# overview
Using a multi-disciplinary toolset, we probe the molecular mechanisms that macrophages use to activate an innate immune response that is rapid, robust, and regulated. We mainly study how RNA binding proteins control the ability of macrophages to respond to infection, using a variety of bacterial and viral models. By working to uncover how RNA binding proteins work and how macrophages functionalize RNA binding proteins to orchestrate a fine-tuned innate immune response, our work furthers our understanding of a variety of human diseases.

# keywords[]
1.1 Normal Biological Development And Functioning

# keywords[]
1.1 Normal Biological Development And Functioning

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2.2 Factors Relating To The Physical Environment

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2.2 Factors Relating To The Physical Environment

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Intracellular Signaling Peptides And Proteins

# keywords[]
1.1 Normal Biological Development And Functioning

# keywords[]
1.1 Normal Biological Development And Functioning

# keywords[]
Intracellular Signaling Peptides And Proteins

# keywords[]
1.1 Normal Biological Development And Functioning

# educationAndTraining[].organization.label
Hamilton College - (Clinton, New York, United States)

# educationAndTraining[].organization.label
Yale University - (New Haven, Connecticut, United States)

# educationAndTraining[].organization.label
University of California, San Francisco - (San Francisco, California, United States)

# publications[].label
Galectin-8 senses phagosomal damage and recruits selective autophagy adapter TAX1BP1 to control Mycobacterium tuberculosis infection in macrophages

# publications[].label
LRRK2 is required for macrophage homeostasis and the control of type I IFN

# publications[].publisher
The American Association of Immunologists

# publications[].label
Interactions between fungal hyaluronic acid and host CD44 promote internalization by recruiting host autophagy proteins to forming phagosomes

# publications[].label
LRRK2 maintains mitochondrial homeostasis and regulates innate immune responses to Mycobacterium tuberculosis.

# publications[].label
Serine/arginine-rich splicing factor 7 promotes the type I interferon response by activating Irf7 transcription.

# publications[].label
Mitochondrial dysfunction promotes alternative gasdermin D-mediated inflammatory cell death and susceptibility to infection

# publications[].label
Gasdermins gone wild: new roles for GSDMs in regulating cellular homeostasis.

# publications[].label
LRRK2 regulates innate immune responses and neuroinflammation during Mycobacterium tuberculosis infection

# publications[].label
The Splicing Factor hnRNP M Is a Critical Regulator of Innate Immune Gene Expression in Macrophages.

# publications[].label
PRMT5 Promotes Symmetric Dimethylation of RNA Processing Proteins and Modulates Activated T Cell Alternative Splicing and Ca2+/NFAT Signaling.

# publications[].publisher
The American Association of Immunologists

# publications[].label
SRSF6 balances mitochondrial-driven innate immune outcomes through alternative splicing of BAX

# publications[].label
Mitochondria: Powering the Innate Immune Response to Mycobacterium tuberculosis Infection.

# publications[].label
Brucella activates the host RIDD pathway to subvert BLOS1-directed immune defense.

# publications[].label
Distinct and overlapping roles for two Dicer-like proteins in the RNA interference pathways of the ancient eukaryote Trypanosoma brucei.

# publications[].publisher
Proceedings of the National Academy of Sciences

# publications[].label
Heterogeneous ribonucleoprotein M influences specific cytokine outcomes upon Salmonella Typhimurium infection

# publications[].label
TRIM14 is a key regulator of the type I interferon response during Mycobacterium tuberculosis infection

# publications[].label
SRSF6 balances mitochondrial-driven innate immune outcomes through alternative splicing of BAX.

# publications[].label
Genomic rearrangements and transcriptional analysis of the spliced leader-associated retrotransposon in RNA interference-deficient Trypanosoma brucei.

