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The Tumor Suppressor Par-4 Activates an Extrinsic Pathway for Apoptosis
TLDR
Interestingly, extracellular Par-4 induced apoptosis by binding to the stress response protein, glucose-regulated protein-78 (GRP78), expressed at the surface of cancer cells, and activates an extrinsic pathway involving cell surface GRP78 receptor for induction of apoptosis.
Identification of a Unique Core Domain of Par-4 Sufficient for Selective Apoptosis Induction in Cancer Cells
TLDR
A unique death-inducing domain selective for apoptosis induction in cancer cells (SAC domain) is identified which holds promise for identifying key differences between cancer and normal cells and for molecular therapy of cancer.
Binding and phosphorylation of par-4 by akt is essential for cancer cell survival.
TLDR
Par-4 is essential for PTEN-inducible apoptosis, and inactivation of Par-4 by Akt promotes cancer cell survival, suggesting that inhibition of the PI3K-Akt pathway leads to Par- 4-dependent apoptosis.
Par-4-dependent apoptosis by the dietary compound withaferin A in prostate cancer cells.
TLDR
As Par-4 up-regulation induces apoptosis in most tumor cells, the findings can be extended to high-throughput screens to identify synergistic combinations for both therapy-sensitive and therapy-resistant cancers.
Cancer resistance in transgenic mice expressing the SAC module of Par-4.
TLDR
Findings provide genetic evidence that the SAC domain of Par-4 confers cancer resistance in transgenic mice without compromising normal viability or aging, and may have therapeutic significance.
Suppression of PTEN expression is essential for antiapoptosis and cellular transformation by oncogenic Ras.
TLDR
Evidence is presented that oncogenic Ras suppresses the expression of the tumor suppressor phosphatase and tensin homologue deleted from chromosome 10 (PTEN) via the Raf-MEK-ERK-c-Jun pathway to induce antiapoptosis and cellular transformation, which identifies a novel molecular interface between the oncogens and tumor suppressors pathways that regulates cellular transformation and survival.
Lipopolysaccharide-induced liver apoptosis is increased in interleukin-10 knockout mice.
TLDR
In the livers of knockout mice, markedly increased caspase-3 activity was already evident at the 1-h time point following LPS administration, while in the wild type animals this increase was delayed, suggestive of an IL-10 anti-apoptotic effect.
A role for interleukin-10 in alcohol-induced liver sensitization to bacterial lipopolysaccharide.
TLDR
Alcohol-induced liver sensitization to LPS in wild-type mice may involve down-regulation of IL-10, a anti-inflammatory cytokine known for its hepatoprotective effects that is secreted simultaneously with proinflammatory cytokines.
Thyrotropin via Cyclic AMP Induces Insulin Receptor Expression and Insulin Co-stimulation of Growth and Amplifies Insulin and Insulin-like Growth Factor Signaling Pathways in Dog Thyroid Epithelial
TLDR
In dog thyroid cells, this allows low physiological insulin concentrations to act as a comitogenic factor and might explain in part the enhanced responsiveness to IGFs in response to TSH, raising the possibility that TSH-insulin interactions may play a role in the regulation of thyroid growth and function in vivo.
Novel mechanism of apoptosis resistance in cancer mediated by extracellular PAR-4.
TLDR
A novel intracellular pathway of apoptosis mediated by NF-κB through UACA elevation, which by attenuating endoplasmic reticulum stress and GRP78 translocation to the cell surface can blunt the sensitivity of cancer cells to apoptosis.
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