Lijuan He

Pathogenic activation of receptor tyrosine kinases in mammalian membranes.

Increased expression of the integral membrane protein ErbB2 in Chinese hamster ovary cells expressing the anti-apoptotic gene Bcl-xL.

Physical basis behind achondroplasia, the most common form of human dwarfism.

Specific inhibition of a pathogenic receptor tyrosine kinase by its transmembrane domain.

FGFR3 heterodimerization in achondroplasia, the most common form of human dwarfism.

High-throughput selection of transmembrane sequences that enhance receptor tyrosine kinase activation.

Physical-chemical principles underlying RTK activation, and their implications for human disease.

Effect of the G375C and G346E achondroplasia mutations on FGFR3 activation.

Production of plasma membrane vesicles with chloride salts and their utility as a cell membrane mimetic for biophysical characterization of membrane protein interactions.

Consequences of replacing EGFR juxtamembrane domain with an unstructured sequence.

Strong dimerization of wild-type ErbB2/Neu transmembrane domain and the oncogenic Val664Glu mutant in mammalian plasma membranes.

Quantification of the effects of mutations on receptor tyrosine kinase (RTK) activation in mammalian cells.

Switching from protease-independent to protease-dependent cancer cell invasion.

Three-dimensional matrix fiber alignment modulates cell migration and MT1-MMP utility by spatially and temporally directing protrusions.

Local 3D matrix confinement determines division axis through cell shape.

Collective cancer cell invasion induced by coordinated contractile stresses.