Devin Bready
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View article: Modulation of GPR133 (ADGRD1) signaling by its intracellular interaction partner extended synaptotagmin 1
Modulation of GPR133 (ADGRD1) signaling by its intracellular interaction partner extended synaptotagmin 1 Open
GPR133 (ADGRD1) is an adhesion G-protein-coupled receptor that signals through Gαs/cyclic AMP (cAMP) and is required for the growth of glioblastoma (GBM), an aggressive brain malignancy. The regulation of GPR133 signaling is incompletely u…
View article: The expression profile and tumorigenic mechanisms of CD97 (ADGRE5) in glioblastoma render it a targetable vulnerability
The expression profile and tumorigenic mechanisms of CD97 (ADGRE5) in glioblastoma render it a targetable vulnerability Open
Glioblastoma (GBM) is the most common and aggressive primary brain malignancy. Adhesion G protein-coupled receptors (aGPCRs) have attracted interest for their potential as treatment targets. Here, we show that CD97 (ADGRE5) is the most pro…
View article: The expression profile and tumorigenic mechanisms of CD97 (ADGRE5) in glioblastoma render it a targetable vulnerability
The expression profile and tumorigenic mechanisms of CD97 (ADGRE5) in glioblastoma render it a targetable vulnerability Open
SUMMARY Glioblastoma (GBM) is the most common and aggressive primary brain malignancy. Adhesion G protein-coupled receptors (aGPCRs) have attracted interest for their functional role in gliomagenesis and their potential as treatment target…
View article: PTK7 is a positive allosteric modulator of GPR133 signaling in glioblastoma
PTK7 is a positive allosteric modulator of GPR133 signaling in glioblastoma Open
The adhesion G-protein-coupled receptor GPR133 (ADGRD1) supports growth of the brain malignancy glioblastoma. How the extracellular interactome of GPR133 in glioblastoma modulates signaling remains unknown. Here, we use affinity proteomics…
View article: Modulation of GPR133 (ADGRD1) Signaling by its Intracellular Interaction Partner Extended Synaptotagmin 1 (ESYT1)
Modulation of GPR133 (ADGRD1) Signaling by its Intracellular Interaction Partner Extended Synaptotagmin 1 (ESYT1) Open
Summary GPR133 (ADGRD1) is an adhesion G protein-coupled receptor that signals through Gαs and is required for growth of glioblastoma (GBM), an aggressive brain malignancy. The regulation of GPR133 signaling is incompletely understood. Her…
View article: TMET-19. DEFINING A NOVEL ROLE FOR CD97 IN REGULATING GBM GLYCOLYTIC METABOLISM
TMET-19. DEFINING A NOVEL ROLE FOR CD97 IN REGULATING GBM GLYCOLYTIC METABOLISM Open
Glioblastoma (GBM) is the most common and aggressive primary brain malignancy. Despite multimodal therapy, disease recurrence is inevitable. To identify novel vulnerabilities of GBM, we performed an arrayed CRISPR/Cas9 screen against selec…
View article: PTK7 is a positive allosteric modulator of GPR133 (ADGRD1) signaling in GBM
PTK7 is a positive allosteric modulator of GPR133 (ADGRD1) signaling in GBM Open
GPR133 (ADGRD1), an adhesion G protein-coupled receptor, supports growth of glioblastoma, a brain malignancy. We demonstrated that GPR133 is intramolecularly cleaved, and that dissociation of its N-terminal and C-terminal fragments (NTF an…
View article: CSIG-05. DISSOCIATION OF THE INTRAMOLECULARLY CLEAVED N- AND C-TERMINAL FRAGMENTS OF ADHESION G PROTEIN-COUPLED RECEPTOR GPR133 (ADGRD1) INCREASES ITS CANONICAL SIGNALING IN GLIOBLASTOMA
CSIG-05. DISSOCIATION OF THE INTRAMOLECULARLY CLEAVED N- AND C-TERMINAL FRAGMENTS OF ADHESION G PROTEIN-COUPLED RECEPTOR GPR133 (ADGRD1) INCREASES ITS CANONICAL SIGNALING IN GLIOBLASTOMA Open
