Interleukin-3

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  Subject Areas on Research

  • A humanized mouse model to study mast cells mediated cutaneous adverse drug reactions. 
  • Abelson virus abrogation of interleukin-3 dependence in a lymphoid cell line. 
  • Akt-directed glucose metabolism can prevent Bax conformation change and promote growth factor-independent survival. 
  • An effective strategy for decontamination, ex vivo expansion, and storage of human fetal liver hematopoietic stem cells. 
  • Autologous bone marrow transplantation in acute myelogenous leukemia: in vitro treatment with myeloid-specific monoclonal antibodies and drugs in combination. 
  • CD11c(+)B220(+)Gr-1(+) cells in mouse lymph nodes and spleen display characteristics of plasmacytoid dendritic cells. 
  • Caspase-dependent cleavage of carbamoyl phosphate synthetase II during apoptosis. 
  • Close genetic and physical linkage between the murine haemopoietic growth factor genes GM-CSF and Multi-CSF (IL3). 
  • Contribution of mast cells to bacterial clearance and their proliferation during experimental cystitis induced by type 1 fimbriated E. coli. 
  • Conversion of Bcl-2 to a Bax-like death effector by caspases. 
  • Cooperation between core binding factor and adjacent promoter elements contributes to the tissue-specific expression of interleukin-3. 
  • Cytokine induction of the ability of human monocyte CD44 to bind hyaluronan is mediated primarily by TNF-alpha and is inhibited by IL-4 and IL-13. 
  • Cytokine stimulation of aerobic glycolysis in hematopoietic cells exceeds proliferative demand. 
  • Cytokine stimulation promotes glucose uptake via phosphatidylinositol-3 kinase/Akt regulation of Glut1 activity and trafficking. 
  • Cytokine-regulated expression of activated leukocyte cell adhesion molecule (CD166) on monocyte-lineage cells and in rheumatoid arthritis synovium. 
  • Cytoprotective effects of hematopoietic growth factors on primary human acute myeloid leukemias are not mediated through changes in BCL-2, bax, or p21WAF1/CIP1. 
  • Effects of hematopoietic growth factors following myeloablation in a primate model. 
  • Effects of interleukin-3 on hematopoietic recovery after 5-fluorouracil or cyclophosphamide treatment of cynomolgus primates. 
  • Enhanced HIV-1 activity in bone marrow can lead to myelopoietic suppression partially contributed by gag p24. 
  • Enhanced expression of interleukin-3 and granulocyte-macrophage colony-stimulating factor receptor subunits in murine hematopoietic cells stimulated with hematopoietic growth factors. 
  • Enrichment of peripheral blood stem cells in a primate model following administration of a single dose of rh-IL-1 beta. 
  • Expression of constitutively active Raf-1 in the mitochondria restores antiapoptotic and leukemogenic potential of a transformation-deficient BCR/ABL mutant. 
  • Expression of human interleukin-3 (multi-CSF) is restricted to human lymphocytes and T-cell tumor lines. 
  • Glucose metabolism attenuates p53 and Puma-dependent cell death upon growth factor deprivation. 
  • Granulocyte-macrophage colony-stimulating factor and interleukin-3 mRNAs are produced by a small fraction of blood mononuclear cells. 
  • Growth factor modulation of p53-mediated growth arrest versus apoptosis. 
  • Growth factors can influence cell growth and survival through effects on glucose metabolism. 
  • Hematopoietic growth factors: ESMO Clinical Practice Guidelines for the applications. 
  • Human CD34+ hematopoietic progenitors have low, cytokine-unresponsive O6-alkylguanine-DNA alkyltransferase and are sensitive to O6-benzylguanine plus BCNU. 
  • Identification of a critical regulatory site in the human interleukin-3 promoter by in vivo footprinting. 
  • In the absence of extrinsic signals, nutrient utilization by lymphocytes is insufficient to maintain either cell size or viability. 
  • Interleukin-3 expression by activated T cells involves an inducible, T-cell-specific factor and an octamer binding protein. 
  • Interleukin-3-induced activation of the JAK/STAT pathway is prolonged by proteasome inhibitors. 
  • Isolation of unique STAT5 targets by chromatin immunoprecipitation-based gene identification. 
  • JAK2 is required for induction of the murine DUB-1 gene. 
  • Mechanism of differentiation of human erythroleukaemic cell line K562 by hemin. 
  • Multiple proteins interact with the nuclear inhibitory protein repressor element in the human interleukin-3 promoter. 
  • Peptide-major histocompatibility complex class II complexes with mixed agonist/antagonist properties provide evidence for ligand-related differences in T cell receptor-dependent intracellular signaling. 
  • Positive and negative elements regulate human interleukin 3 expression. 
  • Protein phosphatase 2A activates the proapoptotic function of BAD in interleukin- 3-dependent lymphoid cells by a mechanism requiring 14-3-3 dissociation. 
  • Purification and partial characterization of a human hematopoietic precursor population. 
  • Rapamycin and p53 act on different pathways to induce G1 arrest in mammalian cells. 
  • Regulation of the human interleukin-3 gene. 
  • Relationship of acivicin-induced monocytoid differentiation of human myeloid leukemia cells to acivicin-induced modulation of growth factor, cytokine, and protooncogene mRNA expression. 
  • Reversal of apoptosis by the leukaemia-associated E2A-HLF chimaeric transcription factor. 
  • Small contribution of G1 checkpoint control manipulation to modulation of p53-mediated apoptosis. 
  • Subcutaneous vaccination with irradiated, cytokine-producing tumor cells stimulates CD8+ cell-mediated immunity against tumors located in the "immunologically privileged" central nervous system. 
  • The Bcr-Abl tyrosine kinase activates mitogenic signaling pathways and stimulates G1-to-S phase transition in hematopoietic cells. 
  • The distal cytoplasmic domain of the erythropoietin receptor induces granulocytic differentiation in 32D cells. 
  • The dynamics of bone marrow stromal cells in the proliferation of multipotent hematopoietic progenitors by substance P: an understanding of the effects of a neurotransmitter on the differentiating hematopoietic stem cell. 
  • Vasoactive intestinal peptide (VIP) inhibits the proliferation of bone marrow progenitors through the VPAC1 receptor. 
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  Keywords of People

  • Gunn, Michael Dee, Professor of Medicine, Immunology