Professor, Pediatrics, Mayo Medical School
Pediatric Hematology & Oncology
Dr. Richard J. Bram, MD
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Richard J. Bram is an expert in the field of Pediatric Hematology & Oncology. He studied medicine at Stanford University School of Medicine. Stanford University School of Medicine is one of the top medical schools in the US. Stanford University School of Medicine has a rank of 2 in research and a 25 in primary care He received 1 awards: "Elected Member". Richard J. Bram, MD is also published. He has 56 publications published. The lastest publication: "Co-localization of calcium-modulating cyclophilin ligand with intracellular calcium pools.'
Publications
- Calcium-Modulating Cyclophilin Ligand Is Essential for the Survival of Activated T Cells and for Adaptive Immunity.
- A novel synthetic 1,3-phenyl bis-urea compound targets microtubule polymerization to cause cancer cell death.
- Impaired B Cell Receptor Signaling Is Responsible for Reduced TACI Expression and Function in X-Linked Immunodeficient Mice.
- Anasarca, Hypoalbuminemia, and Anemia: What Is the Correlation?
- Cyclophilin B supports Myc and mutant p53-dependent survival of glioblastoma multiforme cells.
- The anticancer drug Dp44mT inhibits T-cell activation and CD25 through a copper-dependent mechanism.
- BAFF Expression Correlates with Idiopathic Inflammatory Myopathy Disease Activity Measures and Autoantibodies.
- Cyclosporin A impairs the secretion and activity of ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type 1 repeat).
- TBK1 suppression of IgA in the NIK of time.
- Conditional deletion of calcium-modulating cyclophilin ligand causes deafness in mice.
- TACI deficiency impairs sustained Blimp-1 expression in B cells decreasing long-lived plasma cells in the bone marrow.
- Protective antiviral antibody responses in a mouse model of influenza virus infection require TACI.
- HIV-1 Rev-binding protein accelerates cellular uptake of iron to drive Notch-induced T cell leukemogenesis in mice.
- Severe osteogenesis imperfecta in cyclophilin B-deficient mice.
- Transmembrane activator, calcium modulator, and cyclophilin ligand interactor drives plasma cell differentiation in LPS-activated B cells.
- CAML loss causes anaphase failure and chromosome missegregation.
- Deficient TACI expression on B lymphocytes of newborn mice leads to defective Ig secretion in response to BAFF or APRIL.
- Calcium-modulating cyclophilin ligand regulates membrane trafficking of postsynaptic GABA(A) receptors.
- Identification of calcium-modulating cyclophilin ligand as a human host restriction to HIV-1 release overcome by Vpu.
- TACI is required for efficient plasma cell differentiation in response to T-independent type 2 antigens.
- TLR stimulation modifies BLyS receptor expression in follicular and marginal zone B cells.
- Renal upregulation of HO-1 reduces albumin-driven MCP-1 production: implications for chronic kidney disease.
- Selective activation of TACI by syndecan-2.
- TACI-BLyS signaling via B-cell-dendritic cell cooperation is required for naive CD8+ T-cell priming in vivo.
- Fibrocystin interacts with CAML, a protein involved in Ca2+ signaling.
- BLyS and APRIL in rheumatoid arthritis.
- CAML is a p56Lck-interacting protein that is required for thymocyte development.
- TACI and BAFF-R mediate isotype switching in B cells.
- Expression of BLyS and its receptors in B-cell non-Hodgkin lymphoma: correlation with disease activity and patient outcome.
- BCMA is essential for the survival of long-lived bone marrow plasma cells.
- CAML is required for efficient EGF receptor recycling.
- Knockin approaches.
- Kaposi's sarcoma-associated herpesvirus mitochondrial K7 protein targets a cellular calcium-modulating cyclophilin ligand to modulate intracellular calcium concentrati...
- Aberrant expression of B-lymphocyte stimulator by B chronic lymphocytic leukemia cells: a mechanism for survival.
- Cutting Edge: Regulation of TLR4-Driven B Cell Proliferation by RP105 Is Not B Cell Autonomous.
- Nonopsonic antibodies in cystic fibrosis. Pseudomonas aeruginosa lipopolysaccharide-specific immunoglobulin G antibodies from infected patient sera inhibit neutrophil ...
- The C104R mutant impairs the function of transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI) through haploinsufficiency.
- The murine equivalent of the A181E TACI mutation associated with common variable immunodeficiency severely impairs B-cell function.
- Regulation of the T-independent humoral response by TACI.
- Calcium-modulating cyclophilin ligand desensitizes hormone-evoked calcium release.
- Molecular cloning and functional characterization of murine transmembrane activator and CAML interactor (TACI) with chromosomal localization in human and mouse.
- Co-localization of calcium-modulating cyclophilin ligand with intracellular calcium pools.
- NF-AT activation induced by a CAML-interacting member of the tumor necrosis factor receptor superfamily.
- Isolation of a cDNA encoding the chicken homologue of the human calcium-modulating cyclophilin ligand.
- The gene for calcium-modulating cyclophilin ligand (CAMLG) is located on human chromosome 5q23 and a syntenic region of mouse chromosome 13.
- A hydrophobic domain of Ca2+-modulating cyclophilin ligand modulates calcium influx signaling in T lymphocytes.
- Identification of the immunophilins capable of mediating inhibition of signal transduction by cyclosporin A and FK506: roles of calcineurin binding and cellular location.
- Isolation of mutant T lymphocytes with defects in capacitative calcium entry.
- Calcium signalling in T cells stimulated by a cyclophilin B-binding protein.
- Specific protein binding to far upstream activating sequences in polymerase II promoters.
- Isolation of a Saccharomyces cerevisiae centromere DNA-binding protein, its human homolog, and its possible role as a transcription factor.
- A GAL family of upstream activating sequences in yeast: roles in both induction and repression of transcription.
- Nuclear association of a T-cell transcription factor blocked by FK-506 and cyclosporin A.
- CAML regulates Bim-dependent thymocyte death.
- Enhanced immunogenicity of pneumococcal surface adhesin A (PsaA) in mice via fusion to recombinant human B lymphocyte stimulator (BLyS).
Schools
Stanford University School Of Medicine
Stanford University Hospital
Conditions Treated
- Anemia
Doctors Specialties
- Oncology
- Pediatric Hematology
Accepted Insurances
- Choice Plus POS II
- Blue Card PPO
- Blue Cross Blue Shield of Illinois PPO
- Blue Cross Accord
- Cigna PPO
- Great West Healthcare-Cigna PPO
- Open Access Plus
- Choice Care PPO
- MultiPlan PPO
- PHCS Network PPO
- Choice Plus POS
- Options PPO
Awards
- Elected Member
Education
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Stanford University -
Stanford University School of Medicine
Hospital
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Mayo Clinic - Rochester, Minnesota
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