Aberrant activation of the Wnt-β-catenin pathway has been found in a wide range of cancers, especially in cancers derived from intestine, skin, mammary gland and haematopoietic cells. Moreover, the Wnt-β-catenin pathway may preferentially influence stem/progenitor cell expansion in these cancers (Wend et al., 2010). Although many downstream target genes for both normal development and tumorigenesis have been identified in different cellular contexts, the genes that mediate the Wnt-β-catenin pathway activity in maintaining the stem cell properties are still not very clear. c-Myc, a reprogramming factor and a well-known Wnt target, was recently demonstrated to be an important stem cell regulator in normal and cancerous cells (Kim et al., 2010; Smith et al., 2011). However, no study has established a convincing relationship between the Wnt-β-catenin pathway and c-Myc in stem cells. In contrast, recent studies on both iPS and ESCs suggest that the role of the Wnt-β-catenin pathway in ...
Transcriptional regulator which displays a remarkable functional diversity in the regulation of cellular responses. These include the regulation of IFN and IFN-inducible genes, host response to viral and bacterial infections, regulation of many genes expressed during hematopoiesis, inflammation, immune responses and cell proliferation and differentiation, regulation of the cell cycle and induction of growth arrest and programmed cell death following DNA damage. Stimulates both innate and acquired immune responses through the activation of specific target genes and can act as a transcriptional activator and repressor regulating target genes by binding to an interferon-stimulated response element (ISRE) in their promoters. Its target genes for transcriptional activation activity include: genes involved in anti-viral response, such as IFN-alpha/beta, DDX58/RIG-I, TNFSF10/TRAIL, OAS1/2, PIAS1/GBP, EIF2AK2/PKR and RSAD2/viperin; antibacterial response, such as NOS2/INOS; anti-proliferative response, ...
MDM4 inhibits p53- and p73-mediated cell cycle arrest and apoptosis by binding its transcriptional activation domain. It inhibits degradation of MDM2.…
Role of EGF receptor transactivation on LPA-induced LPA1-3 receptor phosphorylation.Cells overexpressing LPA1 (panel A, black bars), LPA2 (panel B, blue bars)
Transcriptional regulator which displays a remarkable functional diversity in the regulation of cellular responses. These include the regulation of IFN and IFN-inducible genes, host response to viral and bacterial infections, regulation of many genes expressed during hematopoiesis, inflammation, immune responses and cell proliferation and differentiation, regulation of the cell cycle and induction of growth arrest and programmed cell death following DNA damage. Stimulates both innate and acquired immune responses through the activation of specific target genes and can act as a transcriptional activator and repressor regulating target genes by binding to an interferon-stimulated response element (ISRE) in their promoters. Its target genes for transcriptional activation activity include: genes involved in anti-viral response, such as IFN-alpha/beta, DDX58/RIG-I, TNFSF10/TRAIL, OAS1/2, PIAS1/GBP, EIF2AK2/PKR and RSAD2/viperin; antibacterial response, such as NOS2/INOS; anti-proliferative response, ...
Among recently investigated potential targets for selective cancer treatment are signal transducers and activators of transcription (STATs). STATs are transcription factors activated in response to cytokines and growth factors and are involved in different cellular processes including proliferation, differentiation and inflammation. Of the seven known mammalian STAT proteins STAT3 was shown to be constitutively activated in many human malignancies. Aberrant STAT3 activity promotes tumor progression through transcriptional activation of genes encoding apoptosis inhibitors, cell-cycle regulators and inducers of angiogenesis. Available data indicate that inhibition of STAT3 signaling leads to an attenuation of cancer cell growth and the induction of apoptosis.. The aim of our investigation was to design a novel STAT3 small molecule inhibitor that would selectively inhibit STAT3 activity, reducing expression of its downstream genes. Thus, we performed computational modeling and small molecule ...
The p53 protein has been divided into four domains; (i) a transcriptional activation domain that contacts TAF components of TFIID (residues 1-40; refs. 18 and 19); (ii) a sequence-specific DNA binding domain (residues 120-290; refs. 16 and 17); (iii) a tetramerization domain (residues 310-360; ref. 20); and (iv) a domain that recognizes and binds to damaged DNA nonspecifically (residues 364-390; refs. 46 and 47). This manuscript describes a new fifth functional domain, localized between residues 61-94, containing a putative proline-rich signaling domain. Deletion of this domain from the p53 protein leaves a normal p53 protein with respect to transcriptional transactivation. Therefore, despite its physical juxtaposition between the transcriptional activation and DNA binding domains, the proline-rich region of p53 is not essential to the function of these domains. Because the proline-rich domain of p53 is dispensable for transactivation, the ΔproAE mutant serves as a useful tool to address the ...
