Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.10.1 (ERK)
 95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunization procedures that induce contact sensitivity to the trinitrophenyl (TNP) hapten in vivo were investigated for their ability to induce TNP-specific cytotoxic T lymphocytes in vivo. Spleen cells from C3H/HeN mice primed for CS responses either by the topical application of picryl chloride or by the adoptive transfer of PCL immune cells show little or no cytolytic activity in vitro against TNP-coupled target cells. Intravenous immunization with TNP-substituted syngeneic spleen cells, a procedure known to make animals unresponsive to agents normally inducing CS, also failed to induce cytolytic activity in spleen cells. However, both PCL sensitization and adoptive transfer, when combined with the injection of TNP-substituted syngeneic spleen cells, induce significant cytolytic activity against TNP-haptenated BW5147 target cells in vitro. Furthermore, i.v. injection of TNP-spleen cells with surface-bound immune complexes of the IgM or IgG1 isotypes, or with a monoclonal TNP-specific contrasuppressor T cell factor also induces strong antigen-specific cytolytic activity against TNP modified targets. TcsF bears serological determinants of T cell receptor alpha and beta chains and adheres to specific antigen columns. All these immunization regimens were shown to induce CS to TNP as well as the generation of contrasuppressor T cells. The CTL generated in the spleens of immunized mice are Thy1+ CD8+ T cells an are antigen-specific and genetically restricted. The implications of these results with respect to the mechanisms by which cytolytic responses are controlled in vivo is discussed.
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PMID:Generation of anti-hapten T cell cytotoxicity in vivo. Relationship to contact sensitivity and the role of contrasuppression. 748 50

The intrahepatic accumulation of the c-myc protooncogene product was observed on immunofluorescence in each of six patients with chronic hepatitis delta virus infection who exhibited the hepatitis D antigen in their livers. The c-myc product was stained in the same nuclei that contained the hepatitis D antigen. C-myc was not observed in acute hepatitis D or in cases of chronic hepatitis delta virus infection without expression of the hepatitis D antigen. The protooncogene product was detected in only 1 of 32 viral and nonviral liver disorders unrelated to hepatitis delta virus. To confirm these observations, we transfected HBsAg-positive (PCL/PRF/5) and HBsAg-negative (HepG2) transformed liver cell lines with a plasmid containing a hepatitis delta virus cDNA trimer under the control of the SV40 early enhancer/promoter sequences. Whereas baseline c-myc expression was barely detectable in mock-transfected PLC/PRF/5 or HepG2 cells, strong c-myc nuclear fluorescence was observed when these same cells were transfected with the hepatitis D antigen expression vector. Similar results were obtained after infection of HeLa cells with a recombinant vaccinia virus expressing the hepatitis D antigen. Detection of c-myc mRNA sequences by means of in situ hybridization suggested that the c-myc product accumulation was not due to increased amounts of its mRNA. The c-myc protein accumulates selectively in the livers of patients with chronic hepatitis delta virus infection and in the same nuclei that contain the hepatitis D antigen. The expression of c-myc in hepatitis D antigen-containing cells does not require the presence of hepatitis B virus infection.
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PMID:Expression of the c-myc protooncogene product in cells infected with the hepatitis delta virus. 752 69

Ligand binding of the B-cell lineage antigen CD40 enhances growth and interleukin-6 (IL-6) secretion in human B cells (the CD40/IL-6 loop). IL-6 has an autocrine and paracrine role in human multiple myeloma (MM) cell growth. With the use of the CD40 monoclonal antibody (MoAb) G28-5, we examined CD40 expression and the effect of CD40 binding on MM clonogenic colony (MCC) formation to characterize the IL-6/CD40 loop activity in MM. CD40 was expressed on plasmacytoid cells in 21 of 28 plasma cell dyscrasia (PCD) bone marrow (BM) biopsies tested (10 of 14 MM, 2 of 2 Waldenstrom's macroglobulinemia [WM], 2 of 2 plasma cell leukemia [PCL], 6 of 8 monoclonal gammopathy of undetermined significance [MGUS], and 1 of 2 primary amyloidosis [AL]). G28-5 binding increased MCCs by 35% to 150% in 11 of 17 CD40+ PCD BM cultures, but did not affect MCC formation in CD40- specimens or normal BM colony forming units (CFU-GEMM, CFU-GM, BFU-E). Responsive cultures originated from BM of patients with MM (2 of 5 cases tested), WM (2 of 2), PCL (2 of 2), and MGUS (5 of 6). CD40-responsiveness was not significantly inhibited by the presence of an anti-IL-6 MoAb (2 of 2 MGUS cultures tested), and did not correlate with the capacity to respond to IL-6 stimulation (n = 17, P > .05) or a detectable level of endogenous IL-6 (n = 15, P > .05). Additional studies were performed with PCD cell lines to characterize the interrelationship of CD40 activation and IL-6 production. Fifty percent to greater than 95% of cells from the RPMI 8226 and ARH77 lines expressed CD40, whereas 6% of U266 cells were CD40+. For RPMI 8226, ARH-77, and U266 cells, the increased MCC formation after anti-CD40 stimulation was not affected by the presence of an anti-IL-6 neutralizing MoAb and was not accompanied by detectable IL-6 secretion. There was no apparent increase in IL-6 mRNA transcription following G28-5 treatment of U266 or RPMI 8226 cells. Our observations indicate that CD40 is expressed in a subset of human myeloma cells present in various PCDs. Cell-line studies suggest that the CD40+ myeloma cell may regulate MM clonogenic colony formation without activating the IL-6 pathway.
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PMID:Anti-CD40 antibody binding modulates human multiple myeloma clonogenicity in vitro. 752 65

