Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    Wiley ; 2004
    In:  Cell Biology International Vol. 28, No. 5 ( 2004-05), p. 403-410
    In: Cell Biology International, Wiley, Vol. 28, No. 5 ( 2004-05), p. 403-410
    Abstract: K562 cells can be induced to differentiate along the erythroid lineage by a variety of chemical compounds, including hemin, butyrate, cisplatin and ara‐C. Differential signaling through MAP kinases has been suggested to be involved in this differentiation process. We have investigated the involvement of ERK activation/inhibition in hemin‐, butyrate‐, cisplatin‐ and ara‐C‐induced erythroid differentiation using the K562 cell line. ERK activity decreased for 2–4 h after administration of either inducing agent. ERK was then activated by hemin and cisplatin, while ERK phosphorylation remained decreased during incubation with butyrate and ara‐C. There was no activation of JNK or p38. The MEK‐1 inhibitors UO126 or PD98059 induced erythroid differentiation in K562 cells and acted additively with butyrate. Inhibition of MEK‐1 reduced the hemoglobin accumulation by hemin and cisplatin; erythroid differentiation by ara‐C was unchanged. The results suggest that inhibition of signaling through ERK in K562 cells may be needed to enter the erythroid differentiation process, while after initiation both activation and inhibition of signaling through ERK enhance erythroid differentiation, which, however, is dependent on the inducing compound.
    Type of Medium: Online Resource
    ISSN: 1065-6995 , 1095-8355
    Language: English
    Publisher: Wiley
    Publication Date: 2004
    detail.hit.zdb_id: 1462519-2
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. Further information can be found on the KOBV privacy pages