
Assistant Professor
Diabetes Center
Email
We study how genes determine cellular decisions in energy metabolism, how organisms coordinate such decisions to maintain energy balance, and how new therapies might modulate these processes to treat diseases such as obesity, diabetes, sarcopenia, and cachexia. We apply genetics, biochemistry, and physiology—all driven by individual curiosity and diverse ways of thought.
Faculty Type
Affiliate Faculty
Publications
POLYCYSTIC OVARY SYNDROME: ORIGINS AND IMPLICATIONS: Gestational anti-Müllerian hormone and testosterone excess combined with maternal adiposity program for polycystic ovary syndrome.
Reproduction (Cambridge, England)
p38α kinase governs muscle strength through PGC1α in mice.
Acta physiologica (Oxford, England)
Development of a functional beige fat cell line uncovers independent subclasses of cells expressing UCP1 and the futile creatine cycle.
Cell metabolism
REPTOR and CREBRF encode key regulators of muscle energy metabolism.
Nature communications
Isolation of extracellular fluids reveals novel secreted bioactive proteins from muscle and fat tissues.
Cell metabolism
RBM43 links adipose inflammation and energy expenditure through translational regulation of PGC1a.
bioRxiv : the preprint server for biology
ATP Hydrolysis by the SNF2 Domain of Dnmt5 Is Coupled to Both Specific Recognition and Modification of Hemimethylated DNA.
Molecular cell
An Evolutionarily Conserved uORF Regulates PGC1α and Oxidative Metabolism in Mice, Flies, and Bluefin Tuna.
Cell metabolism
Noncanoncial signal recognition particle RNAs in a major eukaryotic phylum revealed by purification of SRP from the human pathogen Cryptococcus neoformans.
Nucleic Acids Research
Recognizing the enemy within: licensing RNA-guided genome defense.
Trends in biochemical sciences
The spliceosome as a transposon sensor.
RNA biology
Ers1 links HP1 to RNAi.
Proceedings of the National Academy of Sciences of the United States of America
Combinatorial, site-specific requirement for heterochromatic silencing factors in the elimination of nucleosome-free regions.
Genes & development
Erk1/2 MAP kinases are required for epidermal G2/M progression.
The Journal of Cell Biology
Mek1/2 MAPK kinases are essential for Mammalian development, homeostasis, and Raf-induced hyperplasia.
Developmental cell
Effects of active MEK1 expression in vivo.
Cancer letters
Mek1 alters epidermal growth and differentiation.
Cancer research
Address
513 Parnassus Avenue, HSW, Rm 1118
San Francisco, CA 94143
United States