Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P51532 (transcriptional activator)
 6,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Yeast metallothionein, encoded by the CUP1 gene, and its copper-dependent transcriptional activator ACE1 play a key role in mediating copper resistance in Saccharomyces cerevisiae. Using an ethyl methanesulfonate mutant of a yeast strain in which CUP1 and ACE1 were deleted, we isolated a gene, designated CUP9, which permits yeast cells to grow at high concentrations of environmental copper, most notably when lactate is the sole carbon source. Disruption of CUP9, which is located on chromosome XVI, caused a loss of copper resistance in strains which possessed CUP1 and ACE1, as well as in the cup1 ace1 deletion strain. Measurement of intracellular copper levels of the wild-type and cup9-1 mutant demonstrated that total intracellular copper concentrations were unaffected by CUP9. CUP9 mRNA levels were, however, down regulated by copper when yeast cells were grown with glucose but not with lactate or glycerol-ethanol as the sole carbon source. This down regulation was independent of the copper metalloregulatory transcription factor ACE1. The DNA sequence of CUP9 predicts an open reading frame of 306 amino acids in which a 55-amino-acid sequence showed 47% identity with the homeobox domain of the human proto-oncogene PBX1, suggesting that CUP9 is a DNA-binding protein which regulates the expression of important copper homeostatic genes.
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PMID:Identification and analysis of a Saccharomyces cerevisiae copper homeostasis gene encoding a homeodomain protein. 796 20

The endoderm of C. elegans arises entirely from a single progenitor cell, the E blastomere, whose identity is specified by GATA type transcription factors, including END-1. In response to an inductive interaction mediated through Wnt/MAP kinase signaling pathways, POP-1, a Lef/Tcf-type transcription factor, restricts end-1 transcription to the posterior daughter of the mesendoderm progenitor (EMS cell), resulting in activation of endoderm differentiation by the SKN-1 and MED-1/2 transcription factors. We purified a factor from semi-synchronized early embryos that binds to an end-1 cis regulatory region critical for its endoderm-specific expression. Mass spectrometry identified this protein, PLP-1, as a C. elegans orthologue of the vertebrate pur alpha transcription factor. Expression of end-1 is attenuated in embryos depleted for PLP-1. While removal of plp-1 activity alone does not prevent endoderm development, it strongly enhances the loss of endoderm in mutants defective for the Wnt pathway. In contrast, loss of PLP-1 function does not synergize with mutants in the endoderm-inducing MAPK pathway. Moreover, nuclear localization of PLP-1 during interphase requires components of the MAPK pathway, suggesting that PLP-1 is influenced by MAPK signaling. PLP-1 is transiently asymmetrically distributed during cell divisions, with higher levels in the chromatin of the future posterior daughter of EMS and other dividing cells shortly after mitosis compared to that in their sisters. These findings imply that PLP-1 acts as a transcriptional activator of end-1 expression that may be modulated by MAPK signaling to promote endoderm development.
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PMID:C. elegans pur alpha, an activator of end-1, synergizes with the Wnt pathway to specify endoderm. 1908