Professor, Pathology, University of Virginia School of Medicine
Pathology
Dr. Dennis J. Templeton, MD
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Doctor Dennis J. Templeton, MD works in the field of Pathology. He attended University of California San Diego School of Medicine. University of California San Diego School of Medicine is ranked 17/19 in Research/PrimaryCare. He over the years received 1 awards: "Regional Top Doctor". Doctor Dennis J. Templeton, MD has written publications. He has 61 publications published with PubMed. The lastest paper is: 'Paclitaxel (Taxol)-induced gene expression and cell death are both mediated by the activation of c-Jun NH2-terminal kinase (JNK/SAPK).'
Publications
- Macrophage migration inhibitory factor promotes tumor growth and metastasis by inducing myeloid-derived suppressor cells in the tumor microenvironment.
- Sulforaphane inhibits prostaglandin e2 synthesis by suppressing microsomal prostaglandin e synthase 1.
- PICquant: a quantitative platform to measure differential peptide abundance using dual-isotopic labeling with 12C6- and 13C6-phenyl isocyanate.
- JNK-mediated phosphorylation of Cdc25C regulates cell cycle entry and G(2)/M DNA damage checkpoint.
- MAZIE: a mass and charge inference engine to enhance database searching of tandem mass spectra.
- Purification of reversibly oxidized proteins (PROP) reveals a redox switch controlling p38 MAP kinase activity.
- Urokinase directly activates matrix metalloproteinases-9: a potential role in glioblastoma invasion.
- Regulation of signal transduction through protein cysteine oxidation.
- A second-site suppressor strategy for chemical genetic analysis of diverse protein kinases.
- Keap1 is a redox-regulated substrate adaptor protein for a Cul3-dependent ubiquitin ligase complex.
- Thiol oxidation of cell signaling proteins: Controlling an apoptotic equilibrium.
- Functional implications of antiestrogen induction of quinone reductase: inhibition of estrogen-induced deoxyribonucleic acid damage.
- Reactive quinones differentially regulate SAPK/JNK and p38/mHOG stress kinases.
- Mutation causing premature termination of the polyoma virus medium T antigen blocks cell transformation.
- Nonfunctional mutants of the retinoblastoma protein are characterized by defects in phosphorylation, viral oncoprotein association, and nuclear tethering.
- Reconstitution of novel signalling cascades responding to cellular stresses.
- Construction and expression of a recombinant DNA gene encoding a polyomavirus middle-size tumor antigen with the carboxyl terminus of the vesicular stomatitis virus gl...
- Functional interactions between the retinoblastoma (Rb) protein and Sp-family members: superactivation by Rb requires amino acids necessary for growth suppression.
- N-terminal amino acid sequences of the polyoma middle-size T antigen are important for protein kinase activity and cell transformation.
- Ras stimulates DNA topoisomerase II alpha through MEK: a link between oncogenic signaling and a therapeutic target.
- Interaction between c-Rel and the mitogen-activated protein kinase kinase kinase 1 signaling cascade in mediating kappaB enhancer activation.
- Reduced CTLA-4 protein and messenger RNA expression in umbilical cord blood T lymphocytes.
- Deficiency of transporter for antigen presentation (TAP) in tumor cells allows evasion of immune surveillance and increases tumorigenesis.
- Cell cycle-dependent localization of the CDK2-cyclin E complex in Cajal (coiled) bodies.
- The human retinoblastoma susceptibility gene promoter is positively autoregulated by its own product.
- Activation of SAPK/JNK by TNF receptor 1 through a noncytotoxic TRAF2-dependent pathway.
- Mechanisms involved in stimulation of human immunodeficiency virus type 1 replication by aminooxypentane RANTES.
- Safety-modified episomal vectors for human gene therapy.
- Protein kinases: getting NEKed for S6K activation.
- The cyclin box and C-terminus of cyclins A and E specify CDK activation and substrate specificity.
