Professor of Medicine, Johns Hopkins University School of Medicine

Internal Medicine

Paul Rothman works in the field of Internal Medicine. He went to medical school at Yale University School of Medicine. Yale University School of Medicine is one of the top medical schools in the US. Yale University School of Medicine has a rank of 7 in research and a 57 in primary care He received 1 awards: "Elected Member". Paul B. Rothman is a published doctor. He has 47 publications published. The most current publication "Intestinal Helminths Regulate Lethal Acute Graft-versus-Host Disease and Preserve the Graft-versus-Tumor Effect in Mice."

Publications

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• Intestinal Helminths Regulate Lethal Acute Graft-versus-Host Disease and Preserve the Graft-versus-Tumor Effect in Mice.
• NFIL3-Deficient Mice Develop Microbiota-Dependent, IL-12/23-Driven Spontaneous Colitis.
• Tim-3 Directly Enhances CD8 T Cell Responses to Acute Listeria monocytogenes Infection.
• TH17 cell differentiation is regulated by the circadian clock.
• Sedimentation and Immunoprecipitation Assays for Analyzing Complexes that Repress Transcription.
• Medical research has health and wealth implications.
• Tim-1 Regulates Th2 Responses in an Airway Hypersensitivity Model.
• A SOCS-1 promoter variant is associated with total serum IgE levels.
• The Developmental Regulator Protein Gon4l Associates with Protein YY1, Co-repressor Sin3a, and Histone Deacetylase 1 and Mediates Transcriptional Repression.
• Fyn binds to and phosphorylates T cell immunoglobulin and mucin domain-1 (Tim-1).
• NFIL3 is a regulator of IL-12 p40 in macrophages and mucosal immunity.
• NFIL3/E4BP4 controls type 2 T helper cell cytokine expression.
• NFIL3/E4BP4 is a key transcription factor for CD8{alpha}+ dendritic cell development.
• HOIL-1L Interacting Protein (HOIP) Is Essential for CD40 Signaling.
• The Justy mutation identifies Gon4-like as a gene that is essential for B lymphopoiesis.
• The T cell receptor-mediated phosphorylation of Pyk2 tyrosines 402 and 580 occurs via a distinct mechanism than other receptor systems.
• Identification of DOK genes as lung tumor suppressors.
• IL-4-induced transcription factor NFIL3/E4BP4 controls IgE class switching.
• HOIL-1L interacting protein (HOIP) as an NF-kappaB regulating component of the CD40 signaling complex.
• The transcriptional regulator NFIL3 controls IgE production.
• Loss of SOCS7 in mice results in severe cutaneous disease and increased mast cell activation.
• Chapter 3: Role of SOCS in allergic and innate immune responses.
• The Nalp3 inflammasome is essential for the development of silicosis.
• Pim-1 and Pim-2 kinases are required for efficient pre-B-cell transformation by v-Abl oncogene.
• Antigen-specific immune responses to influenza vaccine in utero.
• Suppressor of cytokine signaling in allergic inflammation.
• PIP3 pathway in regulatory T cells and autoimmunity.
• Downstream of tyrosine kinases-1 and Src homology 2-containing inositol 5'-phosphatase are required for regulation of CD4+CD25+ T cell development.
• Deletion of SOCS7 leads to enhanced insulin action and enlarged islets of Langerhans.
• Repression of an interleukin-4-responsive promoter requires cooperative BCL-6 function.
• Dok1 and SHIP act as negative regulators of v-Abl-induced pre-B cell transformation, proliferation and Ras/Erk activation.
• Early growth response-1 regulates lipopolysaccharide-induced suppressor of cytokine signaling-1 transcription.
• Abl oncogene bypasses normal regulation of Jak/STAT activation.
• Interferon-gamma inhibits STAT6 signal transduction and gene expression in human airway epithelial cells.
• SOCS-1 localizes to the microtubule organizing complex-associated 20S proteasome.
• v-Abl signaling disrupts SOCS-1 function in transformed pre-B cells.
• The transcriptional co-activator p/CIP (NCoA-3) is up-regulated by STAT6 and serves as a positive regulator of transcriptional activation by STAT6.
• Enhancement of MEK/ERK signaling promotes glucocorticoid resistance in CD4+ T cells.
• The heparan sulfate proteoglycan GPC3 is a potential lung tumor suppressor.
• Paralytic autoimmune myositis develops in nonobese diabetic mice made Th1 cytokine-deficient by expression of an IFN-gamma receptor beta-chain transgene.
• Protein phosphatase 2A regulates the stability of Pim protein kinases.
• Functional involvement of Akt signaling downstream of Jak1 in v-Abl-induced activation of hematopoietic cells.
• Cutting edge: Suppressor of cytokine signaling 3 inhibits activation of NFATp.
• JAK-STAT signaling in asthma.
• Oligonucleotide microarray analysis of lung adenocarcinoma in smokers and nonsmokers identifies GPC3 as a potential lung tumor suppressor.
• Cutting edge: STAT6 serves as a positive and negative regulator of gene expression in IL-4-stimulated B lymphocytes.

Schools

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• Yale University

• Ny and Presby Hp Columbia Campus

• Johns Hopkins Hospital Corporate Vice Chairman

• Johns Hopkins School of Medicine Dean of the Medical Faculty

Doctors Specialties

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• Internal Medicine

Accepted Insurances

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• Blue Card PPO
• Blue Preferred PPO
• Geisinger Health Plan
• Choice Care PPO
• Choice Plus POS
• Navigate HMO
• Options PPO

Awards

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• Elected Member

Education

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• New York Presbyterian Hospital - Columbia Campus
• New York Presbyterian Hospital
• Yale University School of Medicine

Hospital

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• Johns Hopkins Hospital
• Johns Hopkins Bayview Medical Center

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