# Function interactions between mitogen-activated protein kinases (MAPKs) and SARS-CoV-2

> **NIH NIH R01** · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · 2024 · $852,747

## Abstract

PROJECT SUMMARY
SARS-CoV-2, the causative agent of the COVID-19 pandemic, modifies the cells that it infects in profound ways.
One such modification is the activation of host cellular mitogen-activated protein kinase (MAPK) pathways, which
contribute to severe inflammation that is a hallmark of severe COVID-19 disease. Inhibition of one MAPK
pathway, the p38/MAPK pathway, reduces SARS-CoV-2 replication by an undefined mechanism. This proposal
aims to measure the impact of human MAPK pathways on SARS-CoV-2 infection using a multidisciplinary
approach that combines state-of-the-art proteomics technologies, medium-throughput genetic screening, and in
vivo and ex vivo models of SARS-CoV-2 infection. These findings will inform the potential application of MAPK
inhibitors for COVID-19 treatment and may identify alternative targets within the MAPK families. MAPK pathways
play critical roles in many disease states, and this work will inform research in these areas by providing molecular
mechanisms for MAPK regulation and providing tools for the unbiased discovery of MAPK substrates and
regulators.

## Key facts

- **NIH application ID:** 10808183
- **Project number:** 5R01AI170596-02
- **Recipient organization:** ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI
- **Principal Investigator:** Jeffrey R Johnson
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $852,747
- **Award type:** 5
- **Project period:** 2023-03-13 → 2028-02-29

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10808183

## Citation

> US National Institutes of Health, RePORTER application 10808183, Function interactions between mitogen-activated protein kinases (MAPKs) and SARS-CoV-2 (5R01AI170596-02). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10808183. Licensed CC0.

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