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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)

Serum and tissue ferritins were quantitated by a radioimmunoassay kit (SPAC KIT, Daiichi Radioisotope Lab.) and a diagnostic implication of serum ferritins in patients with gynecological diseases was evaluated. In order to investigate the potential use of tumor marker as a feto-placental antigen (protein), ferritin from ovarian cancer was compared with ferritins from normal adult and feto-placental organs. Serum ferritin levels were significantly higher (p less than 0.01) in patients with ovarian adenocarcinoma, Krukenberg's tumor, cervical squamous cell carcinoma and other malignant diseases than in normal women. Among adult organs the kidney and spleen showed the highest and the heart the lowest ferritin content. The ferritin contents of the kidney and spleen were 78.4 micrograms and 76.2 micrograms/g wet weight, respectively and that of the heart was 5.7 micrograms/g wet weight. The ferritin contents of other adult organs ranged from 10 to 25 micrograms/g wet weight. On the other hand the placenta showed the highest and the heart and stomach the lowest ferritin content among feto-placental organs. The ferritin content of the placenta was 7 micrograms/g wet weight. The ferritin contents of other fetal organs were only half as in the placenta. The ferritin contents of ovarian cancers ranged 6 to 8 micrograms/g wet weight and was almost identical to that of the placenta.
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PMID:[Gynecological cancer and ferritin--a study on the carcinofetoplacental ferritin]. 682 63

In order to characterise the distribution and role of stem cell factor (SCF), a recently-reported growth factor for normal melanocytes, we carried out an immunohistochemical study on benign and malignant melanocytic tumours with a comparison with the presence of its receptor c-Kit proto-oncogene product (c-KIT). In normal skin, SCF was mainly observed in endothelial cells of blood vessels but not frequently in basal melanocytes, whereas c-KIT was predominantly localised in tissue mast cells. In benign neoplastic melanocytes (common melanocytic naevi), localisation of SCF and c-KIT was complementary: SCF was mostly found in dermal naevus cells while c-KIT was revealed in epidermal naevus cells, although the expression of the latter antigen was not frequent. Malignant melanoma cells showed less frequent expression of these antigens than those in benign lesions. Of five cultured melanoma cell lines, SCF was observed in only one, and c-KIT was not found in any melanoma cells. No quantitative or qualitative alterations assessed by Western blot analysis were induced in the presence of phenotypic modifiers (sodium butyrate and HMBA). Present data suggest that loss of SCF expression in neoplastic melanocytes is commonly associated with malignant transformation of pigment cells rather than loss of its receptor c-KIT.
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PMID:Immunohistochemical localisation of stem cell factor (SCF) with comparison of its receptor c-Kit proto-oncogene product (c-KIT) in melanocytic tumours. 749 98

Receptor-type tyrosine kinases (RTKs) constitute a family of proteins involved in growth and developmental processes. Class III RTKs are characterized by an extracellular region composed of five immunoglobulin-like domains and by a split tyrosine kinase domain. Some of the class III RTKs perform major functions in hematopoiesis and are the focus of this review. They are the colony-stimulating factor-1 (CSF1) and Steel factor (SLF) receptors, encoded by the FMS and KIT protooncogenes, respectively, and the product of the FLT3/FLK2 gene. The structural, biochemical, functional, and pathological features of these three receptors and genes are reviewed.
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PMID:Hematopoietic receptors of class III receptor-type tyrosine kinases. 750 35

We cloned the cDNA for stem cell tyrosine kinase 1 (STK-1), the human homolog of murine Flk-2/Flt-3, from a CD34+ hematopoietic stem cell-enriched library and investigated its expression in subsets of normal human bone marrow. The cDNA encodes a protein of 993 aa with 85% identity and 92% similarity to Flk-2/Flt-3. STK-1 is a member of the type III receptor tyrosine kinase family that includes KIT (steel factor receptor), FMS (colony-stimulating factor 1R), and platelet-derived growth factor receptor. STK-1 expression in human blood and marrow is restricted to CD34+ cells, a population greatly enriched for stem/progenitor cells. Anti-STK-1 antiserum recognizes polypeptides of 160 and 130 kDa in several STK-1-expressing cell lines and in 3T3 cells transfected with a STK-1 expression vector. Antisense oligonucleotides directed against STK-1 sequences inhibited hematopoietic colony formation, most strongly in long-term bone marrow cultures. These data suggest that STK-1 may function as a growth factor receptor on hematopoietic stem and/or progenitor cells.
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PMID:STK-1, the human homolog of Flk-2/Flt-3, is selectively expressed in CD34+ human bone marrow cells and is involved in the proliferation of early progenitor/stem cells. 750 45

Schwann cells are the primary cell type in the disfiguring lesions associated with neurofibromatosis type 1 (NF-1). These lesions also contain abnormally high numbers of mast cells, a cell type which develops in response to stem cell factor. We report here that neonatal and adult rat and human Schwann cells, as well as a transfected rat Schwann cell line and a human Schwannoma line derived from an NF-1 patient, all produced stem cell factor mRNA and protein. In coculture experiments, surface expression of stem cell factor by neonatal rat Schwann cells was profoundly downregulated by contact with dorsal root ganglion neurites. The receptor for stem cell factor, KIT, was not expressed in normal Schwann cells but was expressed in the human Schwannoma line, suggesting that aberrant KIT expression may form an autocrine loop in certain Schwann cell neoplasias.
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PMID:Role for the stem cell factor/KIT complex in Schwann cell neoplasia and mast cell proliferation associated with neurofibromatosis. 751 66

