All

What are you looking for?

All
Projects
Results
Organizations

Quick search

  • Projects supported by TA ČR
  • Excellent projects
  • Projects with the highest public support
  • Current projects

Smart search

  • That is how I find a specific +word
  • That is how I leave the -word out of the results
  • “That is how I can find the whole phrase”

MK-886 enhances tumour necrosis factor-alpha-induced differentiation and apoptosis

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68081707%3A_____%2F06%3A00040473" target="_blank" >RIV/68081707:_____/06:00040473 - isvavai.cz</a>

  • Result on the web

  • DOI - Digital Object Identifier

Alternative languages

  • Result language

    angličtina

  • Original language name

    MK-886 enhances tumour necrosis factor-alpha-induced differentiation and apoptosis

  • Original language description

    We investigated the role of the 5-lipoxygenase (5-LOX) pathway of arachidonic acid metabolism in tumour necrosis factor-alpha (TNF-alpha)-induced differentiation of human leukemic HL-60 cells using MK-886, an inhibitor of 5-LOX activating protein. MK-886augmented cell cycle arrest and differentiation induced by TNF-alpha; however, both effect were probably 5-LOX-independent, because a general LOX inhibitor, NDGA, had no effect. Apoptosis was significantly elevated after combined TNF-alpha and MK-886 treatment, which could be partially associated with changes of Mc1-1 protein expression. NF-ksíB signalling or activation of JNKs were not modulated by MK-886. Thus, in addition to apoptosis, MK-886 can enhance TNF-alpha-induced differentiation.

  • Czech name

    MK-886 zvyšuje diferenciaci a apoptózu indukovanou TNF-alpha

  • Czech description

    S využitím látky MK-886, inhibitoru proteinu aktivujícího 5-lipoxygenázu (5-LOX), byla studována role dráhy 5-LOX přeměny kyseliny arachidonové v diferenciaci indukované TNF-alpha u lidské buněčné leukemické linie HL-60. MK-886 posiloval zástavu buněčného cyklu a diferenciaci indukovanou TNF-alpha, ale tyto efekty jsou pravděpodobně nezávislé na inhibici 5-LOX, protože obecný inhibitor LOX, NDGA, neměl žádné účinky. Po kombinaci TNF-alpha a MK-886 byla významně potencována apoptóza, což částečně souviselo se změnami exprese proteinu Mc1-1. Signálování přes NF-ksíB nebo aktivace JNK nebyla MK-886 modulována. Tak, kromě apoptózy, MK-886 může zvyšovat i diferenciaci indukovanou TNF-alpha.

Classification

  • Type

    J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

  • CEP classification

    BO - Biophysics

  • OECD FORD branch

Result continuities

  • Project

    <a href="/en/project/GA524%2F03%2F0766" target="_blank" >GA524/03/0766: Modulation of proliferation, differentiation and apoptosis of hemopoietic cells - interactions of cytokines, drugs and lipid nutrition compounds</a><br>

  • Continuities

    Z - Vyzkumny zamer (s odkazem do CEZ)

Others

  • Publication year

    2006

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Cancer letters

  • ISSN

    0304-3835

  • e-ISSN

  • Volume of the periodical

    237

  • Issue of the periodical within the volume

    2

  • Country of publishing house

    NL - THE KINGDOM OF THE NETHERLANDS

  • Number of pages

    9

  • Pages from-to

    263-271

  • UT code for WoS article

  • EID of the result in the Scopus database