About

Stacey Glasgow is the Principal Investigator of the Glasgow Lab. She earned her Ph.D. in Integrative Biology from UT Southwestern Medical Center under the mentorship of Dr. Jane E. Johnson. Following her doctoral studies, Stacey completed postdoctoral training with Dr. Benjamin Deneen at the Center for Cell and Gene Therapy at Baylor College of Medicine. She has been recognized with a K01 Mentored Research Scientist Development Award issued by the NIH/NCI, highlighting her contributions to research and her potential for future scientific leadership. Additionally, Dr. Glasgow was awarded the Hellman Fellowship in 2020. Her lab is supported by various funding sources including UCSD startup funds, the National Cancer Institute, and the NIH Mentored Research Scientist Development Award to Promote Diversity. The Glasgow Lab focuses on developmental biology and neuroscience, investigating key biological processes relevant to these fields.

Research topics

• Genetics
• Biology
• Neuroscience
• Bioinformatics
• Medicine
• Pathology

Selected publications

• A fetal oncogene NUAK2 is an emerging therapeutic target in glioblastoma

  2025-06-18

  dataset1st authorCorresponding
  PublisherDOI

• A fetal oncogene NUAK2 is an emerging therapeutic target in glioblastoma

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-01-02 · 2 citations

  preprintOpen accessSenior authorCorresponding

  ABSTRACT Glioblastoma Multiforme (GBM) is the most prevalent and highly malignant form of adult brain cancer characterized by poor overall survival rates. Effective therapeutic modalities remain limited, necessitating the search for novel treatments. Neurodevelopmental pathways have been implicated in glioma formation, with key neurodevelopmental regulators being re- expressed or co-opted during glioma tumorigenesis. Here we identified a serine/threonine kinase, NUAK family kinase 2 (NUAK2), as a fetal oncogene in mouse and human brains. We found robust expression of NUAK2 in the embryonic brain that decreases throughout postnatal stages and then is re-expressed in malignant gliomas. However, the role of NUAK2 in GBM tumorigenesis remains unclear. We demonstrate that CRIPSR-Cas9 mediated NUAK2 deletion in GBM cells results in suppression of proliferation, while overexpression leads to enhanced cell growth in both in vitro and in vivo models. Further investigation of the downstream biological processes dysregulated in the absence of NUAK2 reveals that NUAK2 modulates extracellular matrix (ECM) components to facilitate migratory behavior. Lastly, we determined that pharmaceutical inhibition of NUAK2 is sufficient to impede the proliferation and migration of malignant glioma cells. Our results suggest that NUAK2 is an actionable therapeutic target for GBM treatment.

  PublisherDOI

• Spinal motor neuron development and metabolism are transcriptionally regulated by nuclear factor IA

  Science Advances · 2025-08-01 · 1 citations

  articleOpen accessSenior authorCorresponding

  Neural circuits governing all motor behaviors in vertebrates rely on the proper development of motor neurons and their precise targeting of limb muscles. Transcription factors are essential for motor neuron development, regulating their specification, migration, and axonal targeting. While transcriptional regulation of the early stages of motor neuron specification is well established, much less is known about the role of transcription factors in the later stages of maturation and muscle targeting. Defining the molecular mechanisms of these later stages is critical for elucidating how motor circuits are constructed. Here, we demonstrate that the transcription factor nuclear factor IA (NFIA) is required for motor neuron positioning, axonal branching, and neuromuscular junction formation. Moreover, we find that NFIA is required for proper mitochondrial function and adenosine triphosphate production, providing an important link between transcription factors and metabolism during motor neuron development. Together, these findings underscore the critical role of NFIA in instructing the assembly of spinal circuits for movement.

  PublisherDOI

• A fetal oncogene NUAK2 is an emerging therapeutic target in glioblastoma

  EMBO Molecular Medicine · 2025-08-06

  articleOpen accessSenior author

  Glioblastoma Multiforme (GBM) is a highly malignant brain cancer with limited effective therapies. Neurodevelopmental pathways have been implicated in glioma formation, with key neurodevelopmental regulators being re-expressed or co-opted during glioma tumorigenesis. Here we identified a serine/threonine kinase, NUAK family kinase 2 (NUAK2), as a fetal oncogene in mouse and human brains. We found robust expression of NUAK2 in the embryonic brain that decreases throughout postnatal stages and then is re-expressed in malignant gliomas. However, the role of NUAK2 in GBM tumorigenesis remains unclear. We demonstrate that CRIPSR-Cas9 mediated NUAK2 deletion in GBM cells results in suppression of proliferation, while overexpression leads to enhanced cell growth in both in vitro and in vivo models. Further investigation of the downstream biological processes dysregulated in the absence of NUAK2 reveals that NUAK2 modulates extracellular matrix (ECM) components to facilitate migratory behavior. Lastly, we determined that pharmaceutical inhibition of NUAK2 is sufficient to impede the proliferation and migration of malignant glioma cells. Our results suggest that NUAK2 is an actionable therapeutic target for GBM treatment.

