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Transcription factor - Wikipedia

The osteogenic and oncogenic transcription factor RUNX2 downregulates the RNA polymerase I (RNA Pol I)-mediated transcription of rRNAs and changes histone modifications associated with the rDNA repeat. However, the mechanisms by which RUNX2 suppresses rRNA transcription are not well understood. RUNX2 cofactors such as histone deacetylases (HDACs) play a key role in chromatin remodeling and regulation of gene transcription. Here, we show that RUNX2 recruits HDAC1 to the rDNA repeats in osseous cells. This recruitment alters the histone modifications associated with active rRNA-encoding genes and causes deacetylation of the protein upstream binding factor (UBF, also known as UBTF). Downregulation of RUNX2 expression reduces the localization of HDAC1 to the nucleolar periphery and also decreases the association between HDAC1 and UBF. Functionally, depletion of HDAC1 relieves the RUNX2-mediated repression of rRNA-encoding genes and concomitantly increases cell proliferation and global protein synthesis in osseous cells. Our findings collectively identify a RUNX2-HDAC1-dependent mechanism for the regulation of rRNA-encoding genes and suggest that there is plasticity to RUNX2-mediated epigenetic control, which is mediated through selective mitotic exclusion of co-regulatory factors.

N2 - The osteogenic and oncogenic transcription factor RUNX2 downregulates the RNA polymerase I (RNA Pol I)-mediated transcription of rRNAs and changes histone modifications associated with the rDNA repeat. However, the mechanisms by which RUNX2 suppresses rRNA transcription are not well understood. RUNX2 cofactors such as histone deacetylases (HDACs) play a key role in chromatin remodeling and regulation of gene transcription. Here, we show that RUNX2 recruits HDAC1 to the rDNA repeats in osseous cells. This recruitment alters the histone modifications associated with active rRNA-encoding genes and causes deacetylation of the protein upstream binding factor (UBF, also known as UBTF). Downregulation of RUNX2 expression reduces the localization of HDAC1 to the nucleolar periphery and also decreases the association between HDAC1 and UBF. Functionally, depletion of HDAC1 relieves the RUNX2-mediated repression of rRNA-encoding genes and concomitantly increases cell proliferation and global protein synthesis in osseous cells. Our findings collectively identify a RUNX2-HDAC1-dependent mechanism for the regulation of rRNA-encoding genes and suggest that there is plasticity to RUNX2-mediated epigenetic control, which is mediated through selective mitotic exclusion of co-regulatory factors.

Manipulation of transcription factors (TFs) associated with the ..

DUF579 protein required for normal xylan synthesis ..

that SND2 regulates SCW-associated genes

The E6 and E7 oncoproteins of HR-HPV increase theexpression and activity of DNMT1 (). E6 does so by degrading p53 (,)(). In the cervical cancercell lines SiHa and CaSki, knockdown of E6 is associated with anincrease in p53 and a decrease in DNMT1 expression (,).In contrast, Lin ()showed that p53 negatively regulates DNMT1 expression both in celllines and in lung cancer patients. p53 binds to the specificityprotein 1 (Sp1) and chromatin-remodeling proteins, and this complexthen binds to the promoter region of DNMT1. The formation of thecomplex inhibits Sp1 from activating the transcription of DNMT1(). Normally, Sp1 inducesdegradation of p53 by MDM2-mediated ubiquitination (Sp1/p53/MDM2complex) and induces overexpression of DNMT1 (). Non-small cell lung cancer patientswith mutations in p53 and patients with alterations in p53 and/orSp1 showed hypermethylated promoter regions of tumor-suppressorgenes (p=0.003–0.016), most likely due to DNMT1 overexpression().

HIF-1A and c-Myc cooperatively induce atranscriptional program for glycolysis. HIF plays a crucial role incellular adaptation to hypoxia and regulates the expression ofgenes responsible for glucose metabolism, angiogenesis, and cellsurvival (). Cellular HIFlevels are regulated by both an oxygen-dependent pathway and anoxygen-independent pathway. HIF contains two key regulatorysubunits, HIF1A and endothelial PAS domain protein 1 (EPAS1;HIF-2), and the genes encoding these proteins are overexpressed inhuman cancers (,). Many studies have assessed thesignificance of HIF-1A positive expression in the prediction ofclinical outcome of gastrointestinal cancer. HIF-1A expression isassociated with poor prognosis in esophageal squamous cellcarcinoma (ESCC) (,), gastric cancer (,),colorectal cancer (CRC) () andhepatocellular carcinoma (HCC) (). Low expression of HIF1A may beassociated with a favorable effect of 5-FU-based adjuvantchemotherapy in gastric cancer patients (,).HIF-2A is associated with poor survival in gastric cancer patients() but not CRC patients(,).