Poly(epsilon-caprolactone) (PCL) microspheres containing taxol were prepared by the solvent evaporation method and tested for angiogenesis inhibition using the chick chorioallantoic membrane (CAM) model. Very high encapsulation efficiencies (95%) for taxol in PCL microspheres were obtained. In vitro release studies showed about 25% of the loaded drug was released in 6 weeks from microspheres containing 5% taxol. Studies with the CAM showed that taxol released from the microspheres induced vascular regression and inhibited angiogenesis.
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PMID:Taxol encapsulation in poly(epsilon-caprolactone) microspheres. 754 28

1. Precursors form the neuroepithelium of the developing cortex and also from the adult sub-ventricular zone, can be cloned in vitro after stimulation with fibroblast growth factor (FGF)-2 and have the potential to give rise to both neurons and glia. The generation of neurons from these clones can be stimulated by either a factor derived from an astrocyteprecursor line, Ast-1, or FGF-1. 2. Neuronal differentiation stimulated by FGF-1 can be inhibited by diacylglycerol-lipase inhibitor and mimicked by arachidonic acid, suggesting that the neuronal differentiation is signalled through the PCL gamma pathway. 3. The sequential expression of FGF-2 and FGF-1 within the developing forebrain neuroepithelium fits with the different functions the two FGF play in precursor regulation. 4. We have shown that the precursor response to FGF-1 is regulated by a heparan sulphate proteoglycan (HSPG) expressed within the developing neuroepithelium. Precursors restricted to the astrocyte cell lineage can be stimulated by epidermal growth factor or FGF-2; however, the differentiation into GFAP positive astrocytes appears to require a cytokine acting through the leukaemia inhibitory factor beta receptor.
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PMID:Regulation of neural precursor differentiation in the embryonic and adult forebrain. 758 13

In order to evaluate the contribution of the knee ligaments to restrain joint motions, knowledge about their structural properties is required. Due to the variable relative insertion orientation of the ligaments during knee motion, however, different fiber bundles are recruited, each with their specific mechanical properties. Hence, the structural properties vary as a function of knee motion. For this reason, a relationship between the structural tensile properties and the relative insertion orientation is required in order to define the role of the ligaments in knee mechanics. In the present study, this relationship is determined by performing a series of tensile tests in which the relative orientations of the insertion sites of human knee bone-ligament-bone preparations were varied systematically. The experimentally obtained stiffness was significantly affected by the relative orientation of the insertion sites, but more profoundly for the anterior and posterior cruciate ligaments (ACL and PCL) as compared to the medial and lateral collateral ligaments (MCL and LCL). The average decreases in stiffness per 5 degrees tilt of the insertion sites were estimated at -11.6 +/- 3.5 N mm-1 (ACL), -20.9 +/- 2.7 N mm-1 (PCL), -2.6 +/- 0.9 N mm-1 (MCL) and -3.7 +/- 0.3 N mm-1 (LCL). For the PCL and the MCL these changes in stiffness with tilt were rather insensitive to the side of the femoral insertion site which was lifted. The ACL and the LCL, conversely, displayed significant differences in stiffness changes between the different tilt directions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of variable relative insertion orientation of human knee bone-ligament-bone complexes on the tensile stiffness. 760 74

