ArticleJournal of bacteriology2001
Identification of specific residues in colicin E1 involved in immunity protein recognition.
Article in Journal of bacteriology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Channel domain of colicin A modifies the dimeric organization of its immunity protein.The Journal of biological chemistry · 2010Article
- Colicin biology.Microbiology and molecular biology reviews : MMBR · 2007Review
- Colicin A immunity protein interacts with the hydrophobic helical hairpin of the colicin A channel domain in the Escherichia coli inner membrane.Journal of bacteriology · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
The basis of specificity between pore-forming colicins and immunity proteins was explored by interchanging residues between colicins E1 (ColE1) and 10 (Col10) and testing for altered recognition by their respective immunity proteins, Imm and Cti. A total of 34 divergent residues in the pore-forming domain of ColE1 between residues 419 and 501, a region previously shown to contain the specificity determinants for Imm, were mutagenized to the corresponding Col10 sequences. The residue changes most effective in converting ColE1 to the Col10 phenotype are residue 448 at the N terminus of helix VI and residues 470, 472, and 474 at the C terminus of helix VII. Mutagenesis of helix VI residues 416 to 419 in Col10 to the corresponding ColE1 sequence resulted in increased recognition by Imm and loss of recognition by Cti.
Indexed as
Identifiers
What OpenQuestion holds
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.