We previously demonstrated that GPR133 (ADGRD1), an adhesion GPCR that signals via cytosolic cAMP increase, is de novo expressed in glioblastoma (GBM) and enriched in patient-derived glioblastoma stem cells. Knockdown of GPR133 reduces GBM…
View article: CSIG-07. ACTIVATION OF THE ADHESION G PROTEIN-COUPLED RECEPTOR GPR133 BY ANTIBODIES AGAINST THE N-TERMINUS
CSIG-07. ACTIVATION OF THE ADHESION G PROTEIN-COUPLED RECEPTOR GPR133 BY ANTIBODIES AGAINST THE N-TERMINUS Open
We recently demonstrated that GPR133 (ADGRD1), a member of the adhesion G protein-coupled receptor (aGPCR) family, is necessary for growth of glioblastoma (GBM) and is de novo expressed in GBM relative to normal brain tissue. We therefore …
View article: CBIO-05. SOX2 CHROMATIN ARCHITECTURE AND ENHANCER ACTIVITY IN THE MAINTENANCE AND DEVELOPMENT OF NEURAL STEM CELLS
CBIO-05. SOX2 CHROMATIN ARCHITECTURE AND ENHANCER ACTIVITY IN THE MAINTENANCE AND DEVELOPMENT OF NEURAL STEM CELLS Open
Gain of function mutations in isocitrate dehydrogenase I (IDH1) result in the formation of the oncometabolite 2-hydroxyglutarate (2HG) in adult lower grade gliomas. To gain insight into mechanisms of gliomagenesis, our lab previously creat…
View article: The H3K36me2 writer-reader dependency in H3K27M-DIPG
The H3K36me2 writer-reader dependency in H3K27M-DIPG Open
The H3K36me2 histone modification pathway is an acquired dependency in H3K27M mutant diffuse intrinsic pontine glioma (DIPG).
View article: The H3K36me2 writer-reader dependency in H3K27M-DIPG
The H3K36me2 writer-reader dependency in H3K27M-DIPG Open
The lysine-to-methionine mutation at residue 27 of histone H3 (H3K27M) is a driving mutation in Diffuse Intrinsic Pontine Glioma (DIPG), a highly aggressive form of pediatric brain tumor with no effective treatment and little chance of sur…
View article: Functional impact of intramolecular cleavage and dissociation of adhesion G protein–coupled receptor GPR133 (ADGRD1) on canonical signaling
Functional impact of intramolecular cleavage and dissociation of adhesion G protein–coupled receptor GPR133 (ADGRD1) on canonical signaling Open
GPR133 (ADGRD1), an adhesion G protein-coupled receptor (GPCR) whose canonical signaling activates GαS-mediated generation of cytosolic cAMP, has been shown to be necessary for the growth of glioblastoma (GBM), a brain malignancy. The extr…
View article: Dissociation of the intramolecularly cleaved N- and C-terminal fragments of the adhesion G protein-coupled receptor GPR133 (ADGRD1) increases canonical signaling
Dissociation of the intramolecularly cleaved N- and C-terminal fragments of the adhesion G protein-coupled receptor GPR133 (ADGRD1) increases canonical signaling Open
SUMMARY GPR133 (ADGRD1), an adhesion G protein-coupled receptor (GPCR), is necessary for growth of glioblastoma (GBM), a brain malignancy. The extracellular N-terminus of GPR133 is thought to be autoproteolytically cleaved into an N-termin…
View article: Expression profiling of the adhesion G protein-coupled receptor GPR133 (ADGRD1) in glioma subtypes
Expression profiling of the adhesion G protein-coupled receptor GPR133 (ADGRD1) in glioma subtypes Open
Background Glioma is a family of primary brain malignancies with limited treatment options and in need of novel therapies. We previously demonstrated that the adhesion G protein-coupled receptor GPR133 (ADGRD1) is necessary for tumor growt…
View article: CSIG-21. DE-ORPHANIZING GPR133 - AN ADHESION GPCR REQUIRED FOR GLIOBLASTOMA PROGRESSION
