A5066641861- Cellular Mechanics and Interactions
- Neurofibromatosis and Schwannoma Cases
- Neuroblastoma Research and Treatments
- Sarcoma Diagnosis and Treatment
- Axon Guidance and Neuronal Signaling
- Reflective Practices in Education
- Signaling Pathways in Disease
- Wound Healing and Treatments
- Blood properties and coagulation
- Genetics, Aging, and Longevity in Model Organisms
- Chromatin Remodeling and Cancer
- Erythrocyte Function and Pathophysiology
- 14-3-3 protein interactions
- Lipid Membrane Structure and Behavior
- Nerve injury and regeneration
- Glioma Diagnosis and Treatment
Cincinnati Children's Hospital Medical Center
2020-2022
University of Cincinnati
2020-2022
Kent State University
2017-2019
To define alterations early in tumor formation, we studied nerve tumors neurofibromatosis 1 (NF1), a predisposition syndrome. Affected individuals develop neurofibromas, benign driven by NF1 loss Schwann cells (SCs). By comparing normal to plexiform neurofibroma (PN) using single-cell and bulk RNA sequencing, identified changes 5 SC populations, including de novo progenitor–like (SCP-like) population. Long after Nf1 loss, populations developed PN-specific expression of Dcn, Postn, Cd74, with...
Plexiform neurofibromas are benign nerve sheath Schwann cell tumors characterized by biallelic mutations in the neurofibromatosis type 1 (NF1) tumor suppressor gene. Atypical show additional frequent loss of CDKN2A/Ink4a/Arf and may be precursor lesions aggressive malignant peripheral (MPNST). Here we combined Nf1 developing cells with global Ink4a/Arf identified paraspinal plexiform atypical neurofibromas. Upon transplantation, generated genetically engineered mice (GEM)-PNST similar to...
ABSTRACT Receptor for activated C kinase 1 (RACK1) is a multifunctional ribosomal scaffolding protein that can interact with multiple signaling molecules concurrently through its seven WD40 repeats. We recently found RACK1 localized to mammalian growth cones, prompting an investigation into role during neural development. Here, we show the first time localizes point contacts within mouse cortical cones. Point are adhesion sites link actin network cones extracellular matrix, and necessary...
Abstract Local translation regulates the formation of appropriate connectivity in developing nervous system. However, localization and molecular mechanisms underlying this within growth cones is not well understood. Receptor for activated C kinase 1 (RACK1) a multi-functional ribosomal scaffolding protein that interacts with β-actin mRNA. We recently showed RACK1 localizes to point contacts, which are adhesion sites control cone motility. This suggests local occurs at these important axonal...
<div>Abstract<p>Plexiform neurofibromas are benign nerve sheath Schwann cell tumors characterized by biallelic mutations in the neurofibromatosis type 1 (NF1) tumor suppressor gene. Atypical show additional frequent loss of CDKN2A/Ink4a/Arf and may be precursor lesions aggressive malignant peripheral (MPNST). Here we combined Nf1 developing cells with global Ink4a/Arf identified paraspinal plexiform atypical neurofibromas. Upon transplantation, generated genetically engineered...
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<p>Figure S1</p>
<div>Abstract<p>Plexiform neurofibromas are benign nerve sheath Schwann cell tumors characterized by biallelic mutations in the neurofibromatosis type 1 (NF1) tumor suppressor gene. Atypical show additional frequent loss of CDKN2A/Ink4a/Arf and may be precursor lesions aggressive malignant peripheral (MPNST). Here we combined Nf1 developing cells with global Ink4a/Arf identified paraspinal plexiform atypical neurofibromas. Upon transplantation, generated genetically engineered...
Abstract Plexiform neurofibromas (PN) are benign nerve sheath Schwann cell tumors, which occur in at least 50% of individuals with loss function mutations the NF1 tumor suppressor gene, an off signal for RAS-GTPases. Tumors form, part, through activation RAS-MAPK pathway cells. Though benign, PN can cause significant morbidity and often inoperable due to integration vital peripheral nerves. Recent clinical trials have shown that MEK inhibition shrink most PN, but continued is required...