# publications[].label
Protein Arginine Methyltransferase 5 in T Lymphocyte Biology.

# publications[].label
Global transcriptomics reveals specialized roles for splicing regulatory proteins in the macrophage innate immune response

# publications[].label
The Parkinson's disease-associated variant Lrrk2 G2019S confers hyper-susceptibility to inflammasome-mediated cell death and Mycobacterium tuberculosis pathogenesis

# publications[].publisher
The American Association of Immunologists

# publications[].label
The histone variant H2A.Z promotes splicing of weak introns.

# publications[].label
Splicing Defects of the Profilin Gene Alter Actin Dynamics in an S. pombe SMN Mutant.

# publications[].label
The splicing factor SRSF6 controls Mycobacterium tuberculosis replication through its role in maintaining mitochondrial homeostasis

# publications[].publisher
The American Association of Immunologists

# publications[].label
TRIM14 Is a Key Regulator of the Type I IFN Response during Mycobacterium tuberculosis Infection.

# publications[].publisher
The American Association of Immunologists

# publications[].label
The splicing factor hnRNP M is a critical regulator of innate immune gene expression in macrophages

# publications[].label
Global Transcriptomics Uncovers Distinct Contributions From Splicing Regulatory Proteins to the Macrophage Innate Immune Response.

# publications[].label
Interactions between fungal hyaluronic acid and host CD44 promote internalization by recruiting host autophagy proteins to forming phagosomes.

# publications[].label
454 life sciences: illuminating the future of genome sequencing and personalized medicine.

# publications[].label
Mitochondrial ROS promotes susceptibility to infection via gasdermin D-mediated necroptosis.

# publications[].label
Diverse pathogens activate the host RIDD pathway to subvert BLOS1-directed immune defense

# publications[].label
The Fragile X SyndromeRelated Protein, FMRP, Modulates Innate Immune Gene Expression in Macrophages

# publications[].label
Quantitative Yeast Genetic Interaction Profiling of Bacterial Effector Proteins Uncovers a Role for the Human Retromer in Salmonella Infection.

# publications[].label
Galectin-8 Senses Phagosomal Damage and Recruits Selective Autophagy Adapter TAX1BP1 To Control Mycobacterium tuberculosis Infection in Macrophages.

# publications[].label
Alternative splicing of Bax controls cell death and innate immune responses in macrophages

# publications[].publisher
The American Association of Immunologists

# publications[].label
Hierarchical modularity and the evolution of genetic interactomes across species.

# publications[].label
Genetic interaction mapping reveals a role for the SWI/SNF nucleosome remodeler in spliceosome activation in fission yeast.

# publications[].label
LRRK2 is required for macrophage homeostasis and the control of type I IFN

# publications[].label
Exploring the "Multiple-Hit Hypothesis" of Neurodegenerative Disease: Bacterial Infection Comes Up to Bat.

# publications[].label
Gasdermin D promotes hyperinfLammation by triggering necroptosis in the presence of mitochondrial stress

# publications[].publisher
The American Association of Immunologists

# publications[].label
The opportunistic intracellular bacterial pathogen Rhodococcus equi elicits type I interferon by engaging cytosolic DNA sensing in macrophages.

# publications[].label
PRMT5 promotes symmetric dimethylation of RNA processing proteins and modulates activated T cell alternative splicing and Ca2+/NFAT signaling

# publications[].label
For Better or Worse: Cytosolic DNA Sensing during Intracellular Bacterial Infection Induces Potent Innate Immune Responses.

# researcherOn[].label
Pre-mRNA splicing regulation is critical for controlling macrophage activation

# researcherOn[].awardedBy.label
National Institutes of Health - (Bethesda, Maryland, United States)

# researcherOn[].awardedBy.preferredLabel
DHHS-NIH-National Institute of General Medical Science

# researcherOn[].label
The splicing factor SF3b1 is a master regulator of the innate immune response to Mycobacterium tuberculosis

# researcherOn[].awardedBy.label
National Institutes of Health - (Bethesda, Maryland, United States)

# researcherOn[].awardedBy.preferredLabel
DHHS-NIH-National Institute of Allergy and Infectious Diseases

# researcherOn[].label
The Secreted Effector SseC is a Key Regulator of Retrograde Transport During Salmonella Enterica Serovar Typhimurium Infection

# researcherOn[].awardedBy.label
National Institutes of Health - (Bethesda, Maryland, United States)

# researcherOn[].awardedBy.preferredLabel
DHHS-NIH-National Institute of Allergy and Infectious Diseases

# streetAddress
Texas A&M Health Science Center; Microbial Pathogenesis And Immunology; 1114 TAMUS