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  • 1
    Electronic Resource
    Electronic Resource
    Protein kinase A-regulated Cl− channel in ML-1 human hematopoietic myeloblasts (1994)
    Springer
    The journal of membrane biology 142 (1994), S. 65-75 
    Details
    ISSN: 1432-1424
    Keywords: Patch clamp ; Chloride channel ; cAMP-dependent protein kinase ; Human hematopoietic myeloblast
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract Using the inside-out patch clamp technique, we identified a Cl− channel in patches from the membrane of cultured human hematopoietic myeloblastic leukemia ML-1 cells. The Cl− channel was not seen at negative membrane potentials in excised patches until the membrane potential was depolarized to greater than +40 mV. The channel was also activated by addition of cAMP-dependent protein kinase (PKA) catalytic subunit at physiological membrane potential (−40 mV). Biophysical studies of the Cl− channel revealed that the current-voltage (I-V) relationship of the Cl− channel was outwardly rectifying in symmetrical 142 mm Cl− solutions. Single channel conductances were 48 pS for the outward current measured at +60 mV and 27 pS for the inward current at −60 mV. The open time constant of the channel was dependent on the membrane potential and was significantly prolonged at positive membrane potentials. Channels activated by cAMP-dependent protein kinase spent a significantly longer time in the open state compared to those channels activated by depolarization pulses. Pharmacological properties of the Cl− channel were also studied. Two anion transport inhibitors, anthracene-9-carboxylic acid (9-AC) and 4,4-diisothiocyanatostilbene-2,2-disulfonic acid (DIDS) caused a flickering block of the channel. Half-inhibitory concentrations (IC50) for 9-AC and DIDS were 174 ± 20 and 70±16 μm, respectively. Blockade of the Cl− channel by 9-AC or DIDS was completely reversible. Our findings suggest that outwardly rectifying Cl− channels (ORCC) are present in human hematopoietic myeloblasts. The function of ORCC may be involved in hormone-regulated cell growth, cell volume regulation and immune responses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00233384
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  • 2
    Electronic Resource
    Electronic Resource
    Macrophage-stimulating protein, a ligand for the RON receptor protein tyrosine kinase, suppresses myeloid progenitor cell proliferation and synergizes with vascular endothelial cell growth factor and members of the chemokine family (1996)
    Springer
    Annals of hematology 73 (1996), S. 1-9 
    Details
    ISSN: 1432-0584
    Keywords: Key words Macrophage-stimulating protein ; Vascular endothelial cell growth factor ; Chemokines ; Progenitor cells ; Suppressive synergism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Macrophage-stimulating protein (MSP), originally identified as an inducer of murine resident macrophage responsiveness to chemoattractants, is a ligand for human RON/murine STK receptor protein tyrosine kinases. Since STK was cloned from populations enriched for hematopoietic stem cells, we initiated studies on the effects of MSP on colony formation by granulocyte-macrophage (CFU-GM), erythroid (BFU-E), and multipotential (CFU-GEMM) myeloid progenitor cells. MSP alone had no colony stimulating activity. However, MSP caused about a 50% suppression of CFU-GM colony formation induced by synergistic combinations of SLF or Flt-L plus GM-CSF, G-CSF, or IL-3 and of BFU-E and CFU-GEMM colonies induced by SLF or Flt3-L plus Epo or Epo and IL-3. In contrast, MSP had no effect on progenitors stimulated by one growth factor. MSP also suppressed colony formation by stimulated cord blood progenitors, but only after preinduction to a rapidly cycling state. It was previously reported that several members of the chemokine family synergistically suppress myeloid progenitor proliferation. Likewise, synergistic suppression was observed when MSP was paired with VEGF, MIP-1α, IL-8, PF4, MCP-1, IP-10, or ENA-78, or when VEGF was paired with the chemokines; and the required MSP concentration was more than 100-fold less than for MSP alone. Additionally, MSP or VEGF inhibited proliferation of the human myeloid growth factor-dependent cell line, M07e, but a sustained effect required multiple additions over time. At the least, some of the MSP suppressive effects on myeloid progenitors, as assessed on single isolated CD34+++ marrow cells, appeared to be directly on the progenitors; sustained additions of MSP were required to see this effect. The suppressive action of MSP and its synergism with proteins of the chemokine family may be of relevance to regulation of blood cell production.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002770050192
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    Paper (German National Licenses)
    Fulltext
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