A5047243105- Immune Response and Inflammation
- Wound Healing and Treatments
- NF-κB Signaling Pathways
- Immune cells in cancer
- Hippo pathway signaling and YAP/TAZ
- Adipose Tissue and Metabolism
- Antimicrobial Peptides and Activities
- Wnt/β-catenin signaling in development and cancer
- Electrohydrodynamics and Fluid Dynamics
- Nanoparticle-Based Drug Delivery
- Advanced Nanomaterials in Catalysis
- Metabolism, Diabetes, and Cancer
- Dermatologic Treatments and Research
- Redox biology and oxidative stress
- Peptidase Inhibition and Analysis
- Pediatric health and respiratory diseases
- Chemokine receptors and signaling
- S100 Proteins and Annexins
- Helicobacter pylori-related gastroenterology studies
- Cell Adhesion Molecules Research
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Adipokines, Inflammation, and Metabolic Diseases
- Mitochondrial Function and Pathology
- Immune Cell Function and Interaction
- Nanoparticles: synthesis and applications
Texas A&M University
2021-2025
Bryan College
2022-2024
Texas A&M Health Science Center
2021-2023
University of Michigan
2016-2022
Ann Arbor Center for Independent Living
2016
This works shows enhanced aggregation of silver nanoparticles in simulated gastric fluid when pepsin protein is present.
Mucosal wound repair is coordinated by dynamic crosstalk between endogenous and exogenous mediators specific receptors on epithelial cells infiltrating immune cells. One class of such receptor‐ligand pairs involves formyl peptide (FPRs) that have been shown to influence inflammatory response repair. Here we explored the role murine Fpr2/3, an ortholog human FPR2/receptor for lipoxin A4 (ALX), in orchestrating intestinal mucosal Compared with wild‐type (WT) mice, Fpr2/3 –/– mice exhibited...
Abstract Text Glioblastoma multiforme (GBM) is the most common and deadliest primary malignant brain tumor in adults due to its aggressive, invasive growth therapy resistance. The GBM microenvironment (TME) highly infiltrated by associated macrophages microglia (TAMMs) that undergo metabolic reprogramming acquire immunosuppressive, tumor-supporting properties. However, mechanisms underlying this remain poorly understood. This study aims elucidate role of NF-κB-Inducing Kinase (NIK), a key...
JAM-A is a tight-junction-associated protein that contributes to regulation of intestinal homeostasis. We report interacts with NF2 and LATS1, functioning as an initiator the Hippo signaling pathway, well-known for proliferation. Consistent these findings, we observed increased YAP activity in JAM-A-deficient epithelial cells (IEC). Furthermore, overexpression dimerization-deficient mutant, JAM-A-DL1, failed initiate signaling, phenocopying IEC, whereas JAM-A-WT activated suppressed Lastly,...
NF-κB-inducing kinase (NIK), which is essential for the activation of noncanonical NF-κB pathway, regulates diverse processes in immunity, development, and disease. Although recent studies have elucidated important functions NIK adaptive immune cells cancer cell metabolism, role metabolic-driven inflammatory responses innate remains unclear. In this study, we demonstrate that murine NIK-deficient bone marrow-derived macrophages exhibit defects mitochondrial-dependent metabolism oxidative...
NF-κB-inducing kinase (NIK) is an essential upstream inducer of noncanonical NF-κB signaling and a critical regulator immunity inflammation. Our recent work has demonstrated that NIK regulates mitochondrial respiration adaptive metabolic responses in cancer innate immune cells. However, it not clear whether also roles regulating systemic metabolism. In this study, we demonstrate local effects on developmental processes. findings show NIK-deficient mice exhibit reduced adiposity, as well...
Abstract The interconnected relationship between the central nervous system (CNS) and immune is crucial for brain function. Astrocytes, microglia infiltrating macrophages perform diverse functions maintenance of CNS homeostasis, including inflammatory responses to injury or infection, tissue repair surveillance cancers such as glioblastoma (GBM). Indeed, these cells comprise up 50% GBM tumor mass, yet impact their interactions in regulating neuroinflammation immunosuppression...
Abstract Background NF-κB-inducing kinase (NIK) is a critical regulator of immunity and inflammation NIK loss-of-function mutations have recently been described in patients with primary immunodeficiency disease. Based on our previous work showing that regulates adaptive metabolic responses glucose-starved cancer cells, we investigated whether required for mitochondrial functions bioenergetic processes to nutritional stress knockout (KO) mice, which recapitulate the clinical presentation PID...
Abstract NF-κB-Inducing Kinase (NIK), which is essential for the activation of noncanonical NF-κB pathway, regulates diverse processes in immunity, development, and disease. While recent studies have elucidated important functions NIK adaptive immune cells cancer cell metabolism, role metabolic-driven inflammatory responses innate remains unclear. Here, we demonstrate that NIK-deficient bone marrow-derived macrophages exhibit defects mitochondrial-dependent metabolism oxidative...
Chronisch entzündliche Darmerkrankungen führen zu Ulzerationen und Zerstörung der intestinalen epithelialen Barriere. Das klinische Ausmaß hängt mit pathologischen Freisetzung pro-inflammatorischer Mediatoren wie Platelet Activating Factor (PAF) Tumor Necrosis alpha (TNF-a) zusammen. TNF-a neutralisierende Antikörper werden zur erfolgreichen Remissionsinduktion angewendet, wobei es jedoch bei einer signifikanten Patientenzahl zum Therapieversagen kommt, potentiell durch Inhibition...
Mucosal wound repair is coordinated by a dynamic spatiotemporal cross talk of mediators with receptors on epithelial cells and infiltrating immune cells. After initial recruitment neutrophils, monocytes infiltrate mucosal wounds in close proximity to repairing epithelium. Key regulators include pro‐inflammatory pro‐resolving that help orchestrate temporal cells, resolve acute inflammatory responses regulate cell migration proliferation. Immune derived have been shown activate G‐protein...
Epithelial cells migrate and proliferate to cover denuded mucosal surfaces. The intestinal infiltrating immune epithelium secrete an array of inflammatory mediators that have been proposed modulate wound repair. Here, we report Platelet Activating Factor (PAF), a molecule considered be pro-inflammatory mediator its receptor (PAFR) are upregulated in healing colonic wounds. We show epithelial the PAFR up-regulation is downstream TNF-α mediated signaling leading enhanced repair after PAF...
The intestinal mucosa is lined by a columnar epithelial monolayer that serves as dynamic interface, regulating barrier function and homeostasis. Perturbation of homeostasis, including changes in cell (IEC) proliferation migration, can give rise to pathological states ulcerative colitis cancer. Regulation migration complex process coordinated, part, signaling events emanating from tight junction proteins at cell-cell contacts. One protein has been linked regulation cellular Junctional...