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Modulation of murine erythroleukemic cell differentiation by inhibitors of polyamine biosynthesis 总被引:1,自引:0,他引:1
The differentiation of murine erythroleukemic cells induced by hexamethylene bisacetamide is shown to be differently affected by two inhibitors of polyamine biosynthesis. Methyl glyoxal bis(guanyl hydrazone) (inhibitor or S-adenosyl methionine decarboxylase) inhibited this differentiation process. By using a novel experiment protocol the inhibitory effect of this drug on the induced differentiation was dissociated from pleiotropic effects on cell growth. Methyl glyoxal bis(guanyl hydrazone) only inhibited the induced differentiation if present during the first 6 h of culture of the cells with the inducer. No effect on the induced differentiation was observed if the drug was added to the culture medium 6 h after the inducer. alpha-Difluoro methylornithine (inhibitor of ornithine decarboxylase) stimulated the differentiation of these cells. Polyamine analysis demonstrated that alpha-difluoro methylornithine increased the rapidity and the amplitude of the changes in intracellular polyamines associated with this induced differentiation. The presence of methyl glyoxal bis(guanyl hydrazone) during the first 3 h with the inducer was sufficient to produce opposing changes in the intracellular polyamines. These results suggest that changes in either intracellular polyamines or the activities of polyamine biosynthetic enzymes play a regulatory role in the differentiation process induced in murine erythroleukemic cells by hexamethylene bisacetamide. 相似文献
994.
The localization and immunochemical identification of the novel protein kinase C ϕ (nPKC ϕ) and the atypical protein kinase
C λ (aPKC λ) isoforms in retinas of different species were analyzed by immunohistochemistry and SDS-PAGE/Western blotting.
nPKC ϕ immunoreactivity is associated with bipolar cells of mammalian (rabbit, rat and guinea pig) retinas but not the non-mammalian
goldfish retina which has a lower concentration of nPKC ϕ. However, SDS-PAGE and Western blotting data indicate the antigen
recognized by the nPKC ϕ monoclonal antibody in the retina is of a lower molecular weight than that expected for nPKC ϕ. This
would suggest nPKC ϕ is more susceptible to degradation/breakdown than other PKC isoforms found in the retina or that the
nPKC ϕ antibody may be recognizing an unknown retinal antigen. A comparison of nPKC ϕ and nPKC ϕ is present in the developing
retina at an earlier stage than cPKC α. The typical ‘transport’ of cPKC α toward axonal terminals by phorbol-12,13-dibutyrate
does not occur for nPKC ϕ yet both are translocated from the cytosolic to membrane compartments. The inner plexiform layer
and the inner nuclear layer (putative horizontal cells) of all species examined (rabbit, rat, guinea pig and goldfish) exhibited
positive immunoreactivity for aPKC λ as confirmed by SDS-PAGE/Western blotting.
Special issue dedicated to Dr. Kinya Kuriyama. 相似文献
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A method is described to measure in situ lotic benthic community metabolism partitioned into autotrophic, heterotrophic, bacterial and inorganic components of oxidation. 相似文献
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Sally Martin Callista B. Harper Linda M. May Elizabeth J. Coulson Frederic A. Meunier Shona L. Osborne 《PloS one》2013,8(3)
The lipid phosphatidylinositol 3,5-bisphosphate (PtdIns(3,5)P
2), synthesised by PIKfyve, regulates a number of intracellular membrane trafficking pathways. Genetic alteration of the PIKfyve complex, leading to even a mild reduction in PtdIns(3,5)P
2, results in marked neurodegeneration via an uncharacterised mechanism. In the present study we have shown that selectively inhibiting PIKfyve activity, using YM-201636, significantly reduces the survival of primary mouse hippocampal neurons in culture. YM-201636 treatment promoted vacuolation of endolysosomal membranes followed by apoptosis-independent cell death. Many vacuoles contained intravacuolar membranes and inclusions reminiscent of autolysosomes. Accordingly, YM-201636 treatment increased the level of the autophagosomal marker protein LC3-II, an effect that was potentiated by inhibition of lysosomal proteases, suggesting that alterations in autophagy could be a contributing factor to neuronal cell death. 相似文献