Physician
Rheumatology
Dr. Melvin Medof, MD
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Melvin Medof works in the field of Rheumatology. He attended Keck School of Medicine of USC. Keck School of Medicine of USC is ranked 31 in research and 72 in primary care medicine Dr. Melvin Medof is a published doctor as well. He has 101 publications published. The latest was: Cell surface regulators of complement, 5I2 antigen, and CD59, in the rat eye and adnexal tissues.
Publications
- Shear stress-dependent downregulation of the adhesion-G protein-coupled receptor CD97 on circulating leukocytes upon contact with its ligand CD55.
- Absence of signaling into CD4(+) cells via C3aR and C5aR enables autoinductive TGF-?1 signaling and induction of Foxp3(+) regulatory T cells.
- Deletion of either CD55 or CD97 ameliorates Arthritis in mouse models.
- Decay accelerating factor is essential for successful corneal engraftment.
- Primed CD8(+) T-cell responses to allogeneic endothelial cells are controlled by local complement activation.
- Locally produced and activated complement as a mediator of alloreactive T cells.
- An early complement-dependent and TLR-4-independent phase in the pathogenesis of ethanol-induced liver injury in mice.
- Role of complement in ethanol-induced liver injury.
- Donor deficiency of decay-accelerating factor accelerates murine T cell-mediated cardiac allograft rejection.
- Locally produced C5a binds to T cell-expressed C5aR to enhance effector T-cell expansion by limiting antigen-induced apoptosis.
- IFN-gamma and IL-17 production in experimental autoimmune encephalomyelitis depends on local APC-T cell complement production.
- Locally produced complement fragments C5a and C3a provide both costimulatory and survival signals to naive CD4+ T cells.
- Anti-C5 antibody treatment ameliorates weakness in experimentally acquired myasthenia gravis.
- Decay accelerating factor can control T cell differentiation into IFN-gamma-producing effector cells via regulating local C5a-induced IL-12 production.
- Interaction of decay-accelerating factor with coxsackievirus B3.
- Graft-derived complement as a mediator of transplant injury.
- Structure-based mapping of DAF active site residues that accelerate the decay of C3 convertases.
- Differential contributions of C3, C5, and decay-accelerating factor to ethanol-induced fatty liver in mice.
- Deficiency of decay accelerating factor and CD59 leads to crisis in experimental myasthenia.
- The role of decay-accelerating factor as a receptor for Helicobacter pylori and a mediator of gastric inflammation.
- Decay-accelerating factor modulates induction of T cell immunity.
- Complement regulators in extraocular muscle and experimental autoimmune myasthenia gravis.
- An atomic resolution model for assembly, architecture, and function of the Dr adhesins.
- Decay-accelerating factor deficiency increases susceptibility to dextran sulfate sodium-induced colitis: role for complement in inflammatory bowel Disease.
- Respective roles of decay-accelerating factor and CD59 in circumventing glomerular injury in acute nephrotoxic serum nephritis.
- A corresponding tyrosine residue in the C2/factor B type A domain is a hot spot in the decay acceleration of the complement C3 convertases.
- Solution structure of a functionally active fragment of decay-accelerating factor.
- On the same cell type GPI-anchored normal cellular prion and DAF protein exhibit different biological properties.
- Proprotein interaction with the GPI transamidase.
- Differential cytokine expression of human retinal pigment epithelial cells in response to stimulation by C5a.
- Markedly enhanced susceptibility to experimental autoimmune myasthenia gravis in the absence of decay-accelerating factor protection.
- Resonance assignments of the central complement control protein module pair of human decay accelerating factor.
- Structure of decay-accelerating factor bound to echovirus 7: a virus-receptor complex.
- Decay-accelerating factor confers protection against complement-mediated podocyte injury in acute nephrotoxic nephritis.
- Blockage of complement regulators in the conjunctiva and within the eye leads to massive inflammation and iritis.
- Upregulation of DAF (CD55) on orbital fibroblasts by cytokines. Differential effects of TNF-beta and TNF-alpha.
- Lipid protein interactions: the assembly of CD1d1 with cellular phospholipids occurs in the endoplasmic reticulum.
- Comparative efficiencies of C-terminal signals of native glycophosphatidylinositol (GPI)-anchored proproteins in conferring GPI-anchoring.
- Differential effect of 1,10-phenanthroline on mammalian, yeast, and parasite glycosylphosphatidylinositol anchor synthesis.
- Decay-accelerating factor (DAF), complement receptor 1 (CR1), and factor H dissociate the complement AP C3 convertase (C3bBb) via sites on the type A domain of Bb.
- Tissue distribution of products of the mouse decay-accelerating factor (DAF) genes. Exploitation of a Daf1 knock-out mouse and site-specific monoclonal antibodies.
- Properties of exogenously added GPI-anchored proteins following their incorporation into cells.
- Bulk production and functional analyses of mouse CD55's native and deglycosylated active domains.
- Characterization of the active sites in decay-accelerating factor.
- Glycophosphatidylinositol-anchored protein deficiency as a marker of mutator phenotypes in cancer.
- Tears contain the complement regulator CD59 as well as decay-accelerating factor (DAF).
- Decay-accelerating factor in tears of contact lens wearers and patients with contact lens-associated complications.
- Glycerolphosphoinositide anchors for membrane-tethering proteins.
- Cooperation between decay-accelerating factor and membrane cofactor protein in protecting cells from autologous complement attack.
- Structure/function studies of human decay-accelerating factor.
- Impaired growth and elevated fas receptor expression in PIGA(+) stem cells in primary paroxysmal nocturnal hemoglobinuria.
- Conservation in decay accelerating factor (DAF) structure among primates.
- Cloning of murine glycosyl phosphatidylinositol anchor attachment protein, GPAA1.
