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choriocarcinoma/l tyrosin
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Seite 1 von 76 Ergebnisse
Tyrosine phosphorylation-and epidermal growth factor-dependent regulation of the sodium-coupled amino acid transporter B0 in the human placental choriocarcinoma cell line JAR.
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We have recently cloned an amino acid transporter from the human placental choriocarcinoma cell line JAR which, when functionally expressed in HeLa cells, induces an amino acid transport activity with characteristics known to be associated with the amino acid transport system B(0) (R. Kekuda, P.D.
Serotonin-induced decrease in hypothalamic tyrosine hydroxylase activity and corresponding increase in prolactin release are abolished at midpregnancy and by transplants of rat choriocarcinoma cells.
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We investigated the effect of central serotonin (5-hydroxytryptamine, 5-HT) administration on hypothalamic tuberoinfundibular dopamine neurons and related changes in neuronal activity to circulating PRL levels in two physiological models: 1) pregnant rats expressing (day 8) or not expressing (days
Inhibition of brain-derived neurotrophic factor/tyrosine kinase B signaling suppresses choriocarcinoma cell growth.
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Brain-derived neurotrophic factor (BDNF) signals through its receptor tyrosine kinase (Trk)B to regulate the development trophoblast cells during peri- and postimplantation periods. Possible involvement of this signaling system in malignant human trophoblastic cell growth has not been investigated.
Expression of placenta growth factor, soluble fms-like tyrosine kinase-1, metal-responsive transcription factor-1, heme oxygenase 1 and hypoxia inducible factor-1α mRNAs in pre-eclampsia placenta and the effect of pre-eclampsia sera on their expression of choriocarcinoma cells.
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OBJECTIVE
We studied the effect of pre-eclampsia sera on the expression of placenta growth factor (PlGF), soluble fms-like tyrosine kinase-1 (sFlt-1), metal-responsive transcription factor-1 (MTF-1), heme oxygenase 1 (HO-1) and hypoxia inducible factor-1α (HIF-1α) mRNAs in JEG-3 cells
Detection of fms-oncogene-specific tyrosine kinase activity in human leukemia cells.
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The c-fms protooncogene encodes the receptor for the colony-stimulating factor 1 of macrophages. Its transforming counterpart, the v-fms oncogene has previously been recognized as the transforming gene of the McDonough strain of feline sarcoma virus. We have isolated rabbit antisera against a
Relative expression of epidermal growth factor receptor in placental cytotrophoblasts and choriocarcinoma cell lines.
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The role of transforming growth factor-alpha (TGF-alpha)-epidermal growth factor receptor (EGFR) interactions in regulating benign and malignant trophoblast proliferation were examined. Benign cytotrophoblast (CT) demonstrated mitogenic stimulation in response to TGF-alpha; BeWo and JAr
Suppression of choriocarcinoma invasion and metastasis following blockade of BDNF/TrkB signaling.
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Brain-derived neurotrophic factor (BDNF) acts through its cognate receptor tyrosine kinase-B (TrkB) to regulate diverse physiological functions in reproductive and other tissues. In normal and malignant trophoblastic cells, the BDNF/TrkB signaling promotes cell growth. Due to the highly malignant
Functional nuclear epidermal growth factor receptors in human choriocarcinoma JEG-3 cells and normal human placenta.
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Immunocytochemistry with a monoclonal antiepidermal growth factor (anti-EGF) receptor antibody directed against the extracellular domain which can inhibit ligand binding to the receptors showed that nuclei of choriocarcinoma JEG-3 cells and normal placental trophoblasts were distinctly immunostained
Plasmodium falciparum-infected red blood cells selected for binding to cultured syncytiotrophoblast bind to chondroitin sulfate A and induce tyrosine phosphorylation in the syncytiotrophoblast.
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An important pathogenic complication of malaria during human pregnancy is sequestration of Plasmodium-infected red blood cells (iRBCs) in the placental intervillous spaces. This sequestration is thought to be mediated in part by binding of the iRBCs to receptors expressed on the syncytiotrophoblast
Regulation of deoxyribonucleic acid synthesis in proliferating and differentiating trophoblast cells: involvement of transferrin, transforming growth factor-beta, and tyrosine kinases.
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This report investigates the regulation of DNA synthesis in trophoblast stem cells and differentiating trophoblast cells. Experiments in this study were performed on the Rcho-1 trophoblast cell line, which was established from a transplantable rat choriocarcinoma. Rcho-1 trophoblast cells can be
Expression of the human c-fms proto-oncogene product (colony-stimulating factor-1 receptor) on peripheral blood mononuclear cells and choriocarcinoma cell lines.
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The c-fms gene product is related, and possibly identical, to the receptor for the mononuclear phagocyte colony stimulating factor, CSF-1. Using antisera to a recombinant v-fms--coded polypeptide, glycoproteins encoded by the human c-fms locus were detected in mononuclear cells from normal
Evidence for a novel RasGAP-associated protein of 105 kDa in both mature trophoblasts and differentiating choriocarcinoma cells.
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A novel tyrosine-phosphorylated, RasGAP-associated protein of 105 kDa (p105) is found in normal human term placental trophoblasts, as well as in JEG-3 human choriocarcinoma cells induced to differentiate by okadaic acid (OA). This p105 RasGAP-associated protein is distinct from other
Endogenous production of nitric oxide by vascular endothelial growth factor down-regulates proliferation of choriocarcinoma cells.
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The trophoblast-like choriocarcinoma cell line BeWo expresses a receptor for vascular endothelial growth factor (VEGF) and proliferates in response to VEGF. Nitric oxide (NO) seems to play a key role in the VEGF-induced proliferation of endothelial cells but the NO mechanistic regulation of
Identification of tyrosine-phosphorylated colony-stimulating factor 1 (CSF-1) receptor and a 56-kilodalton protein phosphorylated in intact human cells in response to CSF-1.
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Colony-stimulating factor 1 (CSF-1) selectively supports the survival, proliferation, and maturation of hemopoietic cells of the monocyte/macrophage lineage. Although the cellular receptor for CSF-1, (the c-fms protein) is a protein-tyrosine kinase activated by the binding of CFS-1, the role of
Suppression of hydatidiform molar growth by inhibiting endogenous brain-derived neurotrophic factor/tyrosine kinase B signaling.
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Brain-derived neurotrophic factor (BDNF)/tyrosine kinase B (TrkB) receptor signaling promotes trophoblast growth in normal and abnormal pregnancy. It also regulates the growth of malignant trophoblastic, choriocarcinoma cells. However, possible involvement of this signaling system in hydatidiform
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