Transcription factor AtTCP14 regulates embryonic …

The oncogene, a member of the MYCfamily, encodes the transcription factor c-Myc and is upregulatedin many human cancers, linking altered cellular metabolism totumorigenesis (). gene expressions are often elevated or deregulated in humanneoplasms, and c-Myc seems to be at the crossroads of severalimportant pathways and processes involved in carcinogenesis. deregulation due to gene amplification (), chromosomal translocation orinsertion (), mutations(), and epigeneticmodifications () has beenreported in different types of cancers. The number of studies of expression as detected by immunohistochemistry (IHC) isless than that of HIF1A. overexpression and promoterhypomethylation may have a role in the gastric carcinogenesisprocess and deregulation was associated mainly withpoor prognosis (). expression detected by IHC was associated with poor prognosis inpancreatic cancer (), but itsexpression was not associated with poor prognosis in CRC patients(,) ().

Microphthalmia-associated transcription factor regulates the visual cycle genes Rlbp1 ..

Mutations in the genes encoding proteins implicated in the visual cycle have recently emerged as the underlying genetic defects responsible for a number of retinal disorders,. Among them, mutations in Rlbp1 and Rdh5 are associated with retinal dystrophies and dysfunctions such as retinitis pigmentosa, Newfoundland rod/cone dystrophy, retinitis punctata albescens, and Bothnia dystrophy or fundus albipunctatus,,. To provide a deeper understanding of the role of these two genes, we here focus on the regulation of their expression and identify MITF as one of their major transcriptional regulators.

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that protein synthesis-related genes, ..


27/04/2014 · The little elongation complex ..

These domains include a DNA binding domain, a dimerization domain which determines interaction with the differentiation regulated transcription factor proteins (DP), a transactivation domain enriched in acidic amino acids, and a tumor suppressor protein association domain which is embedded within the transactivation domain.

and its binding partner ELL-associated factors ..

Regeneration of the visual pigment by cells of the retinal pigment epithelium (RPE) is fundamental to vision. Here we show that the microphthalmia-associated transcription factor, MITF, which plays a central role in the development and function of RPE cells, regulates the expression of two visual cycle genes, Rlbp1 which encodes retinaldehyde binding protein-1 (RLBP1), and Rdh5, which encodes retinol dehydrogenase-5 (RDH5). First, we found that Rlbp1 and Rdh5 are downregulated in optic cups and presumptive RPEs of Mitf-deficient mouse embryos. Second, experimental manipulation of MITF levels in human RPE cells in culture leads to corresponding modulations of the endogenous levels of RLBP1 and RDH5. Third, the retinal degeneration associated with the disruption of the visual cycle in Mitf-deficient mice can be partially corrected both structurally and functionally by an exogenous supply of 9-cis-retinal. We conclude that the expression of Rlbp1 and Rdh5 critically depends on functional Mitf in the RPE and suggest that MITF has an important role in controlling retinoid processing in the RPE.

Cap n collar transcription factor regulates multiple genes coding ..

AB - The osteogenic and oncogenic transcription factor RUNX2 downregulates the RNA polymerase I (RNA Pol I)-mediated transcription of rRNAs and changes histone modifications associated with the rDNA repeat. However, the mechanisms by which RUNX2 suppresses rRNA transcription are not well understood. RUNX2 cofactors such as histone deacetylases (HDACs) play a key role in chromatin remodeling and regulation of gene transcription. Here, we show that RUNX2 recruits HDAC1 to the rDNA repeats in osseous cells. This recruitment alters the histone modifications associated with active rRNA-encoding genes and causes deacetylation of the protein upstream binding factor (UBF, also known as UBTF). Downregulation of RUNX2 expression reduces the localization of HDAC1 to the nucleolar periphery and also decreases the association between HDAC1 and UBF. Functionally, depletion of HDAC1 relieves the RUNX2-mediated repression of rRNA-encoding genes and concomitantly increases cell proliferation and global protein synthesis in osseous cells. Our findings collectively identify a RUNX2-HDAC1-dependent mechanism for the regulation of rRNA-encoding genes and suggest that there is plasticity to RUNX2-mediated epigenetic control, which is mediated through selective mitotic exclusion of co-regulatory factors.

a heterodimer of xenobiotic transcription factors, ..

MITF is a member of the microphthalmia family of transcription factors (MiT). It is expressed at various levels in a variety of cell types, including neural crest-derived melanocytes and RPE cells where it plays prominent roles in development,. In mice, for instance, mutant alleles such as microphthalmia-vga9 (Mitf mi−vga9) not only cause loss of pigmentation in the skin, but also microphthalmia and retinal degeneration due to abnormalities in RPE structure and function,. Other Mitf mutant alleles, such as microphthalmia-brownish (MitfMi−b) and microphthalmia-vitiligo (Mitfmi−vit), however, do not lead to microphthalmia but to postnatal retinal degeneration,. MITF is well known to regulate the expression of tyrosinase and tyrosinase-related protein-1, whose mutations are associated with Oculocutaneous Albinism and Pigmentary Glaucoma,, and of BEST1, whose mutations cause Best Macular Dystrophy. Nevertheless, little is known about MITF’s potential involvement in the regulation of the visual cycle and whether the regulation of visual cycle genes by MITF contributes to retinal degeneration.

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