In the context of gene regulation: transactivation is the increased rate of gene expression triggered either by biological processes or by artificial means, through the expression of an intermediate transactivator protein. In the context of receptor signaling, transactivation occurs when one or more receptors activate yet another; receptor transactivation may result from the crosstalk of signaling cascades. Transactivation can be triggered either by endogenous cellular or viral proteins, also called transactivators. These protein factors act in trans (i.e., intermolecularly). HIV and HTLV are just two of the many viruses that encode transactivators to enhance viral gene expression. These transactivators can also be linked to cancer if they start interacting with, and increasing expression of, a cellular proto-oncogene. HTLV, for instance, has been associated with causing leukemia primarily through this process. Its transactivator, Tax, can interact with p40, inducing overexpression of ...
P53 is a short-lived, non-abundant protein that regulates the response of cells to DNA damage, in part through transcriptional activation of genes involved in cell cycle control, DNA repair, and apoptosis. P53 is a tumour suppressor protein; consequently, mice in which the p53 gene has been disrupted develop tumours with high frequency, and deletions or mutations in the p53 gene are prevalent in a majority of human cancers. The protein level and activity of p53 is regulated by MDM2 (murine double minute 2). The MDM2 gene is induced by p53, and MDM2 prevents apoptosis by inhibiting p53 activity and promoting its degradation. ...
Barak, Y; Lupo, A; Zauberman, A; Juven, T; Aloni, Grinstein R.; Gottlieb, E; Rotter, V; and Oren, M, " Targets for transcriptional activation by wild-type p53: endogenous retroviral LTR, immunoglobulin-like promoter, and an internal promoter of the mdm2 gene." (1994). Faculty Research 1990 - 1999. 611 ...
Botella LM، Sánchez-Elsner T، Sanz-Rodriguez F، Kojima S، Shimada J، Guerrero-Esteo M، Cooreman MP، Ratziu V، Langa C، Vary CP، Ramirez JR، Friedman S، Bernabéu C (Dec 2002). "Transcriptional activation of endoglin and transforming growth factor-beta signaling components by cooperative interaction between Sp1 and KLF6: their potential role in the response to vascular injury". Blood. 100 (12): 4001-10. PMID 12433697. doi:10.1182/blood.V100.12.4001. الوسيط ...
NaturalNews) "We may need to seek them out and destroy them where they live," wrote a Merck & Co. employee who was actively plotting to murder or discredit doctors who had voiced concerns regarding the adverse health effects of an anti-inflammatory drug called Vioxx.. Launched in 1999, Vioxx was extremely popular (with more than 80 million users worldwide), as its makers heralded the drug as being the answer to inflammation, minus the nausea that often follows with anti-inflammatory medication.. It was later discovered that the New Jersey-based Merck & Co. was knowingly selling a drug that frequently caused heart attacks and strokes in its unsuspecting victims. A study revealed that Vioxx actually doubled the risk of heart attacks and strokes, prompting the company to voluntary withdraw the drug from the market in 2004.. Prior to the drug being pulled from the market, several Merck & Co. staff exchanged emails in which they discussed a "hit list" they drafted of doctors whom they believed needed ...
TY - JOUR. T1 - Structural proteins of Helicoverpa armigera densovirus 2 enhance transcription of viral genes through transactivation. AU - Xu, Pengjun. AU - Yuan, He. AU - Yang, Xianming. AU - Graham, Robert I.. AU - Liu, Kaiyu. AU - Wu, Kongming. PY - 2017/6/1. Y1 - 2017/6/1. N2 - © 2017, Springer-Verlag Wien. Herein, we report the identification of putative promoters for the non-structural proteins (NS) and capsid structural proteins (VP) of Helicoverpa armigera densovirus (HaDV2) as well as a potential mechanism for how these promoters might be regulated. For the first time, we report that VP is able to transactivate the VP promoter and, to a lesser degree, the NS promoter in densoviruses. In addition to this, another promoter-like sequence designated P2, when co-transfected with the VP gene, enhanced luciferase activity by approximately 35 times compared to a control. This suggests that there are two promoters for VP in HaDV2 and that the VP of parvoviruses might play a more important role ...
