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ABT-888, an Orally Active Poly(ADP-Ribose) Polymerase Inhibitor that Potentiates DNA-Damaging Agents in Preclinical Tumor Models
TLDR
ABT-888 is a potent inhibitor of PARP, has good oral bioavailability, can cross the blood-brain barrier, and potentiates temozolomide, platinums, cyclophosphamide, and radiation in syngeneic and xenograft tumor models. Expand
Potent and selective inhibitors of Akt kinases slow the progress of tumors in vivo
TLDR
The development of a series of potent and selective indazole-pyridine based Akt inhibitors is reported, which inhibit Akt-dependent signal transduction in cells and in vivo in a dose-responsive manner and slow the progression of tumors when used as monotherapy or in combination with paclitaxel or rapamycin. Expand
Intravitreal injection of erythropoietin protects both retinal vascular and neuronal cells in early diabetes.
TLDR
Exogenous EPO administration by intravitreal injection in early diabetes may prevent retinal cell death and protect the BRB function and demonstrate that apoptosis is an major contributor to neuronal cell death in the early course of diabetic retinopathy (DR). Expand
Discovery of the Poly(ADP-ribose) polymerase (PARP) inhibitor 2-[(R)-2-methylpyrrolidin-2-yl]-1H-benzimidazole-4-carboxamide (ABT-888) for the treatment of cancer.
TLDR
Compound 3a is aqueous soluble, orally bioavailable across multiple species, and demonstrated good in vivo efficacy in a B16F10 subcutaneous murine melanoma model in combination with temozolomide (TMZ) and in an MX-1 breast cancer xenograft model in conjunction with either carboplatin or cyclophosphamide. Expand
Cadmium induction of reactive oxygen species activates the mTOR pathway, leading to neuronal cell death.
TLDR
The results indicate that Cd induction of ROS activates mTOR signaling, leading to neuronal cell death, in part by activating the positive regulators IGFR/PI3K and by inhibiting the negative regulators PTEN/AMPK. Expand
Potentiation of Temozolomide Cytotoxicity by Poly(ADP)Ribose Polymerase Inhibitor ABT-888 Requires a Conversion of Single-Stranded DNA Damages to Double-Stranded DNA Breaks
TLDR
It is shown that cells treated with temozolomide need to be exposed to ABT-888 for at least 17 to 24 hours to achieve maximal cytotoxicity, and the extent of cytot toxicity correlates with the level of double-stranded DNA breaks as indicated by γH2AX levels. Expand
Hydrogen peroxide-induced neuronal apoptosis is associated with inhibition of protein phosphatase 2A and 5, leading to activation of MAPK pathway.
TLDR
The findings suggest that inhibitors of MAPKs (JNK, Erk1/2 and p38), activators of phosphatases (PP2A and PP5) or antioxidants may have potentials to prevent and treat oxidative stress-induced neurodegenerative diseases. Expand
Hydrogen peroxide inhibits mTOR signaling by activation of AMPKα leading to apoptosis of neuronal cells
TLDR
It is shown that hydrogen peroxide induced apoptosis of neuronal cells by inhibiting the mammalian target of rapamycin (mTOR)-mediated phosphorylation of ribosomal p70 S6 kinase (S6K1) and eukaryotic initiation factor 4E (eIF4E)-binding protein 1 (4E-BP1), and that H2O2 inhibition of mTOR signaling is at least in part through activation of AMPK. Expand
Curcumin disrupts the Mammalian target of rapamycin-raptor complex.
TLDR
The data indicate that curcumin may represent a new class of mTOR inhibitor, andCurcumin was able to dissociate raptor from mTOR, leading to inhibition of m TORC1 activity. Expand
CaMKII is involved in cadmium activation of MAPK and mTOR pathways leading to neuronal cell death
J. Neurochem. (2011) 119, 1108–1118.
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