PubMed Health⌕ Search

Biomedical subjects

E A Neidhardt

Publications and source records attributed to E A Neidhardt.

9 recordsLinked to original sources

Multiple inhibitor analysis of the brequinar and leflunomide binding sites on human dihydroorotate dehydrogenase.

Brequinar and the active metabolite of leflunomide, A77 1726, have been clearly shown to inhibit human dihydroorotate dehydrogenase (DHODH), but conflicting mechanisms for their inhibition have been reported. DHODH catalyses the conversion of dihydroorotate (DHO) to orotate concurrent with the reduction of ubiquinone. This study presents data that indicates brequinar is a competitive inhibitor versus ubiquinone; A77 1726 is noncompetitive versus ubiquinone and both are uncompetitive versus DHO. 2-Phenyl 5-quinolinecarboxylic acid (PQC), the core moiety of brequinar also shows competitive inhibition versus ubiquinone. Multiple inhibition experiments indicate that PQC (and thus brequinar) and A77 1726 have overlapping binding sites. Both PQC and A77 1726 are also mutually exclusive with barbituric acid (a competitive inhibitor versus DHO). In addition, we failed to observe brequinar binding to E.orotate by isothermal titration calorimetry (ITC). These results indicate that the E.DHO.inhibitor and E.orotate.inhibitor ternary complexes do not form. The absence of these complexes is consistent with the two-site ping-pong mechanism reported for DHODH. This kinetic data suggests that recent crystal structures of human DHODH complexed with orotate and A77 1726 or brequinar may not represent the relevant physiological binding sites for these inhibitors [Liu, S., Neidhardt, E. A., Grossman, T. H., Ocain, T., and Clardy J. (2000) Structure 8, 25-33].

Aniline Compounds↗

Structures of human dihydroorotate dehydrogenase in complex with antiproliferative agents.

BACKGROUND: Dihydroorotate dehydrogenase (DHODH) catalyzes the fourth committed step in the de novo biosynthesis of pyrimidines. As rapidly proliferating human T cells have an exceptional requirement for de novo pyrimidine biosynthesis, small molecule DHODH inhibitors constitute an attractive therapeutic approach to autoimmune diseases, immunosuppression, and cancer. Neither the structure of human DHODH nor any member of its family was known. RESULTS: The high-resolution crystal structures of human DHODH in complex with two different inhibitors have been solved. The initial set of phases was obtained using multiwavelength anomalous diffraction phasing with selenomethionine-containing DHODH. The structures have been refined to crystallographic R factors of 16.8% and 16.2% at resolutions of 1. 6 A and 1.8 A for inhibitors related to brequinar and leflunomide, respectively. CONCLUSIONS: Human DHODH has two domains: an alpha/beta-barrel domain containing the active site and an alpha-helical domain that forms the opening of a tunnel leading to the active site. Both inhibitors share a common binding site in this tunnel, and differences in the binding region govern drug sensitivity or resistance. The active site of human DHODH is generally similar to that of the previously reported bacterial active site. The greatest differences are that the catalytic base removing the proton from dihydroorotate is a serine rather than a cysteine, and that packing of the flavin mononucleotide in its binding site is tighter.

Amino Acid Sequence↗

Production of secreted, soluble human two-domain CD4 protein in Escherichia coli.

The two-domain form of recombinant soluble human CD4 (rsCD4(183)) has been used for structural studies and to probe the interaction of CD4 with its ligands. rsCD4(183) has generally been produced in Escherichia coli in the form of inclusion bodies. The generation of conformationally native protein from these inclusion bodies is a time-consuming and inefficient process, requiring a refolding step. Here, we describe a procedure for producing 2-4 mg of secreted, conformationally native rsCD4(183) per liter of E. coli, completely bypassing the requirement for protein refolding in vitro. Furthermore, the yield of active protein is comparable to that reported for expression systems that generate inclusion bodies.

CD4 Antigens↗

Expression and characterization of E. coli-produced soluble, functional human dihydroorotate dehydrogenase: a potential target for immunosuppression.

Human dihydroorotate dehydrogenase (huDHODH) is essential for de novo biosynthesis of pyrimidines and the target of two immunosuppressive drugs, brequinar and the leflunomide metabolite A77-1726 (Chen et al., 1992; Davis et al., 1996). Using a T7 RNA polymerase expression system, we produced huDHODH as a fusion protein containing an amino-terminal decahistidine tag. Escherichia coli growth and expression conditions were optimized to enhance huDHODH solubility and to permit purification of the enzyme in the absence of detergent. Soluble huDHODH, purified by a simple two-step procedure, was catalytically active, monomeric, and contained a flavin mononucleotide (FMN) cofactor in a 1:1 FMN/protein molar ratio. Kinetic analysis showed that huDHODH uses a two site ping-pong mechanism, where DHO is oxidized at one site and the second substrate, ubiquinone, is reduced at the other. This result is consistent with the mechanism proposed for bovine liver DHODH (Hines and Johnston, 1989).

Animals↗

Naphthalene sulfonate polymers with CD4-blocking and anti-human immunodeficiency virus type 1 activities.

PIC 024-4 and PRO 2000 are naphthalene sulfonate polymers that bind to CD4 with nanomolar affinity and block binding of gp120. Both have activity against human immunodeficiency virus type 1 in H9 cells, peripheral blood mononuclear cells, and primary monocyte/macrophages, are synergistic with zidovudine, and do not inhibit tetanus toxoid-stimulated T-cell proliferation at anti-human immunodeficiency virus type 1 concentrations.

Animals↗

Inhibition of T cell activation and adhesion functions by soluble CD2 protein.