Conjugate inhibits androgen receptor transactivation and translocation in prostate cancer cells.Effect of conjugate on the transactivation of androgen receptor
A 58-amino acid region mediates the core transactivation activity of the glucocorticoid receptor tau 1 activation domain. This tau 1 core domain is unstructured in aqueous buffers, but in the presence of trifluoroethanol three Alpha-helical segments are induced. Two of these putative structural modules have been tested in different combinations with regard to transactivation potential in vivo and binding capacity to the coactivators in vitro, The results show that whereas single modules are not transcriptionally active, any combination of two or three modules is sufficient, with trimodular constructs having the highest activity. However, proteins containing one, two, or three segments bind Ada2 and cAMP-response element-binding protein with similar affinity. A single segment is thus able to bind a target factor but cannot transactivate target genes significantly. The results are consistent with models in which activation domains are comprised of short activation modules that allow multiple ...
To ensure that the attached RNA module both retains targeting functionality as well as the resulting complex drive transcriptional activation at a specific site of interest, transient reporter gene expression of luciferase and fluorescent protein was measured. Two variations of such a transcription activator assay was performed; directly with a dCas9 fused to a transcriptional activator/repressor (VP64, a factor known to enhance gene expression) (Direct activation) or indirectly where the transcriptional activator is fused to an RNA binding protein module on the sgRNA (Bridged activation). Reporter gene activation through direct activation imply the sgRNA variant binds and targets dCas9 efficiently. All the five topologies showed direct activation except TOP3 and TOP4, which showed reduced activity. Bridged activation indicates that the fused RNA accessory domain is intact in mature dCas9 complexes. Bridged activation was observed with TOP1, TOP3 and INT. The results were recapitulated at ...
The activation of the p53 protein by cellular stress signals is fundamental for tumor suppression but also promotes pathological states, such as provoking the side effects of genotoxic cancer therapies. To better understand the mechanisms of p53 action in different contexts, we have leveraged both mouse genetic and genomic approaches. First, we have used mouse genetics to define transcriptional programs involved in p53 function in different in vivo settings, specifically by generating a panel of p53 transcriptional activation domain mutant knock-in mouse strains. These include strains expressing p53 mutants in the first (p5325,26), second (p5353,54), or both transactivation domains (p5325,26,53,54). We have observed that p5325,26 is severely compromised for transactivation of most classical p53 target genes, but retains the ability to activate a subset of p53 targets, while p5325,26,53,54 lacks transactivation activity completely. Interestingly, although unable to induce apoptosis or cell cycle ...
BioAssay record AID 82682 submitted by ChEMBL: Inhibitory activity of compound was tested against transcriptional activation by Tat protein in human cells.
BioAssay record AID 396055 submitted by ChEMBL: Agonist activity at human PPARgamma in U2OS cells by transactivation assay relative to rosiglitazone.
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Hyaluronic acid and its derivative as a multi-functional gene expression enhancer: Protection from non-specific interactions, adhesion to targeted cells, and transcriptional activation ...
reference: Structure of the MDM2 oncoprotein bound to the p53 tumor suppressor transactivation domain., Kussie PH, Gorina S, Marechal V, Elenbaas B, Moreau J, Levine AJ, Pavletich NP, Science 1996 Nov 8;274(5289):948-53. PMID: 8875929 ...
