Professor, Internal Medicine, University of Michigan Medical School
Endocrinology
Dr. Peter Arvan, MD
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Peter Arvan, MD works in the field of Endocrinology. He went to Yale University School of Medicine. Yale University School of Medicine is a one of the best medicals schools. Yale University School of Medicine has a rank of 7 in research and a 57 in primary care He received 2 awards: "CMS Meaningful Use Stage 1 Certification" and "Elected Member". Peter Arvan is also published. He has 101 publications published. The lastest publication: "A single amino acid change in the acetylcholinesterase-like domain of thyroglobulin causes congenital goiter with hypothyroidism in the cog/cog mouse: a model of human...' Peter Arvan accepts all Medicare patients.
Publications
- Monitoring C-Peptide Storage and Secretion in Islet β-Cells In Vitro and In Vivo.
- Thyroglobulin From Molecular and Cellular Biology to Clinical Endocrinology.
- Pancreatic β-Cell Adaptive Plasticity in Obesity Increases Insulin Production but Adversely Affects Secretory Function.
- Competitive Inhibition of the Endoplasmic Reticulum Signal Peptidase by Non-cleavable Mutant Preprotein Cargos.
- Proinsulin misfolding and endoplasmic reticulum stress during the development and progression of Diabetes☆
- Molecular aspects of pancreatic beta cell failure and Diabetes.
- INS-gene mutations: from genetics and beta cell biology to clinical Disease.
- Defective Transport of the Obesity Mutant PC1/3 N222D Contributes to Loss of Function.
- Inefficient Translocation of Preproinsulin Contributes to Pancreatic Beta Cell Failure and Late Onset Diabetes.
- Endoplasmic Reticulum Oxidoreductin-1alpha (Ero1alpha) Improves Folding and Secretion of Mutant Proinsulin and Limits Mutant Proinsulin-Induced ER Stress.
- Neuroendocrinology: Regulated secretory cells go to the BAR for a bud.
- UDP-glucose:glycoprotein glucosyltransferase (UGGT1) promotes substrate solubility in the endoplasmic reticulum.
- Proinsulin Intermolecular Interactions During Secretory Trafficking in Pancreatic Beta Cells.
- Islet autoantigens: structure, function, localization, and regulation.
- How does type 1 Diabetes develop?: the notion of homicide or β-cell suicide revisited.
- New insights into thyroglobulin pathophysiology revealed by the study of a family With congenital goiter.
- Protein sorting and secretion granule formation in regulated secretory cells.
- Transient aggregation of nascent thyroglobulin in the endoplasmic reticulum: relationship to the molecular chaperone, BiP.
- Protein targeting via the "constitutive-like" secretory pathway in isolated pancreatic islets: passive sorting in the immature granule compartment.
- Protein discharge from immature secretory granules displays both regulated and constitutive characteristics.
- Regulated and constitutive protein targeting can be distinguished by secretory polarity in Thyroid epithelial cells.
- Folding and assembly of newly synthesized thyroglobulin occurs in a pre-Golgi compartment.
- Phasic release of newly synthesized secretory proteins in the unstimulated rat exocrine pancreas.
- Relative lack of ATP-driven H+ translocase activity in isolated parotid secretory granules.
- Isolated secretion granules from parotid glands of chronically stimulated rats possess an alkaline internal pH and inward-directed H+ pump activity.
- Similarities and differences among neuroendocrine, exocrine, and endocytic vesicles.
- Protein production and secretion in exocrine cells.
- Constitutive protein secretion from the exocrine pancreas of fetal rats.
- Plasma membrane of the rat parotid gland: preparation and partial characterization of a fraction containing the secretory surface.
- Osmotic properties and internal pH of isolated rat parotid secretory granules.
- Secretory membranes of the rat parotid gland: preparation and comparative characterization.
- Intracellular transport of proinsulin in pancreatic beta-cells. Structural maturation probed by disulfide accessibility.
- Calnexin and BiP act as sequential molecular chaperones during thyroglobulin folding in the endoplasmic reticulum.
