ArticlePloS one2017
N-terminally truncated POM121C inhibits HIV-1 replication.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Mis-localized nucleoporin POM121C potently inhibits nuclear entry of HIV-1 but leads to the outgrowth of viral escape mutants.Journal of virology · 2026Article
- POM121 induces chemoresistance toward cisplatin in non-small cell lung cancer.Cytotechnology · 2025Article
- Article
- Nuclear pore protein POM121 regulates subcellular localization and transcriptional activity of PPARγ.Cell death & disease · 2024Article
- POM121 is a novel marker for predicting the prognosis of laryngeal cancer.Histology and histopathology · 2020Article
- POM121 is identified as a novel prognostic marker of oral squamous cell carcinoma.Journal of Cancer · 2019Article
- The transmembrane nucleoporin Pom121 ensures efficient HIV-1 pre-integration complex nuclear import.Virology · 2018Article
- FAM13A and POM121C are candidate genes for fasting insulin: functional follow-up analysis of a genome-wide association study.Diabetologia · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have identified host cell factors that regulate early stages of HIV-1 infection including viral cDNA synthesis and orientation of the HIV-1 capsid (CA) core toward the nuclear envelope, but it remains unclear how viral DNA is imported through the nuclear pore and guided to the host chromosomal DNA. Here, we demonstrate that N-terminally truncated POM121C, a component of the nuclear pore complex, blocks HIV-1 infection. This truncated protein is predominantly localized in the cytoplasm, does not bind to CA, does not affect viral cDNA synthesis, reduces the formation of 2-LTR and diminished the amount of integrated proviral DNA. Studies with an HIV-1-murine leukemia virus (MLV) chimeric virus carrying the MLV-derived Gag revealed that Gag is a determinant of this inhibition. Intriguingly, mutational studies have revealed that the blockade by N-terminally-truncated POM121C is closely linked to its binding to importin-β/karyopherin subunit beta 1 (KPNB1). These results indicate that N-terminally-truncated POM121C inhibits HIV-1 infection after completion of reverse transcription and before integration, and suggest an important role for KPNB1 in HIV-1 replication.
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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.