Lloyd A. Greene

Nerve growth factor selectively regulates expression of transcripts encoding ribosomal proteins.

Nerve growth factor (NGF) down-regulates the Bcl-2 homology 3 (BH3) domain-only protein Bim and suppresses its proapoptotic activity by phosphorylation.

The basic region and leucine zipper transcription factor MafK is a new nerve growth factor-responsive immediate early gene that regulates neurite outgrowth.

Endoplasmic reticulum stress and the unfolded protein response in cellular models of Parkinson's disease.

POSH acts as a scaffold for a multiprotein complex that mediates JNK activation in apoptosis.

Regulated expression of ATF5 is required for the progression of neural progenitor cells to neurons.

Malignant pheochromocytoma: current status and initiatives for future progress.

B-myb and C-myb play required roles in neuronal apoptosis evoked by nerve growth factor deprivation and DNA damage.

Highly efficient small interfering RNA delivery to primary mammalian neurons induces MicroRNA-like effects before mRNA degradation.

Analysis of gene expression changes in a cellular model of Parkinson disease.

Regulation of neuron survival and death by p130 and associated chromatin modifiers.

Downregulation of activating transcription factor 5 is required for differentiation of neural progenitor cells into astrocytes.

ATF5 regulates the proliferation and differentiation of oligodendrocytes.

CHOP/GADD153 is a mediator of apoptotic death in substantia nigra dopamine neurons in an in vivo neurotoxin model of parkinsonism.

Bim is a direct target of a neuronal E2F-dependent apoptotic pathway.

Puma and p53 play required roles in death evoked in a cellular model of Parkinson disease.

Siah1 interacts with the scaffold protein POSH to promote JNK activation and apoptosis.

Regulation of apoptotic c-Jun N-terminal kinase signaling by a stabilization-based feed-forward loop.

You can't go home again: transcriptionally driven alteration of cell signaling by NGF.

Activation of the apoptotic JNK pathway through the Rac1-binding scaffold protein POSH.

Direct interaction of the molecular scaffolds POSH and JIP is required for apoptotic activation of JNKs.

RTP801 is elevated in Parkinson brain substantia nigral neurons and mediates death in cellular models of Parkinson's disease by a mechanism involving mammalian target of rapamycin inactivation.

Proapoptotic Nix activates the JNK pathway by interacting with POSH and mediates death in a Parkinson disease model.

Cell cycle molecules define a pathway required for neuron death in development and disease.

Bim is elevated in Alzheimer's disease neurons and is required for beta-amyloid-induced neuronal apoptosis.

The transcription factor ATF5 is widely expressed in carcinomas, and interference with its function selectively kills neoplastic, but not nontransformed, breast cell lines.

Pro-apoptotic Bim induction in response to nerve growth factor deprivation requires simultaneous activation of three different death signaling pathways.

Identification of POSH2, a novel homologue of the c-Jun N-terminal kinase scaffold protein POSH.

Glucagon-like peptide-1 (GLP-1) diminishes neuronal degeneration and death caused by NGF deprivation by suppressing Bim induction.

The transcription factor ATF5: role in neurodevelopment and neural tumors.

RTP801 is induced in Parkinson's disease and mediates neuron death by inhibiting Akt phosphorylation/activation.

Cell death pathways in Parkinson's disease: proximal triggers, distal effectors, and final steps.

Identification of a novel DNA binding site and a transcriptional target for activating transcription factor 5 in c6 glioma and mcf-7 breast cancer cells.

Cbl negatively regulates JNK activation and cell death.

Rapamycin protects against neuron death in in vitro and in vivo models of Parkinson's disease.

Sertad1 plays an essential role in developmental and pathological neuron death.

RTP801/REDD1 regulates the timing of cortical neurogenesis and neuron migration.

Gata2 is required for migration and differentiation of retinorecipient neurons in the superior colliculus.

Akt as a victim, villain and potential hero in Parkinson's disease pathophysiology and treatment.

Reciprocal actions of ATF5 and Shh in proliferation of cerebellar granule neuron progenitor cells.

Sh3rf2/POSHER Protein Promotes Cell Survival by Ring-mediated Proteasomal Degradation of the c-Jun N-terminal Kinase Scaffold POSH (Plenty of SH3s) Protein.