دورية أكاديمية
أعرض في EDS

Functional Analysis of KAP1/TRIM28 Requirements for HIV-1 Transcription Activation.

التفاصيل البيبلوغرافية
العنوان: Functional Analysis of KAP1/TRIM28 Requirements for HIV-1 Transcription Activation.
المؤلفون: Randolph K; Department of Microbiology, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA., Hyder U; Department of Microbiology, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA., Challa A; Department of Microbiology, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA., Perez E; Department of Microbiology, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA., D'Orso I; Department of Microbiology, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
المصدر: Viruses [Viruses] 2024 Jan 13; Vol. 16 (1). Date of Electronic Publication: 2024 Jan 13.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: MDPI Country of Publication: Switzerland NLM ID: 101509722 Publication Model: Electronic Cited Medium: Internet ISSN: 1999-4915 (Electronic) Linking ISSN: 19994915 NLM ISO Abbreviation: Viruses Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Basel, Switzerland : MDPI
مواضيع طبية MeSH: HIV-1*/genetics , Transcriptional Activation* , Tripartite Motif-Containing Protein 28*/genetics, Humans ; Mutagenesis ; RING Finger Domains
مستخلص: HIV-1 latency maintenance and reactivation are regulated by several viral and host factors. One such factor is Krüppel-associated box (KRAB)-associated protein 1 (KAP1: also named TRIM28 or TIF1β). While initial studies have revealed KAP1 to be a positive regulator of latency reversal in transformed and primary CD4 + T cells, subsequent studies have proposed KAP1 to be a repressor required for latency maintenance. Given this discrepancy, in this study, we re-examine KAP1 transcription regulatory functions using a chemical genetics strategy to acutely deplete KAP1 expression to avoid the accumulation of indirect effects. Notably, KAP1 acute loss partially decreased HIV-1 promoter activity in response to activating signals, a function that can be restored upon complementation with exogenous KAP1, thus revealing that KAP1-mediated activation is on target. By combining comprehensive KAP1 domain deletion and mutagenesis in a cell-based reporter assay, we genetically defined the RING finger domain and an Intrinsically Disordered Region as key activating features. Together, our study solidifies the notion that KAP1 activates HIV-1 transcription by exploiting its multi-domain protein arrangement via previously unknown domains and functions.
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معلومات مُعتمدة: F99 CA264296 United States CA NCI NIH HHS; R01 AI114362 United States AI NIAID NIH HHS; R03 CA259672 United States CA NCI NIH HHS
فهرسة مساهمة: Keywords: HIV-1 gene expression; KAP1; TIF1β; TRIM28; latency; transcription
المشرفين على المادة: EC 2.3.2.27 (TRIM28 protein, human)
EC 2.3.2.27 (Tripartite Motif-Containing Protein 28)
تواريخ الأحداث: Date Created: 20240123 Date Completed: 20240220 Latest Revision: 20240523
رمز التحديث: 20240523
مُعرف محوري في PubMed: PMC10819576
DOI: 10.3390/v16010116
PMID: 38257816
قاعدة البيانات: MEDLINE
الوصف
تدمد:1999-4915
DOI:10.3390/v16010116