scholarly journals A Novel Functional Epitope Formed by Domains 1 and 4 of the Human Common β-Subunit Is Involved in Receptor Activation by Granulocyte Macrophage Colony-stimulating Factor and Interleukin 5

2003 ◽  
Vol 278 (12) ◽  
pp. 10572-10577 ◽  
Author(s):  
James M. Murphy ◽  
Sally C. Ford ◽  
Ursula M. Wiedemann ◽  
Paul D. Carr ◽  
David L. Ollis ◽  
...  
Keyword(s):  
Receptor Activation ◽  
Β Subunit ◽  
Colony Stimulating Factor ◽  
Interleukin 5 ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

scholarly journals Interleukin-5 is at 5q31 and is deleted in the 5q- syndrome

Blood ◽  
1988 ◽  
Vol 71 (4) ◽  
pp. 1150-1152
Author(s):  
GR Sutherland ◽  
E Baker ◽  
DF Callen ◽  
HD Campbell ◽  
IG Young ◽  
...  
Keyword(s):  
Growth Hormone ◽  
In Situ Hybridization ◽  
Colony Stimulating Factor ◽  
Interleukin 5 ◽  
Viral Oncogene ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Viral Oncogene Homolog

Human interleukin-5 (IL-5) is a selective eosinophilopoietic and eosinophil-activating growth hormone. By in situ hybridization this gene is mapped to chromosome 5q23.3 to 5q32. It is shown to be deleted in two patients with the 5q-syndrome and in one patient previously diagnosed with myelodysplasia whose condition had progressed to acute myeloblastic leukemia. The clustering of other genes involved in hematopoiesis (IL-3, granulocyte-macrophage colony-stimulating factor, feline sarcoma viral oncogene homolog, colony-stimulating factor 1) to the same region as IL-5 suggests a nonrandom localization and raises interesting questions concerning the evolution and regulation of these genes.

scholarly journals Differential activation of leukotriene biosynthesis by granulocyte- macrophage colony-stimulating factor and interleukin-5 in an eosinophilic substrain of HL-60 cells

Blood ◽  
1995 ◽  
Vol 86 (9) ◽  
pp. 3507-3516 ◽  
Author(s):  
KA Scoggan ◽  
AW Ford-Hutchinson ◽  
DW Nicholson
Keyword(s):  
Binding Sites ◽  
Affinity Binding ◽  
Colony Stimulating Factor ◽  
High Affinity Binding ◽  
Interleukin 5 ◽  
Gm Csf ◽  
High Affinity ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Cytokines can stimulate eosinophils to produce cysteinyl leukotrienes (LTs) in the lung that provoke tissue destruction associated with asthma. Priming of an eosinophilic substrain of HL-60 cells (HL-60#7) with recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) before ionophore challenge was found to produce an apparent 45% increase in total LT production in a dose-dependent manner (ED50 = 150 pmol/L) that could be accounted for by a decrease in the time required for maximal formation of LTs. GM-CSF had no effect on the kinetic parameters of LTC4 synthase and therefore probably acts upstream of this catalytic event. Incubation with interleukin-5 (IL-5), however, had no effect on LT biosynthesis. This differential priming ability was not a consequence of different receptor populations or differences in the affinity or stability of the ligand-receptor complexes of GM-CSF and IL-5. GM-CSF and IL-5 each displayed similar populations of high-affinity binding sites and neither GM-CSF nor IL-5 were able to cross-compete for the other's receptor binding sites. Analysis of phosphotyrosine patterns suggest that IL-5 is incapable of transducing a signal in eosinophilic HL-60#7 cells even though IL-5 and GM-CSF receptors mediate signal transduction via a common beta-chain component that is also necessary for high-affinity binding. Overall, this unique system may permit the dissection of distinct events responsible for specific intracellular signals transduced separately by GM-CSF or IL-5.

scholarly journals A mutation of the common receptor subunit for interleukin-3 (IL-3), granulocyte-macrophage colony-stimulating factor, and IL-5 that leads to ligand independence and tumorigenicity

Blood ◽  
1994 ◽  
Vol 83 (10) ◽  
pp. 2802-2808 ◽  
Author(s):  
R D'Andrea ◽  
J Rayner ◽  
P Moretti ◽  
A Lopez ◽  
GJ Goodall ◽  
...  
Keyword(s):  
Large Family ◽  
Mutant Form ◽  
Sequence Motifs ◽  
Colony Stimulating Factor ◽  
Interleukin 5 ◽  
Interleukin 3 ◽  
Conserved Sequence ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Abstract The cytokines interleukin-3, interleukin-5, and granulocyte-macrophage colony-stimulating factor bind with high affinity to a receptor complex that contains a ligand-specific alpha-chain and a common beta-chain, h beta c. We report here the isolation of a mutant form of h beta c, from growth factor-independent cells, that arose spontaneously after infection of a murine factor-dependent hematopoietic cell line (FDC-P1) with a retroviral h beta c expression construct. Analysis of this h beta c mutation shows that a small (37 amino acid) duplication of extracellular sequence that includes two conserved sequence motifs is sufficient to confer ligand-independent growth on these cells and lead to tumourigenicity. Because this is a conserved region in the cytokine receptor superfamily, our results suggest that the large family of cytokine receptors has the capacity to become oncogenically active.

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