High throughput screening of a 4096 compound library of boronic acid and acridine containing branched peptides revealed compounds that have dissociation constants in the low nanomolar regime for HIV-1 RRE IIB RNA. We demonstrate that branched peptide boronic acids , , and inhibit the production of p24, an HIV-1 capsid protein, in a dose-dependent manner.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4957400PMC
http://dx.doi.org/10.1039/C6MD00171HDOI Listing

Publication Analysis

Top Keywords

branched peptide
8
hiv-1 rre
8
intercalator lewis
4
lewis acid-base
4
acid-base branched
4
peptide complex
4
complex formation
4
formation boosting
4
boosting affinity
4
affinity hiv-1
4

Similar Publications

TSLP acts on regulatory T cells to maintain their identity and limit allergic inflammation.

Sci Immunol

January 2025

Laboratory of Molecular Immunology and Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health (NIH), Bethesda, MD 20892, USA.

Thymic stromal lymphopoietin (TSLP) is a type I cytokine that promotes allergic responses and mediates type 2 immunity. A balance between effector T cells (T), which drive the immune response, and regulatory T cells (T), which suppress the response, is required for proper immune homeostasis. Here, we report that TSLP differentially acts on T versus T to balance type 2 immunity.

View Article and Find Full Text PDF

The current study aimed to evaluate the efficacy and safety of Compound Danshen Dripping Pills (CDDP) in improving cardiac function among patients with acute anterior ST-segment elevation myocardial infarction (AAMI). Between February 2021 and February 2023, 247 eligible patients with AAMI after primary percutaneous coronary intervention (pPCI) were enrolled and randomly assigned (1∶1) to receive CDDP ( = 126) or placebo ( = 121), with a follow-up of 48 weeks. Compared with the placebo group, the CDDP group demonstrated a significant increase in left ventricular ejection fraction (LVEF) values after 24 weeks of the treatment (least squares mean: 3.

View Article and Find Full Text PDF

Background: Andersen-Tawil syndrome (ATS) is a rare autosomal dominant disorder caused by variants in the gene. It is associated with periodic paralysis, dysmorphic features and cardiac arrhythmias. The syndrome exhibits incomplete penetrance, leading to a broad spectrum of clinical manifestations, making diagnosis challenging.

View Article and Find Full Text PDF

Background: Meier-Gorlin syndrome (MGORS) is a rare autosomal inherited form of primordial dwarfism. Pathogenic variants in 13 genes involved in DNA replication initiation have been identified in this disease, but homozygous intronic variants have never been reported. Additionally, whether growth hormone (GH) treatment can increase the height of children with MGORS is unclear.

View Article and Find Full Text PDF

METTL3-Mediated m6A Modification of ISG15 mRNA Regulates Doxorubicin-Induced Endothelial Cell Apoptosis.

J Cell Mol Med

January 2025

Zhengzhou Key Laboratory of Cardiovascular Aging, Henan Province Key Laboratory for Prevention and Treatment of Coronary Heart Disease, National Health Commission key Laboratory of Cardiovascular Regenerative Medicine, Central China Fuwai Hospital of Zhengzhou University, Fuwai Central China Cardiovascular Hospital & Central China Branch of National Center for Cardiovascular Diseases, Zhengzhou, Henan, China.

N6-adenosine methylation (m6A) of RNA is involved in the regulation of various diseases. However, its role in chemotherapy-related vascular endothelial injury has not yet been elucidated. We found that methyltransferase-like 3 (METTL3) expression was significantly reduced during doxorubicin (DOX)-induced apoptosis of vascular endothelial cells both in vivo and in vitro, and that silencing of METTL3 further intensified this process.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!