ArticleJournal of bacteriology2011
Active role of the interdomain linker of AraC.
Article in Journal of bacteriology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- Arginine 37 of Glycine Linker Dictates Regulatory Function of HapR.Frontiers in microbiology · 2020Article
- Arabinose Alters Both Local and Distal H-D Exchange Rates in the Escherichia coli AraC Transcriptional Regulator.Biochemistry · 2019Article
- A large family of anti-activators accompanying XylS/AraC family regulatory proteins.Molecular microbiology · 2016Article
- DOMMINO 2.0: integrating structurally resolved protein-, RNA-, and DNA-mediated macromolecular interactions.Database : the journal of biological databases and curation · 2016Article
- The length of glycine-rich linker in DNA-binding domain is critical for optimal functioning of quorum-sensing master regulatory protein HapR.Molecular genetics and genomics : MGG · 2014Article
- The LacI-Type transcriptional regulator AraR acts as an L-arabinose-responsive repressor of L-arabinose utilization genes in Corynebacterium glutamicum ATCC 31831.Journal of bacteriology · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in the interdomain linker of the gene for the AraC regulatory protein of Escherichia coli that severely interfere with the protein's ability either to repress or to activate transcription have been found. These mutations have relatively small effects on the dimerization domain's ability to bind arabinose or to dimerize the protein or on the DNA-binding domain's affinity for a single DNA half-site. The linker mutations, however, dramatically change the affinity of AraC for binding to two direct-repeat DNA half-sites. Less dramatically, the induction-deficient linker variants also display altered DNA sequence selectivity. These results show that changing the sequence of the interdomain linker can profoundly affect the dimerization domain-DNA-binding domain interactions in AraC. The smaller effects on the functions of the individual domains could be the direct result of the linker alterations but more likely are the indirect result of the altered dimerization domain-DNA-binding domain interactions. In summary, the linker does not simply function as a passive and flexible connector between the domains of AraC but, instead, is more directly involved in the protein's dimerization domain-DNA-binding domain interactions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.