KIT constitutes the cell surface transmembrane receptor protein tyrosine kinase for a growth factor variously termed steel factor (SLF), stem cell factor, mast cell growth factor, or Kit ligand. Inherited mutations of the KIT gene result in piebaldism in humans and dominant white spotting (W) in mice. Patches of hypopigmented skin and hair in these disorders represent regions lacking in melanocytes, the result of defective melanoblast differentiation, migration, proliferation, or survival during embryonic development. Here we show that incubation of normal human melanocytes with a KIT antisense oligodeoxynucleotide greatly inhibits cell proliferation in culture, whereas incubation with a KIT sense oligodeoxynucleotide has no effect. The KIT oligodeoxynucleotides also had little or no effect on cell survival.
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PMID:Inhibition of proliferation of human melanocytes by a KIT antisense oligodeoxynucleotide: implications for human piebaldism and mouse dominant white spotting (W). 751 54

Piebaldism is an autosomal dominant genetic disorder of pigmentation characterized by congenital patches of white skin and hair that lack melanocytes. Piebaldism results from mutations of the KIT proto-oncogene, which encodes the cell-surface receptor transmembrane tyrosine kinase for an embryonic growth factor, Steel factor. Several pathologic mutations of the KIT gene have now been identified in different patients with piebaldism. Correlation of these mutations with the associated piebald phenotypes has led to the recognition of a hierarchy of three classes of mutations that result in a graded series of piebald phenotypes, and to improved understanding of the mechanisms that underlie dominant genetic disorders.
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PMID:Molecular basis of human piebaldism. 752 36

We examined the expression of Fc epsilon-RI and Fc gamma-RII/III on mouse bone marrow cells enriched for hematopoietic progenitors including mast cell progenitors. Bone marrow cells were depleted of mature hematopoietic lineages and a primitive population of cells that express the proto-oncogene c-kit (KIT+ lineage- cells) was isolated. KIT+ lineage- cells stain positively using the Ab 2.4G2, indicating surface expression of Fc gamma-RII and/or Fc gamma-RIII. Fluorescent staining of intracytoplasmic domains of Fc gamma-RII and Fc gamma-RIII revealed that these cells express primarily Fc gamma-RII on their surface. KIT+ lineage- cells did express Fc gamma RIII alpha-chain protein, but predominately in the nuclear/perinuclear area. We could not detect surface expression of Fc epsilon-RI by KIT+ lineage- cells, although a heterogeneous population of KIT- cells does bind IgE with high affinity and may reflect cells of the basophilic lineage. KIT+ lineage- cells cultured with SCF and IL-3 generate numerous mast cells, whereas equivalent numbers of KIT- cells or naive bone marrow cells do not. In these cultures, surface expression of Fc epsilon-RI is detected on a small number of cells by day 3 of culture with increased surface expression levels correlating roughly with metachromatic granule formation. The fact that Fc gamma-RIII and Fc epsilon-RI are not expressed on the cell surface of KIT+ lineage- cells but appear later in hematopoietic development makes it unlikely that these receptors influence early hematopoietic differentiation. The role that might justify such a complete surface expression of Fc gamma-RII by bone marrow progenitors remains to be identified.
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PMID:Murine KIT+ lineage- bone marrow progenitors express Fc gamma-RII but do not express Fc epsilon-RI until mast cell granule formation. 752 15

Hepatocyte growth factor (HGF) is a mesenchymal derived growth factor known to induce proliferation and "scattering" of epithelial and endothelial cells. Its receptor is the tyrosine kinase encoded by the c-MET protooncogene. Here we show that highly purified recombinant HGF stimulates hemopoietic progenitors to form colonies in vitro. In the presence of erythropoietin, picomolar concentrations of HGF induced the formation of erythroid burst-forming unit colonies from CD34-positive cells purified from human bone marrow, peripheral blood, or umbilical cord blood. The growth stimulatory activity was restricted to the erythroid lineage. HGF also stimulated the formation of multipotent CFU-GEMM colonies. This effect is synergized by stem cell factor, the ligand of the tyrosine kinase receptor encoded by the c-KIT protooncogene, which is active on early hemopoietic progenitors. By flow cytometry analysis, the receptor for HGF was found to be expressed on the cell surface in a fraction of CD34+ progenitors. Moreover, in situ hybridization experiments showed that HGF receptor mRNA is highly expressed in embryonic erythroid cells (megaloblasts). HGF mRNA was also found to be produced in the embryonal liver. These data show that HGF plays a direct role in the control of proliferation and differentiation of erythroid progenitors, and they suggest that it may be one of the long-sought mediators of paracrine interactions between stromal and hemopoietic cells within the hemopoietic microenvironment.
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PMID:Hepatocyte growth factor induces proliferation and differentiation of multipotent and erythroid hemopoietic progenitors. 752 22

We have mapped five genes encoding protein tyrosine kinases (PTKs) to the pericentromeric region of human chromosome 4. PTK4 and TYRO4, which encode nonreceptor intracellular PTKs, are located at 4p12 and 4q13, respectively. The other three genes, PDGFRA, KIT, and KDR, encode type III transmembrane receptor PTKs for known ligands. We have developed a contig of 29 yeast artificial chromosomes (YACs) spanning approximately 2 Mb of DNA at 4q12 that includes PDGFRA, KIT, and KDR, and we have used this YAC contig to map 12 different sequence-tagged sites in this region. PDGFRA, KIT, and KDR thus constitute a cluster of genes at 4q12 encoding closely related type III receptor PTKs. Mutations of the human KIT gene result in piebaldism, an autosomal dominant disorder of melanocyte development.
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PMID:A YAC contig spanning a cluster of human type III receptor protein tyrosine kinase genes (PDGFRA-KIT-KDR) in chromosome segment 4q12. 752 18


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