# overview
The goal of our research is to understand the molecular mechanisms that control NF-kappaB regulatory networks in the central nervous system (CNS). NF-kappaB is a ubiquitously expressed, evolutionarily conserved transcription factor that responds to a variety of signals and regulates fundamental processes, including cell growth and proliferation, inflammation, invasion and angiogenesis. Indeed, aberrant NF-kappaB activity or expression is associated with many cancers, as it can promote tumorigenesis, tumor progression and resistance to therapy. Our focus is on glioblastoma, a common and highly lethal CNS tumor that is very resistant to current treatment strategies.

# keywords[]
5 Development Of Treatments And Therapeutic Interventions

# keywords[]
3201 Cardiovascular Medicine And Haematology

# keywords[]
1.1 Normal Biological Development And Functioning

# keywords[]
1.1 Normal Biological Development And Functioning

# keywords[]
Positive Regulatory Domain I-binding Factor 1

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Intracellular Signaling Peptides And Proteins

# keywords[]
Glutamate Plasma Membrane Transport Proteins

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

# educationAndTraining[].organization.label
University of North Carolina at Chapel Hill - (Chapel Hill, North Carolina, United States)

# educationAndTraining[].organization.label
Columbia University - (New York, New York, United States)

# publications[].label
NON-CANONICAL NF-B SIGNALING DRIVES THE AGGRESSIVE INVASIVENESS OF GLIOBLASTOMA

# publications[].label
Transcriptional Induction of NF-kB-Inducing Kinase by E2F4/5 Facilitates Collective Invasion of Glioma Cells.

# publications[].label
A genetic analysis of glucocorticoid receptor signaling. Identification and characterization of ligand-effect modulators in Saccharomyces cerevisiae.

# publications[].label
NF-kappaB mediates inhibition of mesenchymal cell differentiation through a posttranscriptional gene silencing mechanism.

# publications[].label
Ex Vivo Blockade of NF-[dappa]B Signaling in Alloreactive T Cells Prevents Murine Graft-Versus-Host Disease (GVHD).

# publications[].label
NF-B-Inducing Kinase (NIK) Governs the Mitochondrial Respiratory Capacity, Differentiation, and Inflammatory Status of Innate Immune Cells

# publications[].label
NIK promotes metabolic adaptation of glioblastoma cells to bioenergetic stress.

# publications[].label
Erratum: Nuclear factor-B is an important modulator of the altered gene expression profile and malignant phenotype in squamous cell carcinoma (Cancer Research (September 2004) 64 (6511-6523)

# publications[].label
NF-B-Inducing Kinase Maintains Mitochondrial Efficiency and Systemic Metabolic Homeostasis

# publications[].label
Transcriptional induction of NF-B-inducing kinase by E2F4/5 facilitates collective invasion of GBM cells.

# publications[].label
Targeting NF-B-Inducing Kinase (NIK) in Immunity, Inflammation, and Cancer.

# publications[].label
Nuclear factor-kappaB is an important modulator of the altered gene expression profile and malignant phenotype in squamous cell carcinoma.

# publications[].publisher
American Association for Cancer Research (AACR)

# publications[].label
NF-kappaB-dependent and - independent roles for NIK in regulating GBM cell invasion

# publications[].publisher
American Association for Cancer Research (AACR)

# publications[].label
Ex vivo inhibition of NF-kappaB signaling in alloreactive T-cells prevents graft-versus-host disease.

# publications[].label
Conjugation of Dasatinib with MHI-148 Has a Significant Advantageous Effect in Viability Assays for Glioblastoma Cells.

# publications[].label
NIK regulates MT1-MMP activity and promotes glioma cell invasion independently of the canonical NF-B pathway.

# publications[].label
Cyanine-Gemcitabine Conjugates as Targeted Theranostic Agents for Glioblastoma Tumor Cells.

# publications[].label
Erratum: Inhibition of acute graft-versus-host disease with retention of graft-versus-tumor effects by the proteasome inhibitor bortezomib (Proceedings of the National Academy of Sciences of the United States of America (May 25, 2004) 101, 21 (8120-8125))

# publications[].label
Inhibition of acute graft-versus-host disease with retention of graft-versus-tumor effects by the proteasome inhibitor bortezomib.