CSIG-21. DE-ORPHANIZING GPR133 - AN ADHESION GPCR REQUIRED FOR GLIOBLASTOMA PROGRESSION Open
We previously found GPR133 (ADGRD1), an orphan adhesion GPCR, is de novo expressed in glioblastoma (GBM) and enriched in patient-derived glioblastoma stem cells (GSCs). Knockdown of GPR133 reduces GBM cell proliferation and tumorsphere for…
View article: STEM-17. LOW GRADE ASTROCYTOMA MUTATIONS COOPERATE TO DISRUPT SOX2 GENOMIC ARCHITECTURE AND BLOCK DIFFERENTIATION VIA PREVIOUSLY UNIDENTIFIED ENHANCER ELEMENTS
STEM-17. LOW GRADE ASTROCYTOMA MUTATIONS COOPERATE TO DISRUPT SOX2 GENOMIC ARCHITECTURE AND BLOCK DIFFERENTIATION VIA PREVIOUSLY UNIDENTIFIED ENHANCER ELEMENTS Open
Neomorphic mutations in isocitrate dehydrogenase I (IDH1) result in the formation of the oncometabolite 2-hydroxyglutarate (2HG) in a significant subset of gliomas and other tumors including acute myeloid leukemias. Preclinical evidence su…
View article: Mutant Isocitrate Dehydrogenase Inhibitors as Targeted Cancer Therapeutics
Mutant Isocitrate Dehydrogenase Inhibitors as Targeted Cancer Therapeutics Open
The identification of heterozygous neomorphic isocitrate dehydrogenase (IDH) mutations across multiple cancer types including both solid and hematologic malignancies has revolutionized our understanding of oncogenesis in these malignancies…
View article: Molecular Pathogenesis of Low-Grade Glioma
Molecular Pathogenesis of Low-Grade Glioma Open
Advances in genome sequencing have elucidated the genetics of low-grade glioma. Available evidence indicates a neomorphic mutation in isocitrate dehydrogenase (IDH) initiates gliomagenesis. Mutant IDH produces the oncometabolite 2-hydroxyg…
View article: Native RNA sequencing on nanopore arrays redefines the transcriptional complexity of a viral pathogen
Native RNA sequencing on nanopore arrays redefines the transcriptional complexity of a viral pathogen Open
Viral genomes exhibit a higher gene density and more diversified transcriptome than the host cell. Coding potential is maximized through the use of multiple reading frames, placement of genes on opposing strands, inefficient or modified us…
View article: Exogenous Gene Transmission of Isocitrate Dehydrogenase 2 Mimics Ischemic Preconditioning Protection
Exogenous Gene Transmission of Isocitrate Dehydrogenase 2 Mimics Ischemic Preconditioning Protection Open
Ischemic preconditioning confers organ-wide protection against subsequent ischemic stress. A substantial body of evidence underscores the importance of mitochondria adaptation as a critical component of cell protection from ischemia. To id…
View article: Low-Grade Astrocytoma Mutations in IDH1, P53, and ATRX Cooperate to Block Differentiation of Human Neural Stem Cells via Repression of SOX2
Low-Grade Astrocytoma Mutations in IDH1, P53, and ATRX Cooperate to Block Differentiation of Human Neural Stem Cells via Repression of SOX2 Open
Low-grade astrocytomas (LGAs) carry neomorphic mutations in isocitrate dehydrogenase (IDH) concurrently with P53 and ATRX loss. To model LGA formation, we introduced R132H IDH1, P53 shRNA, and ATRX shRNA into human neural stem cells (NSCs)…
View article: 378. Isocitrate Dehydrogenase 2 Overexpression Ameliorates Ischemia Reperfusion Injury to the Kidney
378. Isocitrate Dehydrogenase 2 Overexpression Ameliorates Ischemia Reperfusion Injury to the Kidney Open
Acute Kidney Injury (AKI) is a significant contributor to morbidity and mortality, affecting 35% of critical care patients and 7% of hospital admissions nationwide. Furthermore, the 60 day mortality rate for AKI patients requiring renal re…