| pubmed-article:10835355 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10835355 | lifeskim:mentions | umls-concept:C0036025 | lld:lifeskim |
| pubmed-article:10835355 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:10835355 | lifeskim:mentions | umls-concept:C0080347 | lld:lifeskim |
| pubmed-article:10835355 | lifeskim:mentions | umls-concept:C0001455 | lld:lifeskim |
| pubmed-article:10835355 | lifeskim:mentions | umls-concept:C0333051 | lld:lifeskim |
| pubmed-article:10835355 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
| pubmed-article:10835355 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:10835355 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:10835355 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
| pubmed-article:10835355 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:10835355 | pubmed:dateCreated | 2000-7-20 | lld:pubmed |
| pubmed-article:10835355 | pubmed:abstractText | The Saccharomyces cerevisiae protein kinase Rim15 was identified previously as a component of the Ras/cAMP pathway acting immediately downstream of cAMP-dependent protein kinase (cAPK) to control a broad range of adaptations in response to nutrient limitation. Here, we show that the zinc finger protein Gis1 acts as a dosage-dependent suppressor of the rim15Delta defect in nutrient limitation-induced transcriptional derepression of SSA3. Loss of Gis1 results in a defect in transcriptional derepression upon nutrient limitation of various genes that are negatively regulated by the Ras/cAMP pathway (e.g. SSA3, HSP12 and HSP26). Tests of epistasis as well as transcriptional analyses of Gis1-dependent expression indicate that Gis1 acts in this pathway downstream of Rim15 to mediate transcription from the previously identified post-diauxic shift (PDS) element. Accordingly, deletion of GIS1 partially suppresses, and overexpression of GIS1 exacerbates the growth defect of mutant cells that are compromised for cAPK activity. Moreover, PDS element-driven expression, which is negatively regulated by the Ras/cAMP pathway and which is induced upon nutrient limitation, is almost entirely dependent on the presence of Gis1. | lld:pubmed |
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| pubmed-article:10835355 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10835355 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10835355 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10835355 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10835355 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:10835355 | pubmed:issn | 0261-4189 | lld:pubmed |
| pubmed-article:10835355 | pubmed:author | pubmed-author:BürckertNN | lld:pubmed |
| pubmed-article:10835355 | pubmed:author | pubmed-author:De VirgilioCC | lld:pubmed |
| pubmed-article:10835355 | pubmed:author | pubmed-author:EggerPP | lld:pubmed |
| pubmed-article:10835355 | pubmed:author | pubmed-author:PedruzziII | lld:pubmed |
| pubmed-article:10835355 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10835355 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:10835355 | pubmed:volume | 19 | lld:pubmed |
| pubmed-article:10835355 | pubmed:owner | NLM | lld:pubmed |
