Andrew Brohl
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Andrew Brohl has a total of 13 co-authors. Here are the top co-authors by number of shared publications:
- Elsa R. Flores
Department of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA
1 shared publication - Goodwin G. Jinesh
Moffitt Cancer Center
1 shared publication - Isha Godwin
Department of Cardiothoracic Surgery Royal Brompton Hospital London United Kingdom
1 shared publication John Lockhart
Moffitt Cancer Center
1 shared publicationLing Cen
Moffitt Cancer Center
1 shared publicationMarco Napoli
Moffitt Cancer Center
1 shared publication
Latest Publications
- Open Access
- 31 October 2025
- Published by Springer Nature in Research Square
CEBPB, C19MC, and Defective Autophagy Drive Novel Podosomal Belt to Macropinocytosis Transition, Lipid Accumulation, and HBV A-to-I RNA-editing
Obesity and neurodegeneration are clinically associated diseases with defective autophagy. However, the genetic, biological, and metabolic underpinnings connecting these diseases are not well-understood. Here we identified a Mitochondria obesity/neurodegeneration (M on ) gene-signature that is shared between obesity, and neurodegenerative diseases. We demonstrate that, CEBPB elevates M on -gene-signature, to form podosomal belts, and enhance ROS production. Inhibiting autophagy collapses podosomal-belts through macropinocytosis to accumulate vacuoles, lipid-droplets, nuclear Notch-1 (nNICD), DEPTOR, and HBV-polymerase mRNAs. Conversely, hemin counteracts these events and suppresses DEPTOR and HBV-polymerase mRNAs by A-to-I-RNA-editing and nonsense-mediated decay. Furthermore, we CRISPR-engineered the antiviral chromosome-19 miRNA cluster (C19MC) to demonstrate that C19MC-miRNAs augment CEBPB, M on -gene-signature, ROS, and recapitulate CEBPB-driven phenotypes, in response to autophagy inhibition. Hemin, or a γ-Secretase inhibitor counteract these phenotypes in CRISPR-C19MC-engineered cells. Therefore, a CEBPB and C19MC-driven M on -gene-signature regulates the podosomal belt, lipid droplet, HBV, and DEPTOR mRNA dynamics to genetically link obesity, and neurodegeneration at the cellular level.
- 31 October 2025
- Published by Springer Nature in Research Square
Open AccessCEBPB, C19MC, and Defective Autophagy Drive Novel Podosomal Belt to Macropinocytosis Transition, Lipid Accumulation, and HBV A-to-I RNA-editing
Obesity and neurodegeneration are clinically associated diseases with defective autophagy. However, the genetic, biological, and metabolic underpinnings connecting these diseases are not well-understood. Here we identified a Mitochondria obesity/neurodegeneration (M on ) gene-signature that is shared between obesity, and neurodegenerative diseases. We demonstrate that, CEBPB elevates M on -gene-signature, to form podosomal belts, and enhance ROS production. Inhibiting autophagy collapses podosomal-belts through macropinocytosis to accumulate vacuoles, lipid-droplets, nuclear Notch-1 (nNICD), DEPTOR, and HBV-polymerase mRNAs. Conversely, hemin counteracts these events and suppresses DEPTOR and HBV-polymerase mRNAs by A-to-I-RNA-editing and nonsense-mediated decay. Furthermore, we CRISPR-engineered the antiviral chromosome-19 miRNA cluster (C19MC) to demonstrate that C19MC-miRNAs augment CEBPB, M on -gene-signature, ROS, and recapitulate CEBPB-driven phenotypes, in response to autophagy inhibition. Hemin, or a γ-Secretase inhibitor counteract these phenotypes in CRISPR-C19MC-engineered cells. Therefore, a CEBPB and C19MC-driven M on -gene-signature regulates the podosomal belt, lipid droplet, HBV, and DEPTOR mRNA dynamics to genetically link obesity, and neurodegeneration at the cellular level.