Assistant Professor of Pathology, Boston Children's Hospital

Hematology

John P. Manis is an expert in the field of Hematology. He went to medical school at State University of New York Upstate Medical University. John P. Manis, MD is a published doctor. He has 30 publications published. The most current publication "A novel mutation in the POLE2 genecausing combined immunodeficiency."

Publications

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• Defective lymphoid organogenesis underlies the immune deficiency caused by a heterozygous S32I mutation in IκBα.
• Differential role of nonhomologous end joining factors in the generation, DNA damage response, and myeloid differentiation of human induced pluripotent stem Cells.
• TRIF Signaling Is Essential for TLR4-Driven IgE Class Switching.
• Focal adhesion kinase regulates the localization and retention of pro-B Cells in bone marrow microenvironments.
• BAL1 and Its Partner E3 Ligase, BBAP, Link Poly(ADP-Ribose) Activation, Ubiquitylation, and Double-Strand DNA Repair Independent of ATM, MDC1, and RNF8.
• Immature B Cells preferentially switch to IgE with increased direct S? to S{varepsilon} recombination.
• Signatures of murine B-Cell development implicate Yy1 as a regulator of the germinal center-specific program.
• AID-induced genotoxic stress promotes B Cell differentiation in the germinal center via ATM and LKB1 signaling.
• Downstream class switching leads to IgE antibody production by B lymphocytes lacking IgM switch regions.
• Analysis of mice lacking DNaseI hypersensitive sites at the 5' end of the IgH locus.
• BBAP monoubiquitylates histone H4 at lysine 91 and selectively modulates the DNA damage response.
• Oncogenic transformation in the absence of Xrcc4 targets peripheral B Cells that have undergone editing and switching.
• Fixing DNA breaks during class switch recombination.
• Knock out, knock in, knock down--genetically manipulated mice and the Nobel Prize.
• SOCS3 protein developmentally regulates the chemokine receptor CXCR4-FAK signaling pathway during B lymphopoiesis.
• 53BP1 and p53 synergize to suppress genomic instability and Lymphomagenesis.
• MDC1 maintains genomic stability by participating in the amplification of ATM-dependent DNA damage signals.
• H2AX prevents DNA breaks from progressing to chromosome breaks and translocations.
• Artemis-independent functions of DNA-dependent protein kinase in Ig heavy chain class switch recombination and development.
• p63 and p73 are not required for the development and p53-dependent apoptosis of T Cells.
• 53BP1 links DNA damage-response pathways to immunoglobulin heavy chain class-switch recombination.
• Artemis and p53 cooperate to suppress oncogenic N-myc amplification in progenitor B Cells.
• Developmental defects and p53 hyperacetylation in Sir2 homolog (SIRT1)-deficient mice.
• Novel antibody switching defects in human patients.
• Deficiencies of GM-CSF and interferon gamma link inflammation and Cancer.
• Internal IgH class switch region deletions are position-independent and enhanced by AID expression.
• The function of AID in somatic mutation and class switch recombination: upstream or downstream of DNA breaks.
• IgH class switch recombination to IgG1 in DNA-PKcs-deficient B Cells.
• A novel mutation in the POLE2 gene causing combined immunodeficiency.

Schools

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• Upstate Medical University College of Health Professions

• Georgetown University Hospital Dc

• New England Med Center

• New Eng Med Center

Procedures Preformed

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• Plasmapheresis

Conditions Treated

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• Acute Leukemia
• Anemia
• Breast Cancer
• Cryoglobulinemia
• View All

Doctors Specialties

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• Hematology
• Medical Oncology
• Oncology

Accepted Insurances

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Education

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• Brigham and Women's Hospital
• Tufts Medical Center
• Georgetown University Hospital
• State University of New York Upstate Medical University

Hospital

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• Brigham and Women's Hospital

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