  PublisherOA PDFDOI

• Spinal motor neuron development and metabolism are transcriptionally regulated by Nuclear Factor IA

  bioRxiv (Cold Spring Harbor Laboratory) · 2024 · 1 citations

  Senior authorCorresponding
  • Biology
  • Neuroscience
  • Genetics

  Neural circuits governing all motor behaviors in vertebrates rely on the proper development of motor neurons and their precise targeting of limb muscles. Transcription factors are essential for motor neuron development, regulating their specification, migration, and axonal targeting. While transcriptional regulation of the early stages of motor neuron specification is well-established, much less is known about the role of transcription factors in the later stages of maturation and terminal arborization. Defining the molecular mechanisms of these later stages is critical for elucidating how motor circuits are constructed. Here, we demonstrate that the transcription factor Nuclear Factor-IA (NFIA) is required for motor neuron positioning, axonal branching, and neuromuscular junction formation. Moreover, we find that NFIA is required for proper mitochondrial function and ATP production, providing a new and important link between transcription factors and metabolism during motor neuron development. Together, these findings underscore the critical role of NFIA in instructing the assembly of spinal circuits for movement.

  PublisherOA PDFDOI

• The Role of Neurodevelopmental Pathways in Brain Tumors

  Frontiers in Cell and Developmental Biology · 2021 · 67 citations

  Senior authorCorresponding
  • Neuroscience
  • Biology
  • Bioinformatics

  Disruptions to developmental cell signaling pathways and transcriptional cascades have been implicated in tumor initiation, maintenance and progression. Resurgence of aberrant neurodevelopmental programs in the context of brain tumors highlights the numerous parallels that exist between developmental and oncologic mechanisms. A deeper understanding of how dysregulated developmental factors contribute to brain tumor oncogenesis and disease progression will help to identify potential therapeutic targets for these malignancies. In this review, we summarize the current literature concerning developmental signaling cascades and neurodevelopmentally-regulated transcriptional programs. We also examine their respective contributions towards tumor initiation, maintenance, and progression in both pediatric and adult brain tumors and highlight relevant differentiation therapies and putative candidates for prospective treatments.

  PublisherOA PDFDOI

• Nuclear factor I-A regulates diverse reactive astrocyte responses after CNS injury

  Journal of Clinical Investigation · 2019-09-08 · 79 citations

  articleOpen access

  Reactive astrocytes are associated with every form of neurological injury. Despite their ubiquity, the molecular mechanisms controlling their production and diverse functions remain poorly defined. Because many features of astrocyte development are recapitulated in reactive astrocytes, we investigated the role of nuclear factor I-A (NFIA), a key transcriptional regulator of astrocyte development whose contributions to reactive astrocytes remain undefined. Here, we show that NFIA is highly expressed in reactive astrocytes in human neurological injury and identify unique roles across distinct injury states and regions of the CNS. In the spinal cord, after white matter injury (WMI), NFIA-deficient astrocytes exhibit defects in blood-brain barrier remodeling, which are correlated with the suppression of timely remyelination. In the cortex, after ischemic stroke, NFIA is required for the production of reactive astrocytes from the subventricular zone (SVZ). Mechanistically, NFIA directly regulates the expression of thrombospondin 4 (Thbs4) in the SVZ, revealing a key transcriptional node regulating reactive astrogenesis. Together, these studies uncover critical roles for NFIA in reactive astrocytes and illustrate how region- and injury-specific factors dictate the spectrum of reactive astrocyte responses.

  PublisherOA PDFDOI

• A glial blueprint for gliomagenesis

  Nature reviews. Neuroscience · 2018-05-18 · 144 citations

  reviewOpen access
  PublisherOA PDFDOI

• Pancreatic Cell Fate Determination Relies on Notch Ligand Trafficking by NFIA

  Cell Reports · 2018-12-01 · 20 citations

  articleOpen access

  Notch is activated globally in pancreatic progenitors; however, for progenitors to differentiate into endocrine cells, they must escape Notch activation to express Neurogenin-3. Here, we find that the transcription factor nuclear factor I/A (NFIA) promotes endocrine development by regulating Notch ligand Dll1 trafficking. Pancreatic deletion of NFIA leads to cell fate defects, with increased duct and decreased endocrine formation, while ectopic expression promotes endocrine formation in mice and human pancreatic progenitors. NFIA-deficient mice exhibit dysregulation of trafficking-related genes including increased expression of Mib1, which acts to target Dll1 for endocytosis. We find that NFIA binds to the Mib1 promoter, with loss of NFIA leading to an increase in Dll1 internalization and enhanced Notch activation with rescue of the cell fate defects after Mib1 knockdown. This study reveals NFIA as a pro-endocrine factor in the pancreas, acting to repress Mib1, inhibit Dll1 endocytosis and thus promote escape from Notch activation.

  PublisherOA PDFDOI

• lnc’edin to Myelin

  Neuron · 2017-01-01 · 2 citations

  articleOpen access1st author
  PublisherOA PDFDOI

Recent grants

• The Sox9/NFIA Transcriptional Network In Malignant Glioma

  NIH · $702k · 2015–2020

Frequent coauthors

• Benjamin Deneen

  Baylor College of Medicine

  33 shared

• Malgorzata Borowiak

  Adam Mickiewicz University in Poznań

  16 shared

• Jolanta Chmielowiec

  University of Zielona Góra

  16 shared

• Katrina Wamble

  Baylor College of Medicine

  16 shared

• Hyun Kyoung Lee

  Texas Children's Hospital

  8 shared

• Lita Duraine

  Baylor College of Medicine

  8 shared

• David H. Rowitch

  University of Cambridge

  7 shared

• Lesley Chaboub

  University of Pennsylvania

  7 shared

Labs

• Glasgow LabPI

  Not provided

Awards & honors

• K01 Mentored Research Scientist Development Award issued by…