SynthesisMolecular biology reports2025
Recent progress in molecular mechanisms of Salmonella effectors involved in gut epithelium invasion.
Synthesis in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Review
- Modulation of host functions by bacterial serine/threonine protein kinase effector proteins.The Journal of biological chemistry · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Salmonella enterica is one of the leading infectious pathogens for gastrointestinal illness and affects millions worldwide. Being a foodborne pathogen, Salmonella has developed several molecular strategies to overcome unfavorable conditions in the intestine and to enter and survive in the gut epithelium. This specialized process of host-pathogen interaction is achieved by a series of complex events of adhesion, invasion, and survival. These processes are profoundly regulated by effector proteins encoded in specialized Salmonella pathogenicity islands (SPI). Type-3 Secretion System (T3SS), a molecular assembly of several proteins, is a key for initiating and establishing the interaction of pathogen to host cell. It works as a molecular syringe to deliver effector proteins for a complex invasion process of a pathogen in the host. In this review, we discuss the molecular role of the effector proteins in the invasion of Salmonella pathogen into the gut epithelium of the host. Primarily, effector proteins like SipB and SipC help Salmonella to form translocation assembly and stabilize the host cell structure, allowing bacteria to enter the host cell. Whereas, SopE and SopB further promote membrane ruffling. Next, SptP restores the normal shape of the host cell to ensure the pathogen survives inside the host cell. The pathogen forms a niche, Salmonella-containing vacuoles (SCVs), inside the host cell with the help of SteA, SteC, and PipB2. Further, effectors of the SPI-2 T3SS, including SseB, SseC, and SseD stablize the SCVs and support prolonged bacterial survival. This systematic review provides molecular aspects of these sequential events for the entry of Salmonella into gut epithelium.
Indexed as
Identifiers
40522423What 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.