# overview
Mitochondria are complex and dynamic organelles integral to many processes including energy generation, programmed cell death, signal transduction, and immunity. Research in my laboratory centers on understanding how mitochondria regulate innate immunity and inflammatory processes to influence human health and disease.

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1.1 Normal Biological Development And Functioning

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1.1 Normal Biological Development And Functioning

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Intracellular Signaling Peptides And Proteins

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1.1 Normal Biological Development And Functioning

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Hypoxia-Inducible Factor 1, Alpha Subunit

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1.1 Normal Biological Development And Functioning

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Mitochondrial Amino Acid Trna Synthetases

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Physical Injury - Accidents And Adverse Effects

# educationAndTraining[].organization.label
North Carolina State University - (Raleigh, North Carolina, United States)

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Yale University - (New Haven, Connecticut, United States)

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Yale University - (New Haven, Connecticut, United States)

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LRRK2 is required for macrophage homeostasis and the control of type I IFN

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The American Association of Immunologists

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A virus-acquired host cytokine controls systemic aging by antagonizing apoptosis.

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Machine learning prediction of cancer cell metabolism from autofluorescence lifetime images

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Induction of macrophage nitric oxide production by Gram-negative flagellin involves signaling via heteromeric Toll-like receptor 5/Toll-like receptor 4 complexes.

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The American Association of Immunologists

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Mitochondrial dysfunction promotes alternative gasdermin D-mediated inflammatory cell death and susceptibility to infection

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Neutralizing interleukin-6 in tumor-bearing mice does not abrogate behavioral fatigue induced by Lewis lung carcinoma.

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Suppression of NLRX1 in chronic obstructive pulmonary disease.

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American Society for Clinical Investigation

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Loss of mitochondrial ClpP, Lonp1, and Tfam triggers transcriptional induction of Rnf213, a susceptibility factor for moyamoya disease.

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Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA.

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The Splicing Factor hnRNP M Is a Critical Regulator of Innate Immune Gene Expression in Macrophages.

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Age-Dependent Decline in Neuron Growth Potential and Mitochondria Functions in Cortical Neurons.

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Borrelia burgdorferi Engages Mammalian Type I IFN Responses via the cGAS-STING Pathway.

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The American Association of Immunologists

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Borrelia burgdorferi engages mammalian type I interferon responses via the cGAS-STING pathway

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NF-B-Inducing Kinase (NIK) Governs the Mitochondrial Respiratory Capacity, Differentiation, and Inflammatory Status of Innate Immune Cells

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Activation of the cGAS-STING innate immune response in cells with deficient mitochondrial topoisomerase TOP1MT.

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Subversion of innate immune responses by Brucella through the targeted degradation of the TLR signaling adapter, MAL.

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The American Association of Immunologists

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Elevated type I interferon responses potentiate metabolic dysfunction, inflammation, and accelerated aging in mtDNA mutator mice.

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American Association for the Advancement of Science (AAAS)

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ClpP-Deletion Causes Azoospermia, with Meiosis-I Delay and Insufficient Biosynthesis of Spermatid Factors, Due to Mitochondrial Dysfunction with Accumulation of Perrault Proteins ERAL1, PEO1, and HARS2

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Loss of Mitochondrial Protease CLPP Activates Type I IFN Responses through the Mitochondrial DNAcGASSTING Signaling Axis

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The American Association of Immunologists

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Neuroimmune mechanisms of cognitive impairment in a mouse model of Gulf War illness.

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Prominent Increases of Nuclear DNAJA3and Cytosolic STAT1 with Nucleic Acid Sensors Underlie Innate Immunity Activation in ClpP-null Mouse

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Type I interferon potentiates metabolic dysfunction, inflammation, and accelerated aging in mtDNA mutator mice

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TRIM14 Is a Key Regulator of the Type I IFN Response during Mycobacterium tuberculosis Infection.

# publications[].publisher
The American Association of Immunologists

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The splicing factor hnRNP M is a critical regulator of innate immune gene expression in macrophages

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Recognition and signaling by toll-like receptors.

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NF-B-Inducing Kinase Governs the Mitochondrial Respiratory Capacity, Differentiation, and Inflammatory Status of Innate Immune Cells.

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The American Association of Immunologists

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Impact of pharmacological agents on mitochondrial function: a growing opportunity?

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Mitochondrial DNA stress primes the antiviral innate immune response.

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Mitochondrial ROS promotes susceptibility to infection via gasdermin D-mediated necroptosis.

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Identification of a sequence in human toll-like receptor 5 required for the binding of Gram-negative flagellin.

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A conserved PLPLRT/SD motif of STING mediates the recruitment and activation of TBK1.

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Gasdermin D promotes hyperinfLammation by triggering necroptosis in the presence of mitochondrial stress

# publications[].publisher
The American Association of Immunologists

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Clpp-Deletion Causes Azoospermia, with Meiosis-I Delay and Insufficient Biosynthesis of Spermatid Factors, Due to Mitochondrial Dysfunction with Accumulation of Perrault Proteins ERAL1, PEO1, and HARS2

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Assessing Mitochondrial DNA Release into the Cytosol and Subsequent Activation of Innate Immune-related Pathways in Mammalian Cells.