The CD2 (T11) molecule belongs to a family of cell-surface glycoproteins that function as adhesion molecules in the immune system. Human CD2 is found exclusively on cells of the T lineage: peripheral T lymphocytes, NK cells, and thymocytes. CD2 binds specifically to the surface glycoprotein LFA-3. CD2/LFA-3 adhesion is the basis for the formation of rosettes between T cells and sheep erythrocytes (SRBC) which bear the sheep homologue of LFA-3. More importantly, CD2/LFA-3 adhesion functions in the immune system to augment T cell activation; it initiates conjugate formation between participating T cells and antigen-presenting cells (APC). We investigated the effects of soluble forms of CD2 (sCD2), produced in either baculovirus or CHO expression systems, on the rosetting of T cells with SRBC and on the activation of T cells by antigen plus major histocompatibility complex (MHC) molecules. Rosette formation between T cells and SRBC was completely inhibited by as little as 1 microM sCD2. Furthermore, sCD2 effectively inhibited (at micromolar concentrations) the T cell proliferative response to recall antigens including rubella, tetanus toxoid, and herpes simplex virus (HSV-1), as well as alloantigens in a mixed lymphocyte culture. These findings are consistent with the notion that the CD2/LFA-3 interaction augments antigen-specific T cell functions. The use of a CD2 "decoy" molecule rather than anti-CD2 or anti-LFA-3 antibodies to block the CD2/LFA-3 interaction rules out secondary antibody effects, via the Fc portion, as the basis for inhibition of T cell activation and directly stresses the importance of this adhesion interaction in T cell responses.

Antigens, CD↗

N-glycosylation is required for human CD2 immunoadhesion functions.

The T-lymphocyte glycoprotein receptor, CD2, mediates cell-cell adhesion by binding to the surface molecule CD58 (LFA-3) on many cell types including antigen presenting cells. Two domains comprise the CD2 extracellular segment, with all adhesion functions localized to the amino-terminal domain that contains a single N-glycosylation site at Asn65. We have defined an important role for the N-linked glycans attached to Asn65 of this domain in mediating CD2-CD58 interactions and also characterize its N-glycotype structure. Analysis of deglycosylated soluble recombinant CD2 as well as a mutant transmembrane CD2 molecule containing a single Asn65-Gln65 substitution demonstrates that neither deglycosylated CD2 nor the mutant CD2 transmembrane receptor binds CD58 or monoclonal antibodies directed at native CD2 adhesion domain epitopes. Electrospray ionization-mass spectrometry demonstrates that high mannose oligosaccharides ((Man)nGlcNAc2, n = 5-9) are the only N-glycotypes occupying Asn65 when soluble CD2 is expressed in Chinese hamster ovary cells. Based on a model of human CD2 secondary structure, we propose that N-glycosylation is required for stabilizing domain 1 in the human receptor. Thus, N-glycosylation is essential for human CD2 adhesion functions.

Amino Acid Sequence↗

Rapid, two-step purification process for the preparation of pyrogen-free murine immunoglobulin G1 monoclonal antibodies.

A cost-efficient process was specifically designed for the preparation of gram amounts of highly pure murine immunoglobulin (Ig) G1 monoclonal antibodies (mAbs). This rapid, simple and scalable purification process employs a unique binding and elution protocol for IgG1 mAbs on a silica-based, mixed-mode ion-exchange resin followed by conventional anion-exchange chromatography. mAbs are bound to BakerBond ABx medium at pH 5.6 directly from serum-supplemented hybridoma culture supernatants. Contaminating proteins and nucleic acids are removed by an intermediate wash at pH'6.5, followed by the specific elution of IgG1 mAbs with 100 mM Tris-HCl (pH 8.5). The mAb eluate is then loaded directly on to QAE-Sepharose Fast Flow medium and eluted with 10 mM sodium phosphate buffer (pH 7.4), containing 150 mM sodium chloride. The resulting IgG1 mAbs are greater than 98% pure, free from measurable endotoxin, formulated in a physiological buffer and suitable for in vivo applications.

Animals↗

Structural and functional characterization of the CD2 immunoadhesion domain. Evidence for inclusion of CD2 in an alpha-beta protein folding class.

The T-lymphocyte transmembrane glycoprotein CD2 plays an important physiological role in facilitating adhesion between T-lymphocytes and their cognate cellular partners. This interaction is mediated by binding of CD2 to the broadly distributed surface polypeptide LFA-3 and augments the recognition function of the CD3-Ti antigen-major histocompatibility complex receptor via stabilization of conjugate formation between cells. To define better the structural components of the CD2 extracellular region which are important in contact-mediated cellular adhesion, a single-domain CD2 immunoadhesion protein has been prepared from papain digestion of a soluble two-domain CD2 molecule. This amino-terminal domain fragment binds to LFA-3 on human B-cells with a dissociation constant of 0.4 microM, possesses functional immunoadhesion epitopes as defined by the binding of monoclonal antibodies raised to native CD2, and retains the ability to inhibit sheep erythrocyte rosette formation with human T-cells. Thus, all of the immunoadhesion functions ascribed to CD2 reside within the amino-terminal domain. Circular dichroism analysis of the isolated CD2 adhesion domain suggests the presence of substantial alpha-helical character (22%), consistent with earlier computer modeling analyses that predicted a pattern of alternating alpha-helices and beta-sheets within the extracellular region of CD2. Despite the existence of short stretches of sequence homology between CD2 and immunoglobulin superfamily members, the circular dichroism data provide supporting biophysical evidence for classification of CD2 in an alpha-beta (either alpha/beta or alpha + beta) protein folding class.

Amino Acid Sequence↗