ArticleFunctional & integrative genomics2025
CutIn: a ready-to-use construct for rapid generation of urgently needed transgenic cell lines in emerging infection research.
Article in Functional & integrative genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Site-directed exogenous gene knock-in for stable cell line generation remains a multi-step procedure that heavily relies on expertise. Therefore, there is a need for a competent and easily manageable method, particularly when there is an urgent demand for cell lines, especially for emerging infection research. We present here a universal construct called CutIn that expresses the Cas9 protein and dual sgRNAs targeting a host cell genome locus and the ampicillin resistance (AmpR) gene of a cotransfected donor plasmid commercially available. This construct specifically induces double-strand breaks (DSBs) in cotransfected plasmids and host cell genomes, thereby facilitating whole plasmid integration through nonhomologous end joining (NHEJ) repair mechanisms. As pilot tests, adeno-associated virus integration site 1 (AAVS1) or hypoxanthine phosphoribosyl transferase (HPRT) locus was selected as host genome target, commonly used human cell lines 293T, HeLa and HCT116 were employed. CutIn was subjected for reporter plasmid knock-in in all three cell lines, either AAVS1 and AmpR or HPRT and AmpR loci were efficiently targeted. Fluorescent protein, human angiotensin-converting enzyme 2 (ACE2) and dengue virus (DENV) infection reporter transgenic cells were rapidly obtained via CutIn-mediated whole expression vector integration. This method is designed to be user-friendly and shows potential for supporting the investigation of emerging/re-emerging infectious diseases. Further validation in diverse research contexts will be necessary to fully assess its applicability and effectiveness.
Indexed as
Identifiers
40111512What 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.