Physician
Pathology
Dr. Jay M. McDonald, MD
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Doctor Jay M. McDonald, MD practices Pathology. He studied medicine at Wayne State University School of Medicine. Wayne State University School of Medicine has a rank of 63 in research and a 85 in primary care He received 1 awards: "Elected Member". Jay M. McDonald is a published doctor as well. He has 61 publications published. The latest was: Characterization of Calmodulin-Fas Death Domain Interaction: An Integrated Experimental and Computational Study.
Publications
- Characterization of Calmodulin-Fas Death Domain Interaction: An Integrated Experimental and Computational Study.
- PARP-1 Regulates Resistance of Pancreatic Cancer to TRAIL Therapy.
- Structural insight for the roles of fas death domain binding to FADD and oligomerization degree of the fas - FADD complex in the death inducing signaling complex forma...
- The Dark Side of Publishing: Promoting Ethics in AJP 2003 to 2008.
- Reduced CaM/FLIP binding by a single point mutation in c-FLIP(L) modulates Fas-mediated apoptosis and decreases tumorigenesis.
- Calmodulin mediates FAS-induced FADD-independent survival signaling in pancreatic cancer cells via activation of Src-ERK.
- Trifluoperazine regulation of calmodulin binding to Fas: A computational study.
- Nucleosides accelerate inflammatory osteolysis, acting as distinct innate immune activators.
- Tamoxifen enhances therapeutic effects of gemcitabine on cholangiocarcinoma tumorigenesis.
- Disorders of bone remodeling.
- Calmodulin-an often-ignored signal in osteoclasts.
- Free fatty acids enhance breast cancer cell migration through plasminogen activator inhibitor-1 and SMAD4.
- Molecular mechanisms of tamoxifen therapy for cholangiocarcinoma: role of calmodulin.
- Calcium/calmodulin-dependent kinase II regulates notch-1 signaling in prostate cancer cells.
- Conformation and free energy analyses of the complex of calcium-bound calmodulin and the Fas death domain.
- Phospholipase Cgamma2 mediates RANKL-stimulated lymph node organogenesis and osteoclastogenesis.
- Oxidative stress induces vascular calcification through modulation of the osteogenic transcription factor Runx2 by AKT signaling.
- Solution structure of a calmodulin-binding domain in the carboxy-terminal region of HIV type 1 gp160.
- Calmodulin binding to the Fas-mediated death-inducing signaling complex in cholangiocarcinoma cells.
- Conditional disruption of calcineurin B1 in osteoblasts increases bone formation and reduces bone resorption.
- Future developments in therapy.
- Osteoblast and osteoclast differentiation in modeled microgravity.
- A matter of trust: introducing the journal scientific integrity policy.
- Cyclosporin A elicits dose-dependent biphasic effects on osteoblast differentiation and bone formation.
- Fas-mediated apoptosis in cholangiocarcinoma cells is enhanced by 3,3'-diindolylmethane through inhibition of AKT signaling and FLICE-like inhibitory protein.
- Modulation of osteoclastogenesis induced by nucleoside reverse transcriptase inhibitors.
- Pathogenesis of osteopenia/osteoporosis induced by highly active anti-retroviral therapy for AIDS.
- NFATc1: a novel anabolic therapeutic target for osteoporosis.
- Point mutations in the C-terminus of HIV-1 gp160 reduce apoptosis and calmodulin binding without affecting viral replication.
- Calmodulin is a critical regulator of osteoclastic differentiation, function, and survival.
- RhoA and cytoskeletal disruption mediate reduced osteoblastogenesis and enhanced adipogenesis of human mesenchymal stem cells in modeled microgravity.
- Fas binding to calmodulin regulates apoptosis in osteoclasts.
- Regulators of apoptosis in cholangiocarcinoma.
- Calmodulin and calmodulin-dependent kinase IIalpha regulate osteoblast differentiation by controlling c-fos expression.
- RANKL regulates Fas expression and Fas-mediated apoptosis in osteoclasts.
- Osteoclastogenesis: the role of calcium and calmodulin.
- Modeled microgravity disrupts collagen I/integrin signaling during osteoblastic differentiation of human mesenchymal stem cells.
- AZT enhances osteoclastogenesis and bone loss.
- Modeled microgravity inhibits osteogenic differentiation of human mesenchymal stem cells and increases adipogenesis.
- Calmodulin binding to the Fas death domain. Regulation by Fas activation.
- Notch signaling and ERK activation are important for the osteomimetic properties of prostate cancer bone metastatic cell lines.
- Osteoclast apoptosis: the role of Fas in vivo and in vitro.
- The combination of calmodulin antagonists and interferon-gamma induces apoptosis through caspase-dependent and -independent pathways in cholangiocarcinoma cells.
- The role of calmodulin in the regulation of osteoclastogenesis.
- A new Editor-in-Chief's view toward the future.
- Effects of cyclosporine on osteoclast activity: inhibition of calcineurin activity with minimal effects on bone resorption and acid transport activity.
- Regulation of the formation of osteoclastic actin rings by proline-rich tyrosine kinase 2 interacting with gelsolin.
- IFN-gammaupregulates apoptosis-related molecules and enhances Fas-mediated apoptosis in human cholangiocarcinoma.
- Tamoxifen (TMX)/Fas induced growth inhibition of human cholangiocarcinoma (HCC) by gamma interferon (IFN-gamma).
- Guidelines and recommendations for laboratory analysis in the diagnosis and management of diabetes mellitus.
- Expression of transcription factor E2F1 and telomerase in glioblastomas: mechanistic linkage and prognostic significance.
- Epidermal growth factor receptor variant III status defines clinically distinct subtypes of glioblastoma.
- A multigene predictor of outcome in glioblastoma.
- Elevated phospho-S6 expression is associated with metastasis in adenocarcinoma of the lung.
- Dominant inhibition of Fas ligand-mediated apoptosis due to a heterozygous mutation associated with autoimmune lymphoproliferative syndrome (ALPS) Type Ib.
- Calmodulin binding to cellular FLICE-like inhibitory protein modulates Fas-induced signalling.
- Survivin promoter-based conditionally replicative adenoviruses target cholangiocarcinoma.
- Microgravity: the immune response and bone.
- Reciprocal co-expression of Fas and Fas ligand in human cholangiocarcinoma.
- Modeled microgravity and hindlimb unloading sensitize osteoclast precursors to RANKL-mediated osteoclastogenesis.
Schools
Wayne State University School Of Medicine
Oregon
Wayne State University Affil Hospital
Washington University
Doctors Specialties
- Pathology
Accepted Insurances
- MultiPlan PPO
- PHCS Network PPO
Awards
- Elected Member
Education
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Washington University - Barnes-Jewish Hospital -
Oregon Health & Science University -
Wayne State University School of Medicine
Hospital
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Birmingham Veterans Affairs Medical Center
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