Michael Emerman

Professor

Fred Hutchinson Cancer Research Center

United States

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Michael Emerman is a Professor at the Fred Hutchinson Cancer Center in the United States. His research focuses on HIV-1 transmission mechanisms and mechanisms of viral restriction, particularly involving the CARD8 inflammasome and Mx proteins. Recent publications include studies on transcriptional blocks to HIV latency reversal and the role of integrator complexes in HIV-1 reactivation.

Articles (18)

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2025

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2020

Collaborators (3)

Patrick Mitchell

Assistant Professor

University of Washington

UNITED STATES

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Nicholas Chesarino

Lecturer

Ohio State University

UNITED STATES

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Molly Ohainle

Assistant Professor

University of California, Berkeley

UNITED STATES

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Michael Emerman

Research Interests

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About

Articles (18)

CARD8 inflammasome activation during HIV-1 cell-to-cell transmission

CARD8 inflammasome activation during HIV-1 cell-to-cell transmission

Heterozygous and generalist MxA super-restrictors overcome breadth-specificity tradeoffs in antiviral restriction

A conserved opal termination codon optimizes a temperature-dependent tradeoff between protein production and processing in alphaviruses

Integrator complex subunit 12 knockout overcomes a transcriptional block to HIV latency reversal

Integrator complex subunit 12 knockout overcomes a transcriptional block to HIV latency reversal

Antiviral Mx proteins have an ancient origin and widespread distribution among eukaryotes

Capsid-dependent lentiviral restrictions

A human-specific motif facilitates CARD8 inflammasome activation after HIV-1 infection

A CRISPR Screen of HIV Dependency Factors Reveals That CCNT1 Is Non-Essential in T Cells but Required for HIV-1 Reactivation from Latency

A Virus-Packageable CRISPR System Identifies Host Dependency Factors Co-Opted by Multiple HIV-1 Strains

A modular CRISPR screen identifies individual and combination pathways contributing to HIV-1 latency

HIV-1 Vif Gained Breadth in APOBEC3G Specificity after Cross-Species Transmission of Its Precursors

Highly-potent, synthetic APOBEC3s restrict HIV-1 through deamination-independent mechanisms

Mutational resilience of antiviral restriction favors primate TRIM5α in host-virus evolutionary arms races

APOBEC3C Tandem Domain Proteins Create Super Restriction Factors against HIV-1

TRIM34 restricts HIV-1 and SIV capsids in a TRIM5α-dependent manner

Polymorphisms in Human APOBEC3H Differentially Regulate Ubiquitination and Antiviral Activity

Collaborators (3)

Patrick Mitchell

Nicholas Chesarino

Molly Ohainle

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