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

# publications[].label
NF-B-inducing kinase maintains mitochondrial efficiency and systemic metabolic homeostasis.

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

# publications[].publisher
The American Association of Immunologists

# publications[].label
IKK-dependent, NF-B-independent control of autophagic gene expression.

# publications[].label
Topographic organization of sensory projections to the olfactory bulb.

# publications[].label
Essential role for epidermal growth factor receptor in glutamate receptor signaling to NF-kappaB.

# publications[].label
Loss of epithelial RelA results in deregulated intestinal proliferative/apoptotic homeostasis and susceptibility to inflammation.

# publications[].publisher
The American Association of Immunologists

# publications[].label
NIK/MAP3K14 Regulates Mitochondrial Dynamics and Trafficking to Promote Cell Invasion.

# publications[].label
Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) promotes glioma cell invasion through induction of NF-B-inducing kinase (NIK) and noncanonical NF-B signaling.

# publications[].label
The NF-B RelB protein is an oncogenic driver of mesenchymal glioma.

# publications[].label
Blimp-1/PRDM1 mediates transcriptional suppression of the NLR gene NLRP12/Monarch-1.

# publications[].publisher
The American Association of Immunologists

# publications[].label
Positive and negative regulation of EAAT2 by NF-kappaB: a role for N-myc in TNFalpha-controlled repression.

# researcherOn[].label
Investigating Novel Functions for NIK/MAP3K14 in High-Grade Glioma

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

# researcherOn[].awardedBy.preferredLabel
DHHS-NIH-National Institute of Neurological Disorders and Stroke

# researcherOn[].label
Cyanine-Conjugated Kinase Inhibitors (Cy-KIs) as Potential Glioblastoma Theranostics

# researcherOn[].awardedBy.label
Cancer Prevention and Research Institute of Texas - (Austin, Texas, United States)

# researcherOn[].label
Novel roles for NIK in high-grade glioma: regulation of mitochondrial dynamics to control cell migration and invasion

# researcherOn[].awardedBy.label
Cancer Prevention and Research Institute of Texas - (Austin, Texas, United States)

# researcherOn[].label
NIK Promotes a Leader Cell Phenotype in Glioma

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

# researcherOn[].awardedBy.preferredLabel
DHHS-NIH-National Institute of Neurological Disorders and Stroke

# streetAddress
8447 Riverside Pkwy, MREB II, rm 4348; Department of Cell Biology & Genetics; Texas A&M University School of Medicine,1359 TAMUS

# etdChairOf[].label
McFadden, Kassandra Nicole (2018-12). NF-kB Inducing Kinase (NIK) Is an Inducer of Glioma Invasion. Master's Thesis.

# etdChairOf[].label
Keeney, Justin N. (2023-07). NF-kB Inducing Kinase (NIK) Drives Metabolic Reprogramming of Myeloid Cells in Immunity and Cancer. Doctoral Dissertation.

# etdChairOf[].label
Jung, Jiung (2018-05). NIK, a Novel Regulator of Mitochondrial Dynamics and Invasion in High-Grade Glioma. Doctoral Dissertation.

# etdChairOf[].label
Kamradt, Michael Leo (2021-01). NIK/MAP3K14 IS A BIOENERGETIC STRESS SENSOR AND PROMOTER OF OXIDATIVE PHOSPHORYLATION. Doctoral Dissertation.

# etdChairOf[].label
Pflug, Kathryn M (2021-11). NF-?B-Inducing Kinase Regulation of Development, Metabolism, and Disease. Doctoral Dissertation.

# etdChairOf[].label
Cherry, Evan Michael (2017-01). Noncanonical NF-?B Signaling in Glioma is Activated by TWEAK and Promotes Invasion. Doctoral Dissertation.