Metabolic Fuel Choice:
Causes and Consequences in Health and Disease
Welcome to the Danial Lab
Our lab investigates the metabolic mechanisms that regulate cellular and organismal adaptation to physiologic and pathologic stress conditions. Within this context, we study fundamental aspects of metabolic biology, including causes and consequences of cellular fuel utilization patterns and how processing of carbon substrates translates into specific metabolic signals
that shape cell fate and function. To this end, we apply multi-disciplinary approaches that
draw on biochemistry, mouse models, mitochondrial physiology, chemical biology, proteomics and metabolomics. This research program has led to advances in understanding anabolic
and catabolic mechanisms that link altered cellular fuel usage and nutrient
signaling to diseases such as cancer, diabetes and seizure disorders.
Our Mission Statement
We believe in a research culture that promotes the highest standard of scientific rigor
and integrity, encourages effective communication and feedback, nurtures inclusion and collaboration, and helps trainees overcome limiting beliefs and practice resilience.
We value mentoring and being mentored as we strive for scientific innovation and excellence.
By following these guiding principles, we provide a fertile ground for training the
next generation of scientists, educators, innovators, entrepreneurs and leaders.
Glucose-Dependent Partitioning of Arginine to the Urea Cycle Protects
ꞵ-cells from Inflammation
is linked to diverse disease processes,
but the intrinsic mechanisms that determine cellular sensitivity to inflammation are incompletely understood.
Metabolic Signatures Uncover Distinct Targets in Molecular Subsets of Diffuse Large B Cell Lymphoma
Molecular signatures have identiﬁed several subsets of diffuse large B cell lymphoma (DLBCL) and rational targets within the
B cell receptor
(BCR) signaling axis.
HCF-1 Regulates De Novo Lipogenesis through a Nutrient-Sensitive Complex with ChREBP
Carbohydrate response element binding protein (ChREBP) is a key transcriptional regulator of de novo lipogenesis (DNL) in response to
in hepatic steatosis.
BAD-Dependent Regulation of Fuel Metabolism and KATP Channel Activity
Confers Resistance to Epileptic Seizures
can be substantially modulated by alterations in metabolism, as evident from the anticonvulsant effect of diets that reduce glucose utilization and promote ketone body metabolism.
“The true sign of intelligence is not knowledge but imagination.”