Transcription Factors (Human Molecular Genetics Series)
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Table 1 Primers used for the mutational screening of the entire TCF-4 coding sequence.
Biochemistry: Molecular Genetics
Characterization of Alternative Exons and Splice Sites. Acknowledgments We thank Drs. Footnotes The costs of publication of this article were defrayed in part by the payment of page charges. Science Washington DC , : , Clevers H.
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Oncogene , 18 : , Cell Genet , 88 : , Sparks A. Cancer Res , 58 : , Previous Next. If the Sp1 sequence variation is the only frequent functional polymorphism in this gene still remains to be established. Importantly, there is evidence that the COLIA1 T allele has direct biological effects, which could explain the observed associations. The first report on the polymorphism demonstrated that the putative Sp1 binding site containing the G-to-T polymorphism binds the Sp1 transcription factor protein [ ].
On the basis of these so-called null mutations in OI patients, it can be speculated that an increased proportion of the COLIA1 homotrimer, such as could be the case in GT and TT subjects, would lead to a more fragile bone. This notion is strongly supported by the observation that the T allele was found to be associated with decreased bone strength in that the yield strength of bone taken from the femoral neck was approximately half in GT heterozygotes compared to that of GG homozygotes [ ]. The phenotype of homozygous oim mice includes skeletal fractures, generalized osteopenia, and small body size [ ]—aspects of osteoporosis that are also observed in human TT homozygotes.
Thus, in summary, a strong case is being built to implicate this polymorphism in osteoporosis. There is probably a concomitant effect on bone structure and quality resulting in substantially increased fracture risk, mostly independent of BMD. Whether the Sp1 sequence variation is the only frequent functional polymorphism in this gene remains to be established.
Pleiotropic effects of this gene and interactions with environmental factors and other osteoporosis candidate genes have to be further explored. Maria Angelica Cortez, Estrogens are widely accepted as major contributors to breast cancer development. Some estrogen-regulated miRNAs are associated with estrogen response elements, whereas several others are located in the intergenic regions of estrogen-regulated genes.
A few miRNAs are regulated by secondary estrogen responses via estrogen-regulated transcript factors and are likely associated with epigenetic alteration Bhat-Nakshatri et al. In studies of chronic 6—12 weeks exposure to estradiol E 2 , in a mammary carcinogenesis model in female rats Kovalchuk et al. Interestingly, following even longer exposure to E 2 , the spectrum of miRNA expression changed significantly, as expression of only miR was downregulated, whereas expression of miR , miR , miR , miRp , and miRa was upregulated.
In a study on human breast cancer cells, Maillot et al. However, the direct impact of E 2 on its expression is still controversial, as different groups have reported contrasting effects of this exposure Bhat-Nakshatri et al. Philippa D. Darbre, in Endocrine Disruption and Human Health , In addition to direct binding of the ER to DNA, ERs can regulate gene expression through interactions with other protein transcription factors.
Figure 3. Indirect genomic action of estrogen. EDs may interfere in this pathway by binding to intracellular ER and setting off a similar sequence of events, but with altered consequences to mRNA levels. Interference has also been noted between ER and other transcriptional regulators when the response elements are juxtapositioned in the DNA.
This was first shown through identifying interference in the genomic action of ER by binding of an arylhydrocarbon receptor AhR with its nuclear translocator Arnt to its juxtapositioned dioxin response element in the DNA Figure 3. Juxtapositioned response elements, such as dioxin response elements in the DNA that bind the AhR and its nuclear translocator Arnt , can influence the ability of estrogen-ER complexes to bind to an ERE .
Goldman, in Encyclopedia of Genetics , As there is a vast difference in how tissue-specific in contrast to housekeeping genes must be regulated, it is not surprising that the promoters of these genes differ as well. GC boxes provide binding sites for the transcription factor Sp1 and, like the TATA box, direct the start of transcription. Since there are several GC boxes in the promoters of many housekeeping genes, the transcription start site is ambiguous.
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These data indicate that androgens exert a direct trophic effect on MN-1 cells expressing the wild-type androgen receptor. In contrast, there is a diminished response to ligand in cells expressing the mutant androgen receptor designated Q65 , suggesting that poly Q expansion has caused a partial loss of receptor function. Thus, our system models both the trophic effects mediated by activation of the wild-type receptor and the partial loss-of-function that results from expansion of the poly Q tract.
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These data show that our model will enable us to study the molecular basis of the alteration in function that the androgen receptor undergoes as a result of poly Q expansion. Since the wild-type lines Q and Q behaved similarly in these and all other biochemical analyses, subsequent results will be shown for line Q only, although similar data have been obtained from line Q The diminished trophic effect mediated by activation of the mutant receptor correlates with lower steady-state levels of androgen receptor protein as determined by western blot and Scatchard analysis.
Although the wild-type and mutant receptors have similar ligand-binding affinity in the cell lines used in these studies, cells expressing the mutant receptor only have about half the number of ligand-binding sites 46 , Similar results have been obtained from radiolabeled ligand-binding studies using scrotal fibroblasts derived from some but not all Kennedy's disease patients As seen in Figure 2 A, mutant protein is expressed at lower levels than the wild-type protein in the absence of ligand.
Ligand increases the steady-state levels of both the wild-type and mutant receptors. In contrast to the differences in steady-state protein levels, androgen receptor mRNA levels are quite similar between cells expressing the wild-type and mutant receptors. These data suggest that the exogenous mutant protein is more rapidly degraded than the wild-type protein. To directly test this hypothesis, we performed pulse-chase analysis to measure the half-lives of the wild-type and mutant androgen receptor proteins Fig. In contrast, the half-life of the wild-type receptor is about 3 hours.
Both the wild-type and mutant receptors are stabilized by ligand shown in red. Similar data characterizing the half-life of the wild-type androgen receptor and its ligand-dependent stabilization have been reported previously Treatment with the proteasome inhibitor lactacystin resulted in marked accumulation of both forms of the androgen receptor Fig. Collectively, these data suggest one possible mechanism by which poly Q expansion causes decreased levels of soluble androgen receptor protein, as seen in patients with Kennedy's disease. We next used our cell culture model and oligonucleotide arrays to compare the function of the wild-type and mutant androgen receptors as ligand-activated transcription factors.
For these experiments, cells were treated with ligand or vehicle control for 24 hours. Expression analysis was performed on duplicate samples using Affymetrix GeneChip software. This software package provides a qualitative measure of expression differences between samples increased, decreased or unchanged.
As duplicate experiments allowed us to perform a four-way comparison, our criteria for calling a gene up- or downregulated were that it must be called increased or decreased in three out of four comparisons. We have found similarly high concordance by confirmatory northern blots on a subset of a dozen genes data not shown.