- Polarized distribution and delivery of plasma membrane proteins in Thyroid follicular epithelial cells.
- Distinct molecular mechanisms for protein sorting Within immature secretory granules of pancreatic beta-cells.
- Formation of the insulin-containing secretory granule core occurs Within immature beta-granules.
- Hormonal regulation of thyroglobulin export from the endoplasmic reticulum of cultured thyrocytes.
- Intracellular iodination of thyroglobulin in filter-polarized thyrocytes leads to the synthesis and basolateral secretion of Thyroid hormone.
- Disulfide-linked aggregation of thyroglobulin normally occurs during nascent protein folding.
- Polarized secretion of thrombospondin is opposite to thyroglobulin in Thyroid epithelial cells.
- An endoplasmic reticulum storage disease causing congenital goiter with hypoThyroidism.
- Oligomeric assembly of thrombospondin in the endoplasmic reticulum of Thyroid epithelial cells.
- Congenital hypoThyroid goiter with deficient thyroglobulin. Identification of an endoplasmic reticulum storage disease with induction of molecular chaperones.
- Intracellular protein transport to the thyrocyte plasma membrane: potential implications for Thyroid physiology.
- Differential sorting of lysosomal enzymes out of the regulated secretory pathway in pancreatic beta-cells.
- Thyroglobulin transport along the secretory pathway. Investigation of the role of molecular chaperone, GRP94, in protein export from the endoplasmic reticulum.
- Polarized apical targeting directed by the signal/anchor region of simian virus 5 hemagglutinin-neuraminidase.
- Enhanced binding to the molecular chaperone BiP slows thyroglobulin export from the endoplasmic reticulum.
- Mannose 6-phosphate receptors are sorted from immature secretory granules via adaptor protein AP-1, clathrin, and syntaxin 6-positive vesicles.
- Endocrinopathies in the family of endoplasmic reticulum (ER) storage diseases: Disorders of protein trafficking and the role of ER molecular chaperones.
- Sorting and storage during secretory granule biogenesis: looking backward and looking forward.
- A single amino acid change in the acetylcholinesterase-like domain of thyroglobulin causes congenital goiter with hypoThyroidism in the cog/cog mouse: a model of human...
- Polarized targeting of epithelial cell proteins in thyrocytes and MDCK cells.
- Disruption of disulfide bonds exhibits differential effects on trafficking of regulated secretory proteins.
- Disease models provide insights into post-golgi protein trafficking, localization and processing.
- Protein traffic from the secretory pathway to the endosomal system in pancreatic beta-cells.
- Proinsulin endoproteolysis confers enhanced targeting of processed insulin to the regulated secretory pathway.
- Cell type-dependent differences in Thyroid peroxidase cell surface expression.
- Secretion, gamma-carboxylation, and endoplasmic reticulum-associated degradation of chimeras With mutually exchanged Gla domain between human protein C and prothrombin.
- Endoplasmic reticulum (ER)-associated degradation of misfolded N-linked glycoproteins is suppressed upon inhibition of ER mannosidase I.
- Thyroglobulin is selected as luminal protein cargo for apical transport via detergent-resistant membranes in epithelial cells.
- Caveolin-1 binding to endoplasmic reticulum membranes and entry into the regulated secretory pathway are regulated by serine phosphorylation. Protein sorting at the le...
- Intracellular retention of newly synthesized insulin in yeast is caused by endoproteolytic processing in the Golgi complex.
- MAL mediates apical transport of secretory proteins in polarized epithelial Madin-Darby canine kidney cells.
- Polarized trafficking of thyrocyte proteins in MDCK cells.
- Secretory pathway quality control operating in Golgi, plasmalemmal, and endosomal systems.
- Lumenal protein multimerization in the distal secretory pathway/secretory granules.
- Folding of thyroglobulin in the calnexin/calreticulin pathway and its alteration by loss of Ca2+ from the endoplasmic reticulum.
- Behavior in the eukaryotic secretory pathway of insulin-containing fusion proteins and single-chain insulins bearing various B-chain mutations.
- Role of the connecting peptide in insulin biosynthesis.
