Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P62988 (Ubiquitin)
 4,326 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nucleotide sequence of the polyubiquitin gene UbC of HeLa S3 cells and its upstream region was determined and characterized. Recognition sequences for the transcription factors HSF, NF kappa B, AP-1(c-jun), NF-IL6 and Sp1 were found in the upstream control region, a result consistent with the observation of a distinct regulatory response for the UbC gene compared with that of another polyubiquitin gene UbB. Employing a PCR procedure to amplify the entire coding region from genomic DNA, we found a heterogeneity in the repeat number (eight and nine repeats) of the ubiquitin coding units, which resulted from an apparent deletion of either the seventh or the eighth unit in the predominant nine-ubiquitin-unit coding gene. In addition, by comparison with the nucleotide sequence of the UbC gene of human leukocytes previously determined, we found a significant number of nucleotide discrepancies. However, these discrepancies could be substantially reduced by realigning the units so that the first and second ubiquitin units of the sequence determined here are translocated to the boundary between the eighth and the ninth units.
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PMID:Heterogeneous structure of the polyubiquitin gene UbC of HeLa S3 cells. 891 96

Transcription of the polyubiquitin gene UBI4 of Saccharomyces cerevisiae is strongly induced by a variety of environmental stresses, such as heat shock, nutrient depletion and exposure to DNA-damaging agents. This transcriptional response of UBI4 is likely to be the primary mechanism for increasing the pool of ubiquitin for degradation of stress-damaged proteins. Deletion and promoter fusion studies of the 5' regulatory sequences indicated that two different elements, heat shock elements (HSEs) and stress response element (STREs), contributed independently to heat shock regulation of the UBI4 gene. In the absence of HSEs, STRE sequences localized to the intervals -264 to -238 and -215 to -183 were needed for stress control of transcription after heat shock. Site-directed mutagenesis of the STRE (AG4) at -252 to -248 abolished heat shock induction of UBI4 transcription. Northern analysis demonstrated that cells containing either a temperature-sensitive HSF or non-functional Msn2p/Msn4p transcription factors induced high levels of UBI4 transcripts after heat shock. In cells deficient in both heat stress pathways, heat-induced UBI4 transcript levels were considerably lower but not abolished, suggesting a role for another factor(s) in stress control of its expression.
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PMID:Multiple independent regulatory pathways control UBI4 expression after heat shock in Saccharomyces cerevisiae. 1004 26