogen	62-70	Gat1p	Saccharomyces cerevisiae S288C	0-5
7568152-0	1995	Role of the GATA factors Gln3p and Nil1p of Saccharomyces cerevisiae in the expression of nitrogen-regulated genes.	Nitrogen	90-98	Gat1p	Saccharomyces cerevisiae S288C	35-40
7568152-1	1995	We have isolated the NIL1 gene, whose product is an activator of the transcription of nitrogen-regulated genes, by virtue of the homology of its zinc-finger domain to that of the previously identified activator, the product of GLN3.	Nitrogen	86-94	Gat1p	Saccharomyces cerevisiae S288C	21-25
7568152-2	1995	Disruption of the chromosomal NIL1 gene enabled us to compare the effects of Gln3p and of Nil1p on the expression of the nitrogen-regulated genes GLN1, GDH2, and GAP1, coding respectively for glutamine synthetase, NAD-linked glutamate dehydrogenase, and general amino acid permease.	Nitrogen	121-129	Gat1p	Saccharomyces cerevisiae S288C	30-34
7568152-2	1995	Disruption of the chromosomal NIL1 gene enabled us to compare the effects of Gln3p and of Nil1p on the expression of the nitrogen-regulated genes GLN1, GDH2, and GAP1, coding respectively for glutamine synthetase, NAD-linked glutamate dehydrogenase, and general amino acid permease.	Nitrogen	121-129	Gat1p	Saccharomyces cerevisiae S288C	90-95
7568152-4	1995	The results further indicate that Gln3p is inactivated by an increase in the intracellular concentration of glutamine and that Nil1p is inactivated by an increase in intracellular glutamate.	Glutamic Acid	180-189	Gat1p	Saccharomyces cerevisiae S288C	127-132
7798155-1	1995	The cellular level and activity of the general amino acid permease, the product of the GAP1 gene of Saccharomyces cerevisiae, are regulated at the level of transcription by two systems, the products of URE2/GLN3 and NIL1 in response to the nitrogen sources of the growth medium and inactivation in response to the presence of glutamine or glutamate.	Glutamic Acid	339-348	Gat1p	Saccharomyces cerevisiae S288C	216-220
7798155-1	1995	The cellular level and activity of the general amino acid permease, the product of the GAP1 gene of Saccharomyces cerevisiae, are regulated at the level of transcription by two systems, the products of URE2/GLN3 and NIL1 in response to the nitrogen sources of the growth medium and inactivation in response to the presence of glutamine or glutamate.	Glutamine	326-335	Gat1p	Saccharomyces cerevisiae S288C	216-220
34105981-4	2021	It plays a central role in ESR by activating genes for glycerol and fatty acid production (GUP1, GPP1/2, GPD1, GAT1, and OLE1) to preserve plasma membrane integrity.	Fatty Acids	68-78	Gat1p	Saccharomyces cerevisiae S288C	111-115
34066902-0	2021	GAT1 Gene, the GATA Transcription Activator, Regulates the Production of Higher Alcohol during Wheat Beer Fermentation by Saccharomyces cerevisiae.	Alcohols	80-87	Gat1p	Saccharomyces cerevisiae S288C	0-4
34066902-2	2021	The effect of GAT1 gene, the GATA transcription activator, on higher alcohol biosynthesis was investigated to clarify the mechanism of Saccharomyces cerevisiae regulating higher alcohol metabolism under high concentrations of free amino nitrogen (FAN).	Alcohols	69-76	Gat1p	Saccharomyces cerevisiae S288C	14-18
34066902-2	2021	The effect of GAT1 gene, the GATA transcription activator, on higher alcohol biosynthesis was investigated to clarify the mechanism of Saccharomyces cerevisiae regulating higher alcohol metabolism under high concentrations of free amino nitrogen (FAN).	Alcohols	178-185	Gat1p	Saccharomyces cerevisiae S288C	14-18
34066902-2	2021	The effect of GAT1 gene, the GATA transcription activator, on higher alcohol biosynthesis was investigated to clarify the mechanism of Saccharomyces cerevisiae regulating higher alcohol metabolism under high concentrations of free amino nitrogen (FAN).	Nitrogen	237-245	Gat1p	Saccharomyces cerevisiae S288C	14-18
34066902-3	2021	The availability of FAN by strain SDT1K with a GAT1 double-copy deletion was 28.31% lower than that of parent strain S17, and the yield of higher alcohols was 33.91% lower.	Alcohols	146-154	Gat1p	Saccharomyces cerevisiae S288C	47-51
34066902-4	2021	The transcript levels of the downstream target genes of GAT1 and higher alcohol production in the double-copy deletion mutant suggested that a part of the effect of GAT1 deletion on higher alcohol production was the downregulation of GAP1, ARO9, and ARO10.	Alcohols	72-79	Gat1p	Saccharomyces cerevisiae S288C	56-60
34066902-4	2021	The transcript levels of the downstream target genes of GAT1 and higher alcohol production in the double-copy deletion mutant suggested that a part of the effect of GAT1 deletion on higher alcohol production was the downregulation of GAP1, ARO9, and ARO10.	Alcohols	72-79	Gat1p	Saccharomyces cerevisiae S288C	165-169
34066902-4	2021	The transcript levels of the downstream target genes of GAT1 and higher alcohol production in the double-copy deletion mutant suggested that a part of the effect of GAT1 deletion on higher alcohol production was the downregulation of GAP1, ARO9, and ARO10.	Alcohols	189-196	Gat1p	Saccharomyces cerevisiae S288C	56-60
34066902-4	2021	The transcript levels of the downstream target genes of GAT1 and higher alcohol production in the double-copy deletion mutant suggested that a part of the effect of GAT1 deletion on higher alcohol production was the downregulation of GAP1, ARO9, and ARO10.	Alcohols	189-196	Gat1p	Saccharomyces cerevisiae S288C	165-169