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Mitochondrial DNA in innate immune responses and inflammatory pathology.

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Loss of mitochondrial protease CLPP activates type I interferon responses through the mtDNA-cGAS-STING signaling axis

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Innate immune signaling and sex differences contribute to neurocognitive impairment, neuroinflammation, and mitochondrial rewiring in a mouse model of Gulf War illness

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Inflammatory and interferon gene expression signatures in patients with mitochondrial disease.

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MKK3 regulates mitochondrial biogenesis and mitophagy in sepsis-induced lung injury.

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Cisplatin decreases voluntary wheel-running activity but does not impair food-motivated behavior in mice.

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Loss of Mitochondrial Protease CLPP Activates Type I IFN Responses through the Mitochondrial DNA-cGAS-STING Signaling Axis

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Impaired lysosomal acidification triggers iron deficiency and inflammation in vivo.

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Inflammatory and interferon gene expression signatures in patients with mitochondrial disease.

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Gangliosides inhibit flagellin signaling in the absence of an effect on flagellin binding to toll-like receptor 5.

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Cooperative sensing of mitochondrial DNA by ZBP1 and cGAS promotes cardiotoxicity

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Mitochondrial transcription factor A (TFAM) shapes metabolic and invasion gene signatures in melanoma.

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TLR signalling augments macrophage bactericidal activity through mitochondrial ROS.

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TRIM14 is a key regulator of the type I interferon response during Mycobacterium tuberculosis infection

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Cooperative sensing of mitochondrial DNA by ZBP1 and cGAS promotes cardiotoxicity.

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Inactivity of Peptidase ClpP Causes Primary Accumulation of Mitochondrial Disaggregase ClpX With Its Interactors at the Nucleoid and RNA Granule

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3D convolutional neural networks predict cellular metabolic pathway use from fluorescence lifetime decay data.

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Mitochondrial dysfunction as a trigger of innate immune responses and inflammation.

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Activation of the cGAS-STING innate immune response in cells with deficient mitochondrial topoisomerase TOP1MT

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Mitochondrial DNA Stress Signalling Protects the Nuclear Genome.

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Aging-dependent alterations in gene expression and a mitochondrial signature of responsiveness to human influenza vaccination.

# publications[].label
Loss of Mitochondrial Protease CLPP Activates Type I IFN Responses through the Mitochondrial DNA-cGAS-STING Signaling Axis.

# publications[].publisher
The American Association of Immunologists

# publications[].label
Increased presence of nuclear DNAJA3 and upregulation of cytosolic STAT1 and of nucleic acid sensors trigger innate immunity in the ClpP-null mouse.

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cGAS drives noncanonical-inflammasome activation in age-related macular degeneration (vol 24, pg 50, 2017)

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Inactivity of Peptidase ClpP Causes Primary Accumulation of Mitochondrial Disaggregase ClpX with Its Interacting Nucleoid Proteins, and of mtDNA.

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CLPP Depletion Causes Diplotene Arrest; Underlying Testis Mitochondrial Dysfunction Occurs with Accumulation of Perrault Proteins ERAL1, PEO1, and HARS2.

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Mitochondria in innate immune responses.

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The Age-Dependent Decline in Neuron Growth Potential in the CNS is Associated with an Age-Related Dysfunction of Neuronal Mitochondria

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Resolution of cisplatin-induced fatigue does not require endogenous interleukin-10 in male mice.

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IkappaBbeta acts to inhibit and activate gene expression during the inflammatory response.

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Sex differences in the behavioral and immune responses of mice to tumor growth and cancer therapy.

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The molecular basis of tight nuclear tethering and inactivation of cGAS.

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Mitochondrial Dysfunction and Aberrant Immune Activation in the Pathobiology of Gulf War Illness

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United States Army - (Washington D.C., District of Columbia, United States)

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DOD-Army-Medical Research and Materiel Command

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Innate Immune Signaling and Type I Interferon Responses as Novel Modifiers of Mitochondrial Disease Pathology

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United States Army - (Washington D.C., District of Columbia, United States)

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DOD-Army-Medical Research and Materiel Command

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Mitochondrial DNA Instability Engages a Cancer-Related Interferon Program to Modify the Immune Microenvironment and NAD+ Metabolome and Enhance Melanoma Growth

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Cancer Prevention and Research Institute of Texas - (Austin, Texas, United States)

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Type I Interferon Responses in the Pathobiology of Anthracycline-induced Cardiotoxicity

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National Heart Lung and Blood Institute - (Bethesda, Maryland, United States)

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Inborn Errors of Innate Immunity and Impaired Antimicrobial Defenses in Primary Mitochondrial Diseases

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Congressionally Directed Medical Research Programs - (Frederick, Maryland, United States)

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Identification and Role of Type IV Secretion Effector Proteins in Coxiella Burnetii

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National Institutes of Health - (Bethesda, Maryland, United States)

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DHHS-NIH-National Institute of Allergy and Infectious Diseases

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