ArticleiScience2022
Crotonylation sensitizes IAPi-induced disruption of latent HIV by enhancing p100 cleavage into p52.
Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed.
- Histone decrotonylation plays a distinct role in HIV latency.Science advances · 2026Article
- Review
- Lysine crotonylation in disease: mechanisms, biological functions and therapeutic targets.Epigenetics & chromatin · 2025Review
- HIV-1 latency reversal agent boosting is not limited by opioid use.JCI insight · 2024Article
- Potential functions and mechanisms of lysine crotonylation modification (Kcr) in tumorigenesis and lymphatic metastasis of papillary thyroid cancer (PTC).Journal of translational medicine · 2024Article
- HIV-1 latency reversal agent boosting is not limited by opioid use.medRxiv : the preprint server for health sciences · 2024Article
- Novel histone post-translational modifications in Alzheimer's disease: current advances and implications.Clinical epigenetics · 2024Review
- Protein lysine four-carbon acylations in health and disease.Journal of cellular physiology · 2024Review
- Dynamic modulation of the non-canonical NF-κB signaling pathway for HIV shock and kill.Frontiers in cellular and infection microbiology · 2024Review
- Review
- Article
- Systematic analysis of lysine crotonylation in human macrophages responding to MRSA infection.Frontiers in cellular and infection microbiology · 2023Article
- Human Immunodeficiency Virus-1 Latency ReversalFrontiers in microbiology · 2022Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
The eradication of HIV infection is difficult to achieve because of stable viral reservoirs. Here, we show that crotonylation enhances AZD5582-induced noncanonical NF-κB (ncNF-κB) signaling, further augmenting HIV latency reversal in Jurkat and U1 cell line models of latency, HIV latently infected primary CD4+ T cells and resting CD4+ T cells isolated from people living with HIV. Crotonylation upregulated the levels of the active p52 subunit of NF-κB following AZD5582. Biochemical analyses suggest that the ubiquitin E3 ligase TRIM27 is involved in enhanced p100 cleavage to p52. When TRIM27 was depleted, AZD5582-induced HIV latency reversal was reduced. TRIM27 small interfering RNA (siRNA) knockdown reduced both p100 and p52 levels without inhibiting p100 transcription, indicating that TRIM27 not only acts on p100 cleavage but also may impact p100/p52 stability. These observations reveal the complexity of HIV transcriptional machinery, particularly of NF-κB.
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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.