ReviewFrontiers in cellular and infection microbiology2017
Beyond Paralogs: The Multiple Layers of Redundancy in Bacterial Pathogenesis.
Review in Frontiers in cellular and infection microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 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
80 citing papers in PubMed, 125 citations in OpenAlex.
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- Molecular evolution and adaptations ofFrontiers in cellular and infection microbiology · 2026Review
- Intersections between proteostasis and immunity: insights from Caenorhabditis elegans.Disease models & mechanisms · 2026Review
- Obligate intracellular bacteria and host cell death pathways-the matter of life and death.Cell and tissue research · 2025Review
- Drug Design and Delivery for Intracellular Bacteria: Emerging Paradigms.Drug development research · 2025Review
- Essential redundancies fuel Mycobacterium tuberculosis adaptation to the host.PLoS pathogens · 2025Review
- Complement therapeutic factor H-IgG proteins as pre-exposure prophylaxes against Lyme borreliae infections.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Identification of urinary bacterial genes as biomarkers for non-invasive diagnosis of renal lupus.Biomarker research · 2025Article
- OptimizedMicrobiology spectrum · 2025Article
- Beyond anaerobic respiration-new physiological roles for DmsABC and other S-/N-oxide reductases inJournal of bacteriology · 2025Article
- Bacterial pathogens hijack host cell peroxisomes for replication vacuole expansion and integrity.Science advances · 2025Article
- Targeting bacterial transcription factors for infection control: opportunities and challenges.Transcription · 2025Review
- ThemSphere · 2025Article
- A comparative in silico analysis of the vlhA gene regions of Mycoplasma gallisepticum and Mycoplasma synoviae isolates from commercial hen farms in Mexico.Access microbiology · 2025Article
20 more citing papers are in PubMed but not listed here.
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 at 2 institutions in 1 country.
Funding
Abstract
Redundancy has been referred to as a state of no longer being needed or useful. Microbiologists often theorize that the only case of true redundancy in a haploid organism would be a recent gene duplication event, prior to divergence through selective pressure. However, a growing number of examples exist where an organism encodes two genes that appear to perform the same function. For example, many pathogens translocate multiple effector proteins into hosts. While disruption of individual effector genes does not result in a discernable phenotype, deleting genes in combination impairs pathogenesis: this has been described as redundancy. In many cases, this apparent redundancy could be due to limitations of laboratory models of pathogenesis that do not fully recapitulate the disease process. Alternatively, it is possible that the selective advantage achieved by this perceived redundancy is too subtle to be measured in the laboratory. Moreover, there are numerous possibilities for different types of redundancy. The most common and recognized form of redundancy is functional redundancy whereby two proteins have similar biochemical activities and substrate specificities allowing each one to compensate in the absence of the other. However, redundancy can also exist between seemingly unrelated proteins that manipulate the same or complementary host cell pathways. In this article, we outline 5 types of redundancy in pathogenesis: molecular, target, pathway, cellular process, and system redundancy that incorporate the biochemical activities, the host target specificities and the impact of effector function on the pathways and cellular process they modulate. For each type of redundancy, we provide examples from
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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.