- The trafficking of alpha 1-antitrypsin, a post-Golgi secretory pathway marker, in INS-1 pancreatic beta cells.
- Sorting ourselves out: seeking consensus on trafficking in the beta-cell.
- Syntaxin-6 SNARE involvement in secretory and endocytic pathways of cultured pancreatic beta-cells.
- The acetylcholinesterase homology region is essential for normal conformational maturation and secretion of thyroglobulin.
- Secretory protein trafficking: genetic and biochemical analysis.
- Deficiency of ATP2C1, a Golgi ion pump, induces secretory pathway defects in endoplasmic reticulum (ER)-associated degradation and sensitivity to ER stress.
- Proinsulin disulfide maturation and misfolding in the endoplasmic reticulum.
- Intracellular trafficking of Thyroid peroxidase to the cell surface.
- Mixed-disulfide folding intermediates between thyroglobulin and endoplasmic reticulum resident oxidoreductases ERp57 and protein disulfide isomerase.
- Defective thyroglobulin storage in LDL receptor-associated protein-deficient mice.
- Lumenal protein sorting to the constitutive secretory pathway of a regulated secretory cell.
- A conserved histidine in insulin is required for the foldability of human proinsulin: structure and function of an ALAB5 analog.
- Protein disulfide isomerase-like proteins play opposing roles during retrotranslocation.
- A role for Lte1p (a low temperature essential protein involved in mitosis) in proprotein processing in the yeast secretory pathway.
- Oxidoreductase interactions include a role for ERp72 engagement With mutant thyroglobulin from the rdw/rdw rat dwarf.
- Structural features of vps35p involved in interaction With other subunits of the retromer complex.
- Proinsulin maturation, misfolding, and proteotoxicity.
- Dominant-negative behavior of mammalian Vps35 in yeast requires a conserved PRLYL motif involved in retromer assembly.
- Defective protein folding and intracellular retention of thyroglobulin-R19K mutant as a cause of human congenital Goiter.
- Endoplasmic reticulum (ER) chaperone regulation and survival of cells compensating for deficiency in the ER stress response kinase, PERK.
- Seven mutations in the human insulin gene linked to permanent neonatal/infancy-onset Diabetes mellitus.
- The cholinesterase-like domain of thyroglobulin functions as an intramolecular chaperone.
- Single-chain insulins as receptor agonists.
- The cholinesterase-like domain, essential in thyroglobulin trafficking for Thyroid hormone synthesis, is required for protein dimerization.
- Insulin storage and glucose homeostasis in mice null for the granule zinc transporter ZnT8 and studies of the type 2 Diabetes-associated variants.
- Targeted induction of endoplasmic reticulum stress induces cartilage pathology.
- Crystal structure of a "nonfoldable" insulin: impaired folding efficiency despite native activity.
- Misfolded proinsulin affects bystander proinsulin in neonatal Diabetes.
- Contribution of residue B5 to the folding and function of insulin and IGF-I: constraints and fine-tuning in the evolution of a protein family.
- Cis and trans actions of the cholinesterase-like domain Within the thyroglobulin dimer.
Schools
Yale University School Of Medicine
Procedures Preformed
- Continuous Glucose Monitoring
Conditions Treated
- Abnormal Thyroid
- Acromegaly and Gigantism
- Adrenal Insufficiency
- Calcium Metabolism Disorders
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Doctors Specialties
- Endocrinology
Accepted Insurances
Awards
- CMS Meaningful Use Stage 1 Certification
- Elected Member
Education
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Yale New Haven Children's Center -
Yale University School of Medicine -
University of North Carolina Hospitals
Hospital
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University of Michigan Hospitals and Health Centers
Drug Facts
| NPI NUMBER | 1710069240 | |
| NPPES Provider LastName | ARVAN | |
| NPPES Provider FirstName | PETER | |
| NPPES Provider ZIPCode | 48105 | |
| NPPES Provider State | MI | |
| Specialty Description | Endocrinology | |
| Total Claim Count | 385.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1710069240 |
| Last Name Of The Provider | ARVAN |
| First Name Of The Provider | PETER |
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