# TAT Transactivation

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · 2020 · $396,250

## Abstract

   
DESCRIPTION (provided by applicant): The goal of this project is to define structural and functional aspects of CTD kinases that are critical for HIV replication. They are CycT1:CDK9 (P-TEFb), CycL1/L2:CDK11, CycK:CDK12 and CycK:CDK13. P-TEFb is the co-activator of NF-kB and Tat. CDK11 and CDK12 play critical roles in HIV 3' end formation, i.e. cleavage and polyadenylation. CDK13 is important for HIV mRNA splicing. Studies of their regulation in cells and in HIV silencing and reactivation are major goals of this proposal. In addition, we are developing sensitive assays for the release of P-TEFb from its inactive 7SK snRNP in cells, which will be adapted for the analysis of compounds that can be used to reactivate HIV from latency as well as treat many different forms of cancer and inflammation. These studies will inform all strategies aimed at reducing and/or eliminating the reservoir of HIV in infected individuals.

## Key facts

- **NIH application ID:** 9849730
- **Project number:** 5R01AI125104-05
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
- **Principal Investigator:** Boris Matija PETERLIN
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $396,250
- **Award type:** 5
- **Project period:** 2016-02-01 → 2021-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9849730

## Citation

> US National Institutes of Health, RePORTER application 9849730, TAT Transactivation (5R01AI125104-05). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/9849730. Licensed CC0.

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