Gene redistribution

But how far could gene redistribution go There must be some lock-in mechanism for a nuclear-coded cytoplasmically-synthesized polypeptide which is finally located only in the organelle. There must be some devices for retaining the polypeptide within the organelle. Figure 21 is a catalogue of possible lock-in mechanisms for polypeptides coded by nuclear genes. 

Corticosteroids suppress both humoral and cellular immunity. Single doses produce a redistribution of lymphocytes with a concentration dependent decrease of CD4 and CDS positive cells. This in vivo lymphopenic effect correlates with the in vitro inhibition of stimulated T-cell proliferation. Furthermore, corticosteroids are able to inhibit the expression of genes coding for IL-1, IL-2, IL-6, interferon a, and tumor necrosis factor, TNE-a. Chronic administration decreases the size and also the cellu-larity of lymphoid tissues like lymph nodes, spleen, and thymus. Corticosteroids have more effect on the primary immune response and are less effective against previously sensitized immune responses. Their suppressive effects are more pronounced for T-cell immune responses than for the humoral immune response. 

Transactivation of proapoptotic genes is not the only way that p53 protein can activate the apoptotic program. There is evidence that variants of p53, which are independent of Bax protein and do not operate at the transcription level, can also result in apoptosis (see Haffner and Oren, 1995 Ko and Prives, 1996). Thus, a p53-regulated redistribution of the Fas death receptor from the cytosol to the cell membrane has been demonstrated (Beimet et al., 1998). Overall, these mechanisms are poorly understood. 

As mentioned above, one consequence of stalled RNA polymerase II at a DNA adduct is activation of transcription-coupled repair [27], This effect may depend on the type of polymerase, however, since the removal of some types of DNA damage is slower from RNA-polymerase I transcribed ribosomal DNA than from a nuclear gene [160], The lower level of repair in the nucleolus could also reflect the influence of other transcription factors, such as the HMG-domain protein UBF, which bind to cisplatin-mod-ified DNA [145]. When HeLa cells were exposed to cisplatin at concentrations which did not seem to affect nuclear transcription, inhibition of rDNA gene expression was associated with the redistribution of UBF, along with other factors responsible for rRNA transcription [138], These observations indicate how cisplatin might exert a combination of effects. Transcription is stopped due to titration of essential factors by the platinum-DNA adducts, and the same proteins could shield the lesions from the repair activity. 

Crossing-over or recombination at homologous loci is a normal process and results in a redistribution of parental genes. However, mis-pairing may lead to the formation of abnormal structural genes whose... 

Here, C2I catalyzes the ADP-ribosylation of actin, resulting in dramatic redistribution of F-actin. Recently, the gene of C2I has been reported encoding a protein of 431 amino acids (M, 49400) with significant similarity to the enzyme component of iota toxin (see below) (Fuji et a/., 1996). 

GPCRs FP, FIDA, thermal melt FLIPR -like, reporter gene, aequorin, TR-FRET, AlphaScreen , EFC Transfluor P-arrestin redistribution... 

While the dopamine depleted striatum provides a good model for study of the selective effects of D1 and D2 receptor stimulation these effects are abnormal in the sense that the pharmacologic treatments that alter gene regulation in the lesioned striatum are not paralleled in the unlesioned striatum. These differences in effect are not due to a redistribution of the receptor subtypes, as the segregated localization of the D1 and D2 receptor subtypes to striatonigral and striatopallidal neurons occurs in both the lesioned... 

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