Chang-Hyuk Kwon

mTor is required for hypertrophy of Pten-deficient neuronal soma in vivo.

Pten loss causes hypertrophy and increased proliferation of astrocytes in vivo.

Neuron-specific enolase-cre mouse line with cre activity in specific neuronal populations.

Pten regulates neuronal arborization and social interaction in mice.

A seizure-prone phenotype is associated with altered free-running rhythm in Pten mutant mice.

Neurofibromin is required for barrel formation in the mouse somatosensory cortex.

Pten haploinsufficiency accelerates formation of high-grade astrocytomas.

Neurotrophin-dependent dendritic filopodial motility: a convergence on PI3K signaling.

TrkB regulates hippocampal neurogenesis and governs sensitivity to antidepressive treatment.

Malignant astrocytomas originate from neural stem/progenitor cells in a somatic tumor suppressor mouse model.

Inducible site-specific recombination in neural stem/progenitor cells.

Pharmacological inhibition of mTORC1 suppresses anatomical, cellular, and behavioral abnormalities in neural-specific Pten knock-out mice.

Suppression of peroxiredoxin 4 in glioblastoma cells increases apoptosis and reduces tumor growth.

Cytomegalovirus infection leads to pleomorphic rhabdomyosarcomas in Trp53+/- mice.

Impairment of glioma stem cell survival and growth by a novel inhibitor for Survivin-Ran protein complex.

Cytomegalovirus contributes to glioblastoma in the context of tumor suppressor mutations.

Systemic delivery of SapC-DOPS has antiangiogenic and antitumor effects against glioblastoma.

MicroRNA-128 coordinately targets Polycomb Repressor Complexes in glioma stem cells.

Mutations in glioblastoma oncosuppressive pathways pave the way for oncomodulatory activity of cytomegalovirus.

Genetic Validation of the Protein Arginine Methyltransferase PRMT5 as a Candidate Therapeutic Target in Glioblastoma.

Genome-wide shRNA screen revealed integrated mitogenic signaling between dopamine receptor D2 (DRD2) and epidermal growth factor receptor (EGFR) in glioblastoma.

Genetic Modification of T Cells Redirected towards CS1 Enhances Eradication of Myeloma Cells.