- The role of c-Jun N-terminal kinase (JNK) in apoptosis induced by ultraviolet C and gamma radiation. Duration of JNK activation may determine cell death and proliferat...
- Identification of the major autophosphorylation sites of Nyk/Mer, an NCAM-related receptor tyrosine kinase.
- G1 cyclins control the retinoblastoma gene product growth regulation activity via upstream mechanisms.
- Detection of a novel cell cycle-regulated kinase activity that associates with the amino terminus of the retinoblastoma protein in G2/M phases.
- Paclitaxel (Taxol)-induced gene expression and cell death are both mediated by the activation of c-Jun NH2-terminal kinase (JNK/SAPK).
- Mammalian mitogen-activated protein kinase pathways are regulated through formation of specific kinase-activator complexes.
- Raf, but not MEK or ERK, is sufficient for differentiation of hippocampal neuronal cells.
- Comparative studies of a new subfamily of human Ste20-like kinases: homodimerization, subcellular localization, and selective activation of MKK3 and p38.
- Functional interactions between herpesvirus oncoprotein MEQ and cell cycle regulator CDK2.
- Differential activation of MAP kinase signaling pathways and nuclear factor-kappaB in bronchoalveolar cells of smokers and nonsmokers.
- Quinone reductase (NQO1), a sensitive redox indicator, is increased in Alzheimer''s disease.
- Induction of cyclooxygenase-2 by the activated MEKK1 --> SEK1/MKK4 --> p38 mitogen-activated protein kinase pathway.
- Nuclear binding of purified retinoblastoma gene product is determined by cell cycle-regulated phosphorylation.
- Induction of mitogen-activated protein kinase phosphatase 1 by the stress-activated protein kinase signaling pathway but not by extracellular signal-regulated kinase i...
- Identification of 2 serine residues of MEK-1 that are differentially phosphorylated during activation by raf and MEK kinase.
- Regulation of the activity of MEK kinase 1 (MEKK1) by autophosphorylation within the kinase activation domain.
- Constitutive activation of S6 kinase by deletion of amino-terminal autoinhibitory and rapamycin sensitivity domains.
- Sphingolipid metabolites differentially regulate extracellular signal-regulated kinase and stress-activated protein kinase cascades.
- Biological function of the retinoblastoma protein requires distinct domains for hyperphosphorylation and transcription factor binding.
- Activation of stress-activated protein kinase by MEKK1 phosphorylation of its activator SEK1.
- Amino acid-induced translation of TOP mRNAs is fully dependent on phosphatidylinositol 3-kinase-mediated signaling, is partially inhibited by rapamycin, and is indepen...
- Osmotic stress inhibits p70/85 S6 kinase through activation of a protein phosphatase.
- Fas-induced proteolytic activation and intracellular redistribution of the stress-signaling kinase MEKK1.
- Quinone reductase inhibitors block SAPK/JNK and NFkappaB pathways and potentiate apoptosis.
- S6 phosphorylation-independent pathways regulate translation of 5''-terminal oligopyrimidine tract-containing mRNAs in differentiating hematopoietic cells.
- SAPK/JNK regulates cdc2/cyclin B kinase through phosphorylation and inhibition of cdc25c.
- The isothiocyanate class of bioactive nutrients covalently inhibit the MEKK1 protein kinase.
- Oxidative stress inhibits MEKK1 by site-specific glutathionylation in the ATP-binding domain.
- Characterization of the human polymeric immunoglobulin receptor (PIGR) 3''UTR and differential expression of PIGR mRNA during colon tumorigenesis.
- Nutrient isothiocyanates covalently modify and inhibit the inflammatory cytokine macrophage migration inhibitory factor (MIF).
Schools
University of California At San Diego
New England Deaconess Hospital
Doctors Specialties
- Anatomic Pathology
- Pathology
Accepted Insurances
Awards
- Regional Top Doctor
Education
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Beth Israel Deaconess Medical Center -
University of California San Diego School of Medicine
Hospital
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University of Virginia Medical Center
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