Ca2+, lipid second messenger and small GTPase signaling pathways; Control of cell polarity, chemotaxis, and collective migration as well as cell proliferation and differentiation decisions
email: tobias1 at stanford.edu
I am interested in understanding the precise molecular events that allow cells to transition from G1 to S phase and enter the cell cycle. Specifically, I use quantitative and systems-level approaches to study the roles of CDKs and the ubiquitin ligases APC and SCF in regulating the G1/S checkpoint
email: scappell at stanford.com
My research interests are understanding mTOR signaling and nutrient sensing from a global perspective as well as elucidating the mechanism of nutrient sensing at the molecular level.
email: lgan at stanford.edu
In order to migrate as a cohesive group, cells must coordinate their polarization signals, migratory direction and speed, maintenance of cell-cell junctions, and cytoskeletal activity all at both the single cell and group levels. I am interested in how cells within a group are able to achieve this remarkable level of coordination.
email: dgarbett at stanford.edu
Collective cell migration is required during development, for morphogenesis, and for repair following injury. Directional signals guiding collective cell movement are thought to be transmitted mechanically between cells via cell-cell junctions. Using monolayers of primary human endothelial cells (HUVEC) as a model system, I study how forces applied to the junction locally by one cell are sensed by its neighbor and converted into biochemical signals.
email: arnoldh at stanford.edu
The composition of the cellular lipid landscape is essential for the regulation of biological processes. Previously, the functional annotation of membrane lipids in macrophages led to the identification of lipid species differentially regulating receptor signaling. Cell migration and cell division are both fundamental processes that are precisely regulated by conserved signaling pathways combined with the availability of metabolites. My research is centered around the identification of metabolic pathways and specific metabolites regulating cell cycle progression and migration.
email: mkoeberlin at stanford.edu
I am interested in understanding how distinct chromatin modifications regulate the entry, exit, and maintenance of quiescence through control of both chromatin accessibility and site-specific transcriptional control of critical cell cycle genes.
email: lpack at stanford.edu
I am interested in understanding the signaling network in systems level. How signaling proteins induce signaling cascades, cross-regulate, and are correlated with each other.
email: heewony at stanford.edu
I study how asymmetry cytoskeleton organization promotes and maintains morphological and signaling polarity during cell migration. Specifically, I am interested in how the actin cortex and associated ERM proteins alter membrane tension.
email: abisaria at stanford.edu
The rate of cell division is largely dictated by the amount of time individual cells spend in a non-dividing state before entering a cycle of cell division. My research focuses on dissecting the signaling pathways regulating cell-cycle entry.
email: mingyuc at stanford.edu
My research focuses on how stochastic levels of endogenous cellular stress impact cell cycle dynamics and the proliferation decision.
email: ldaigh at stanford.edu
I study the transcriptional regulation of cellular quiescence and cell-cycle entry.
email: yilinfan at stanford.edu
Joint with the Wysocka lab
email: bgu1224 at stanford.edu
I am interested in understanding the mechanism underlying hysteresis in cell cycle entry.
email: chadliu at stanford.edu
I study regulatory dynamics at the G1/S transition, particularly how cells control DNA replication machinery in order to faithfully duplicate their genome.
email: nalinratnayeke at stanford.edu
email: jenniev at stanford.edu