ArticlemicroPublication biology2024
In silico analysis of several frequent SLX4 mutations appearing in human cancers.
Article in microPublication biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Exploring Molecular Characteristics and Therapeutic Strategies for Primary Sinonasal Mucosal Melanoma With Distant Metastasis.Laboratory investigation; a journal of technical methods and pathology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SLX4 is an interactor and activator of structure-specific exonuclease that helps resolve tangled recombination intermediates arising at stalled replication forks. It is one of the many factors that assist with homologous recombination, the major mechanism for restarting replication. SLX4 mutations have been reported in many cancers but a pan cancer map of all the mutations has not been undertaken. Here, using data from the Catalogue of Somatic Mutations in Cancers (COSMIC), we show that mutations occur in almost every cancer and many of them truncate the protein which should severely alter the function of the enzyme. We identified a frequent R1779W point mutation that occurs in the SLX4 domain required for heterodimerization with its partner, SLX1. In silico protein structure analysis of this mutation shows that it significantly alters the protein structure and is likely to destabilize the interaction with SLX1. Although this brief communication is limited to only
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.