PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22232265-1 2012 A malfunction in the yeast HAC1 causes the unfolding-protein response in the endoplasmic reticulum, resulting in stress-sensitive and inositol auxotrophic phenotypes. Inositol 134-142 transcription factor HAC1 Saccharomyces cerevisiae S288C 27-31 22232265-3 2012 The introduction of the truncated human CCT epsilon subunit into yeast cells of which hac1 was disrupted clearly suppressed not only its inositol auxotrophic phenotype but also its stress-sensitive phenotype. Inositol 137-145 transcription factor HAC1 Saccharomyces cerevisiae S288C 86-90 9409765-1 1997 We previously reported that the Saccharomyces cerevisiae ire15 mutation results in an inositol-auxotrophic phenotype, and that human cDNAs can suppress the ire15 mutation (Nikawa, J., 1994. Inositol 86-94 transcription factor HAC1 Saccharomyces cerevisiae S288C 57-62 16041130-2 2005 IRE1- and HAC1-disruptants require high concentrations of inositol for its normal growth. Inositol 58-66 transcription factor HAC1 Saccharomyces cerevisiae S288C 10-14 16041130-5 2005 However, the growth defect of the hac1-alg10 double disrupted was partially, but significantly, suppressed by the addition of inositol to the medium. Inositol 126-134 transcription factor HAC1 Saccharomyces cerevisiae S288C 34-38 11489850-10 2001 Surprisingly, the deletion of either ITC1 or ISW2 in the Delta hac1 strain circumvented the inositol requirement and caused derepression of INO1 even under repression conditions, i.e., in inositol-containing medium. Inositol 92-100 transcription factor HAC1 Saccharomyces cerevisiae S288C 63-67 11489850-10 2001 Surprisingly, the deletion of either ITC1 or ISW2 in the Delta hac1 strain circumvented the inositol requirement and caused derepression of INO1 even under repression conditions, i.e., in inositol-containing medium. Inositol 188-196 transcription factor HAC1 Saccharomyces cerevisiae S288C 63-67 9409765-8 1997 All human cDNAs and yeast multicopy suppressors, which had been isolated as suppressors for the ire15 mutation, were able to suppress the inositol-auxotrophic phenotype but not the defect in KAR2 induction of the hac1-disrupted strain. Inositol 138-146 transcription factor HAC1 Saccharomyces cerevisiae S288C 96-101 8932376-5 1996 ire2/hac1-disrupted yeast cells showed not only the inositol auxotrophic phenotype but also the tunicamycin sensitivity, and failed to induce the expression of KAR2. Inositol 52-60 transcription factor HAC1 Saccharomyces cerevisiae S288C 5-9 9077435-7 1996 Cells lacking Ern4p are unable to induce transcription of any of the five target genes tested and exhibit sensitivity to ER stress and inositol requirement for growth. Inositol 135-143 transcription factor HAC1 Saccharomyces cerevisiae S288C 14-19 8675017-1 1996 The Saccharomyces cerevisiae ire15 mutant has a defect in the expression of the IN01 gene, showing an inositol auxotrophic phenotype. Inositol 102-110 transcription factor HAC1 Saccharomyces cerevisiae S288C 29-34 8537323-1 1995 Saccharomyces cerevisiae ire15 mutant has a defect in the expression of INO1, showing the inositol auxotrophic phenotype [Nikawa, J. Inositol 90-98 transcription factor HAC1 Saccharomyces cerevisiae S288C 25-30 27256815-2 2016 The inositol requiring enzyme 1 (IRE1) signaling pathway activated by the IRE1-mediated unconventional splicing of HAC1 in yeast, bZIP60 in plants and XBP1 in metazoans, is the most ancient branch of the UPR. Inositol 4-12 transcription factor HAC1 Saccharomyces cerevisiae S288C 115-119 8932376-6 1996 These results clearly indicate that the IRE2/HAC1 gene product plays a critical role in the induction of KAR2 expression and in the inositol prototrophy mediated by IRE1. Inositol 132-140 transcription factor HAC1 Saccharomyces cerevisiae S288C 45-49