- Protein transfer of glycosyl-phosphatidylinositol (GPI)-modified murine B7-1 and B7-2 costimulators.
- Glycosylphosphatidylinositol-anchor intermediates associate with triton-insoluble membranes in subcellular compartments that include the endoplasmic reticulum.
- Decay acceleration of the complement alternative pathway C3 convertase.
- Leukemia arising out of paroxysmal nocturnal hemoglobinuria.
- Cell surface regulators of complement, 5I2 antigen, and CD59, in the rat eye and adnexal tissues.
- Assignment of the human GPAA1 gene, which encodes a product required for the attachment of glycosylphosphatidylinositols to proteins, at 8q24.
- Mammalian glycophosphatidylinositol anchor transfer to proteins and posttransfer deacylation.
- Molecular cloning of human homolog of yeast GAA1 which is required for attachment of glycosylphosphatidylinositols to proteins.
- Complementary recognition of alternative pathway activators by decay-accelerating factor and factor H.
- Detection of complement regulatory proteins on soft contact lenses.
- The cytoplasmic juxtamembrane domain of the epidermal growth factor receptor contains a novel autonomous basolateral sorting determinant.
- The affected gene underlying the class K glycosylphosphatidylinositol (GPI) surface protein defect codes for the GPI transamidase.
- Resistance to apoptosis caused by PIG-A gene mutations in paroxysmal nocturnal hemoglobinuria.
- Use of recombinant DAF proteins to localize the epitopes recognized by monoclonal anti-CD55.
- Coordinator''s report: complement regulatory proteins.
- Paroxysmal nocturnal hemoglobinuria: new insights from murine Pig-a-deficient hematopoiesis.
- Accumulation of glucosaminyl(acyl)phosphatidylinositol in an S3 HeLa subline expressing normal dolicholphosphomannose synthase activity.
- Molecular modeling and mechanism of action of human decay-accelerating factor.
- Localization of classical and alternative pathway regulatory activity within the decay-accelerating factor.
- A knock-out model of paroxysmal nocturnal hemoglobinuria: Pig-a(-) hematopoiesis is reconstituted following intercellular transfer of GPI-anchored proteins.
- COOH-terminal processing of nascent polypeptides by the glycosylphosphatidylinositol transamidase in the presence of hydrazine is governed by the same parameters as gl...
- A defect in glycosylphosphatidylinositol (GPI) transamidase activity in mutant K cells is responsible for their inability to display GPI surface proteins.
- Cell-surface engineering with GPI-anchored proteins.
- Antigen-presenting cell engineering. The molecular toolbox.
- Genetic defects underlying paroxysmal nocturnal hemoglobinuria that arises out of aplastic anemia.
- Regulation of glycoinositol phospholipid anchor assembly in human lymphocytes. Absent mannolipid synthesis in affected T and natural killer cell lines from paroxysmal ...
- Deficient biosynthesis of N-acetylglucosaminyl-phosphatidylinositol, the first intermediate of glycosyl phosphatidylinositol anchor biosynthesis, in cell lines establi...
- The molecular basis for paroxysmal nocturnal hemoglobinuria.
- Characterization of alternatively spliced PIG-A transcripts in normal and paroxysmal nocturnal hemoglobinuria cells.
- Metabolism of GPIs in mammalian cells.
- Glycoinositol phospholipid anchor-defective K562 mutants with biochemical lesions distinct from those in Thy-1- murine lymphoma mutants.
- Cloning and characterization of the mouse PIG-A gene.
- Defective and normal haematopoietic stem cells in paroxysmal nocturnal haemoglobinuria.
- Activation of the alternative complement pathway by exposure of phosphatidylethanolamine and phosphatidylserine on erythrocytes from sickle cell Disease patients.
- A candidate mammalian glycoinositol phospholipid precursor containing three phosphoethanolamines.
- Time-dependent loss of surface complement regulatory activity during storage of donor blood.
- Identification of a PIG-A related processed gene on chromosome 12.
- Mammalian glycosylphosphatidylinositol-anchored proteins and intracellular precursors.
- Peripheral blood harvest of unaffected CD34+ CD38- hematopoietic precursors in paroxysmal nocturnal hemoglobinuria.
- Localization of the complement membrane attack complex inhibitor (CD59) in human conjunctiva and lacrimal gland.
- Purified GPI-anchored CD4DAF as a receptor for HIV-mediated gene transfer.
- PIG-A, DAF and proto-oncogene expression in paroxysmal nocturnal haemoglobinuria-associated acute myelogenous leukaemia blasts.
- Stimulation of glycogen synthesis by insulin in human erythroleukemia cells requires the synthesis of glycosyl-phosphatidylinositol.
- Characterization of the murine PIG-A promoter region high constitutive PIG-A gene expression in brain.
- Histocompatibility antigens and gold toxicity: a preliminary report.
- Ability of complement to release systemic Lupus erythematosus immune complexes from cell receptors.
- Circulating immune complexes in neurologic Disease.
Schools
Keck School Of Medicine Of The Univ Of Southern California
La Co Usc Med Center
Columbia Presby Med Center
Pb Brigham Hospital
Procedures Preformed
- Joint Drainage
- Myofascial Trigger Point Injection
- Steroid Injection
- Viscosupplementation With Hyaluronate
Conditions Treated
- Adhesive Capsulitis
- Arthritis
- Carpal Tunnel Syndrome
- Chronic Neck Pain
- View All
Doctors Specialties
- Rheumatology
Accepted Insurances
Education
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VA Greater Los Angeles Healthcare System -
New York Presbyterian Hospital - Columbia Campus -
University of Southern California - LAC+USC Medical Center -
Keck School of Medicine of USC
Hospital
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University Hospitals Case Medical Center
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