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71.
The X-ray scattering diagram from single chromatin subunit particles is registered within a scattering vector intervall from s = 0 to s = 1 1/A. Preliminary results concerning the dimensions and the structure of the nucleosome core particle are communicated.  相似文献   
72.
Cyclin-dependent kinase inhibitor p2(Waf1/Cip1/Sdi1/CAP20) plays the key part in cell cycle arrest at the G1/S checkpoint in response to DNA damage, and is involved in the assembly of active cyclin-kinase complexes, in particular, cyclin D-Cdk4/6. Recent studies extended the range of known p21Waf1 functions. In addition to the cell-cycle control, p21Waf1 participates in important cell processes such as differentiation, senescence, and apoptosis. A balance of p21Waf1 functional activity seems to shift depending on the cell state (senescence, exposure to stress, expression of viral oncogenes). This is due to direct or indirect interaction with various modulators or to modification (phosphorylation, partial proteolysis) of p21Waf1. The review considers the structure of p21Waf1, its posttranslational modification, interactions with various cell or viral proteins, and their effects on the p21Waf1 function and the cell.  相似文献   
73.
The survey of 2,500 persons in different educational organized groups has been carried out by the method based on the study of changes occurring in the standard population of group A meningococci due to its interaction with the surviving culture of human leukocytes. The heterogeneity of humans with regard to the individual antimeningococcal activity of their blood irrespective of their levels of humoral immunity and complement activity has been revealed. The survey has shown the possibility of detecting the groups of risk among the members of organized groups having, according to our data, a significantly higher level of morbidity in generalized meningococcal infection and meningococcal carriership (including epidemiologically important groups A, B and C).  相似文献   
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Epithelial and endothelial cells are susceptible to a subset of apoptosis known as anoikis. This type of programmed cell death is activated upon disruption of cell-substrate contacts. Here we demonstrate that mouse F9 embryonal carcinoma cell line acquires susceptibility to anoikis upon retinoic acid-induced differentiation towards non-malignant pariental endoderm-like cells. F9 cells survival becomes dependent on the substrate by the 4th day of retinoic acid treatment, when cells assume epithelial phenotype as revealed by actin, alpha-actinin and vinculin expression and distribution, and when focal adhesion contacts are formed. Differentiated F9 cells die in suspension by apoptosis as revealed by oligonucleosomal DNA laddering, DAPI staining and DNA flow cytometry analysis. On the contrary, undifferentiated F9 cells form large multicellular aggregates in suspension and survive. Thus, F9 cell line provides a new model to study pathways involved in both anoikis induction and inhibition.  相似文献   
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Rat embryonic fibroblasts, transformed with E1A and cHa-ras oncogenes, are unable to stop in the cell cycle checkpoints under growth factor withdrawal and genotoxic stresses (Bulavin et al., 1999). In the present paper, we showed that sodium butyrate, an inhibitor of histone deacetyase activity, decreased the share of cells being in S-phase, and caused G1/S and G2/M blocks of the cell cycle in the transformants. By means of RT-PCR and immunoblotting, we found that NaB significantly changed the expression of genes involved in proliferation: cyclins D1, A, E and cyclin-dependent kinases Cdk2 and Cdk4, whereas the amount of p21Waf1 and p27Kip1 inhibitors greatly increased. Along with accumulation of p21Waf1 protein content, that of Cdk2-bound p21 increases. Taken together, these data allow to suggest that NaB treatment does evidently restore the capability of p21Waf1 to inhibit cyclin-kinase activity. One may suppose that inhibition of HDAC activity by sodium butyrate leads to activation of yet unknown HDAC-dependent genes, which is followed by restoration of p21Waf1 function in spite of the E1A oncogene expression.  相似文献   
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