The complete amino acid sequence of a lectin-related 16.5-kDa protein (PCL-RP) isolated from fruit bodies of a lectin-deficient strain of P. cornucopiae is presented. The sequences of six out of the seven peptides generated by digestion with lysylendopeptidase and four of the five peptides generated by cyanogen bromide cleavage were completely analyzed. Overlapping peptides were obtained by arginylendopeptidase digestion. PCL-RP was a single-chain protein consisting of 144 amino acid residues and its N-terminal serine was blocked with acetate. A proline-rich sequence was found in the carboxyl terminal portion. The N-terminal sequence of PCL-RP showed some homology with those of two known Basidiomycete lectins.
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PMID:Complete amino acid sequence of a lectin-related 16.5-kDa protein isolated from fruit bodies of a lectin-deficient strain of Pleurotus cornucopiae. 762 42

This paper describes a novel modeling technique for simulating the motion of the knee joint in three dimensions. For a given range of flexion, the envelope of passive knee joint motion is determined by applying additional translations and rotations necessary to maintain Force Balance in the joint. An initial application of this Force Balance technique has been implemented in MATLAB on a Sparc 10. Results of this application, which describes the knee's motion in the sagittal plane based on the ACL, PCL, MCL, and LCL, are presented here. This model is applicable to the analysis of ligament loss, damage, and repair, and can be adapted to include muscle forces in order to simulate joint motion under load.
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PMID:A technique for simulating the motion of the knee in three dimensions. 765 82

Multiple myeloma (MM) is defined as a tumoral expansion of plasma cells occurring in the bone marrow and sometimes in the peripheral blood (plasma-cell leukemia, PCL). Many reports have demonstrated a clonal expansion of B cells bearing the same idiotypic determinants as the myeloma protein (idiotypic B cells) in MM, suggesting that they could belong to the malignant clone. In order to investigate whether the B-cell population is a malignant component or not, either in the peripheral blood of patients with PCL or in the bone marrow of patients with MM, we derived B-cell lines by infecting, with the Epstein-Barr virus (EBV), cultures in limiting dilution of mononuclear cells from six patients. A limiting dilution culture was used to prevent the elimination of slowly proliferating clones by the more rapidly dividing ones, and thus to get the most exact representation of the B-cell repertoire of these patients. The cloning efficiency of the EBV-infected cells was similar in patients and healthy individuals (range: 1 in 100 to 1 in 1650 B cells). All of the clones obtained from a single patient exhibited different clonal immunoglobulin gene rearrangements (IGR), proving the validity of our cloning technique. No tumoral clones (61 clones analysed) showed the IGR pattern specific of autologous myeloma cells. These results indicate that malignant plasma cells cannot be immortalized with EBV. These results show that, if malignant B cells (pre-switch or post-switch) exist, they could be present only in a minor population, and the corollary of this is that there is a major population of non-malignant B cells in the sites of tumoral proliferation of patients with MM. This is remarkable in view of numerous reports showing a profound defect of the polyclonal B lymphopoiesis in these patients, and even an absence of B lymphocytes. Thus, these results challenge the existence of a major compartment of malignant idiotypic B cells and favor the hypothesis of non-malignant B cells sharing cross-reactive idiotypes with the autologous myeloma protein.
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PMID:Analysis of the B-cell compartment in plasma cell leukemia and multiple myeloma: immunoglobulin gene rearrangement of EBV-infected B-cell lines. 768 18

Pedicellarial toxin, partially purified from the sea urchin Toxopneustes pileolus, dose-dependently and time-dependently caused histamine release from rat peritoneal mast cells. Pedicellarial toxin induced a rapid initial rise in [Ca2+]i within several seconds which was followed by a further slower increase of [Ca2+]i (second rise). The toxin induced a dose-dependent formation of inositol 1,4,5-triphosphate (IP3) as well as the histamine release in mast cells. Furthermore, the toxin stimulated phosphoinositide-specific phospholipase C (PI-PLC) activity in mast cell membranes. 2-Nitro-4-carboxyphenyl-N,N-diphenylcarbamate (NCDC), a PLC inhibitor, inhibited the activation of PI-PCL induced by pedicellarial toxin. Cholera toxin inhibited pedicellarial toxin-induced histamine release, whereas pretreatment of pertussis toxin failed to inhibit it. These results suggest that pedicellarial toxin from T. pileolus activates PI-PCL and the stimulation of PI turnover may lead to the release of IP3 into the cytoplasm, resulting in histamine release from rat mast cells.
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PMID:Mast cell activation by pedicellarial toxin of sea urchin, Toxopneustes pileolus. 768 24


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