Physician
Endocrinology
Dr. Paul M. Yen, MD
Paul M. Yen works in the field of Endocrinology. He went to Johns Hopkins University School of Medicine. Johns Hopkins University School of Medicine is one of the top medical schools in the US. Johns Hopkins University School of Medicine has a rank of 3 in research and a 29 in primary care Paul M. Yen is a published doctor as well. He has 34 publications published. The latest was: Interactions of estrogen- and thyroid hormone receptors on a progesterone receptor estrogen response element (ERE) sequence: a comparison with the vitellogenin A2 cons...
Publications
- Adjunctive β2-agonist treatment reduces glycogen independently of receptor-mediated acid α-glucosidase uptake in the limb muscles of mice with Pompe disease.
- Classification and proposed nomenclature for inherited defects of thyroid hormone action, cell transport, and metabolism.
- Differential AMPK phosphorylation by glucagon and metformin regulates insulin signaling in human hepatic cells.
- Studies of molecular mechanisms associated with increased deiodinase 3 expression in a case of consumptive hypothyroidism.
- Epigallocatechin-3-gallate (EGCG), a green tea polyphenol, stimulates hepatic autophagy and lipid clearance.
- Resveratrol induces insulin gene expression in mouse pancreatic alpha-cells.
- Dynamic exchange at regulatory elements during chromatin remodeling underlies assisted loading mechanism.
- Negative regulation of TSHalpha target gene by thyroid hormone involves histone acetylation and corepressor complex dissociation.
- New insights into thyroid hormone action.
- The rat thyroid hormone receptor (TR) Deltabeta3 displays cell-, TR isoform-, and thyroid hormone response element-specific actions.
- Thyroid hormones and 3,5-diiodothyropropionic acid: new keys for new locks.
- Thyroid hormone-regulated target genes have distinct patterns of coactivator recruitment and histone acetylation.
- Thyroid hormone action at the cellular, genomic and target gene levels.
- Protein synthesis inhibitors and the chemical chaperone TMAO reverse endoplasmic reticulum perturbation induced by overexpression of the iodide transporter pendrin.
- Molecular basis of resistance to thyroid hormone.
- Effects of ligand and thyroid hormone receptor isoforms on hepatic gene expression profiles of thyroid hormone receptor knockout mice.
- Transgenic targeting of a dominant negative corepressor to liver and analyses by cDNA microarray.
- Extreme thyroid hormone resistance in a patient with a novel truncated TR mutant.
- The glucocorticoid receptor interacting protein 1 (GRIP1) localizes in discrete nuclear foci that associate with ND10 bodies and are enriched in components of the 26S ...
- Interactions of estrogen- and thyroid hormone receptors on a progesterone receptor estrogen response element (ERE) sequence: a comparison with the vitellogenin A2 cons...
- Immunohistochemical expression of retinoid X receptor isoforms in human pituitaries and pituitary adenomas.
- Mutant and wild-type androgen receptors exhibit cross-talk on androgen-, glucocorticoid-, and progesterone-mediated transcription.
- Estrogen and thyroid hormone interaction on regulation of gene expression.
- Molecular cloning and properties of a full-length putative thyroid hormone receptor coactivator.
- The peroxisome proliferator-activated receptor alpha is a phosphoprotein: regulation by insulin.
- The isoform-specific expression of the tri-iodothyronine receptor in osteoblasts and osteoclasts.
- Vitamin D receptors repress basal transcription and exert dominant negative activity on triiodothyronine-mediated transcriptional activity.
- T3 or not T3--the slings and arrows of outrageous TR function.
- Region-specific anti-thyroid hormone receptor (TR) antibodies detect changes in TR structure due to ligand-binding and dimerization.
- Roles of 3,5,3'-triiodothyronine and deoxyribonucleic acid binding on thyroid hormone receptor complex formation.
- In vitro transcriptional studies of the roles of the thyroid hormone (T3) response elements and minimal promoters in T3-stimulated gene transcription.
- Roles of v-erbA homodimers and heterodimers in mediating dominant negative activity by v-erbA.
- Phosphorylation selectively increases triiodothyronine receptor homodimer binding to DNA.
Schools
Johns Hopkins University School of Medicine
University Chicago Hosps
National Institute Of Health
Doctors Specialties
- Endocrinology
Accepted Insurances
Education
-
National Institutes of Health Clinical Center -
University of Chicago -
Johns Hopkins University School of Medicine
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