The coiled-coil coactivator (CoCoA) enhances transcriptional activity of nuclear receptors, the xenobiotic aryl hydrocarbon receptor, and the lymphocyte enhancer factors (LEF) in the Wnt/β-catenin signaling pathway. CoCoA is comprised of a large central coiled coil domain flanked by N-terminal and C-terminal activation domains (AD). The N-terminal AD of CoCoA is required for coactivator function with LEF and β-catenin, while the C-terminal AD of CoCoA is required for coactivator function with nuclear receptors. We explored the role of sumoylation in regulating the activities of the two ADs and the coactivator function of CoCoA. The N-terminus of CoCoA is covalently modified by SUMO1 at Lys-29; both PIAS1 and ARIP3 function as E3 ligases. Fusion of SUMO1 to the N-terminus (mimicking sumoylation) reduced coactivator function of CoCoA with LEF1 and the activity of the N-terminal AD. The N- and C-termini of CoCoA can bind to each other, and C-terminal transactivation activity is attenuated in the presence
TY - JOUR. T1 - Transcriptional transactivation functions localized to the glucocorticoid receptor N terminus are necessary for steroid induction of lymphocyte apoptosis. AU - Dieken, E. S.. AU - Miesfeld, R. L.. PY - 1992/1/1. Y1 - 1992/1/1. N2 - Genetic studies have suggested that transcriptional regulation of specific target genes (by either induction or repression) is the molecular basis of glucocorticoid-mediated lymphocyte apoptosis. To examine the role of transcriptional regulation more directly, we developed a complementation assay utilizing stable transfection of wild-type (wt) and mutant (nt(i)) glucocorticoid receptor (GR) cDNA constructs into a GR-deficient S49 murine cell line (7r). Our data confirm that the level of functional GR is rate limiting for S49 apoptosis and moreover that the GR amino terminus (N terminus), which has been deleted from the nt(i) GR, is absolutely required for complementation in this system. Surprisingly, we found that at physiological levels of receptor, ...
We examined how ERK affects the transcriptional activity of LIN-1 to determine if phosphorylation by ERK abrogates LIN-1 activity or converts LIN-1 to a transcriptional activator. If LIN-1 cannot be phosphorylated by ERK because the docking sites for ERK are mutated, then the carboxy-terminus of LIN-1 repressed transcription by about fivefold. By contrast, the carboxy-terminus of LIN-1 activated transcription by ∼80-fold when ERK-docking sites were intact. Stimulating ERK activity with bFGF caused a further 2-fold increase in transcriptional activation. Overall, the difference between transcriptional activation by LIN-1 that cannot be phosphorylated and LIN-1 that is maximally phosphorylated is ∼900-fold. The dramatic ERK-responsive transcriptional activation potential of the carboxy-terminus of LIN-1 strongly supports the model that ERK switches LIN-1 from a transcriptional repressor to a phosphorylated transcriptional activator.. These results extend the similarities between LIN-1 and ...
The present invention discloses steroid/thyroid hormone receptor DNA binding domain compositions that determine target gene specificity. The invention further discloses methods converting the target gene specificity of one receptor into the target gene specificity of another. Still further the invention discloses novel assays for identifying ligands for orphan hormone receptors. These assays are especially useful since they avoid the necessity of constructing chimeric genes and proteins in order to search for ligands that can activate a putative receptor.
High-risk human papillomaviruses are causative agents of cervical cancer. Viral protein E7 is required to establish and maintain the pro-oncogenic phenotype in infected cells, but the molecular mechanisms by which E7 promotes carcinogenesis are only partially understood. Our transcriptome analyses in primary human fibroblasts transduced with the viral protein revealed that E7 activates a group of mitotic genes via the activator B-Myb-MuvB complex. We show that E7 interacts with the B-Myb, FoxM1 and LIN9 components of this activator complex, leading to cooperative transcriptional activation of mitotic genes in primary cells and E7 recruitment to the corresponding promoters. E7 interaction with LIN9 and FoxM1 depended on the LXCXE motif, which is also required for pocket protein interaction and degradation. Using E7 mutants for the degradation of pocket proteins but intact for the LXCXE motif, we demonstrate that E7 functional interaction with the B-Myb-MuvB complex and pocket protein degradation ...
As the key regulatory factor in lipogenesis, SREBPs are targets of hormones such as insulin, glucagon, and growth factors (17, 28, 36). The abundance of the nuclear form of SREBPs is controlled by transcriptional upregulation followed by proteolytic cleavage. However, an increasing body of evidence supports the hypothesis that posttranslational modifications of SREBPs modulate their transactivity and stability (22, 32, 39). In this study, we found that PKA phosphorylated SREBP-1 in cultured hepatoma cells and led to decreased binding and transactivation of SREBP-1. As a result, the expression of SREBP-1-mediated genes was decreased. Because the heterodimer of phosphorylated and unphosphorylated SREBP-1 retained some DNA binding capacity, neither cAMP nor forskolin suppressed the activity of nuclear SREBP-1a fully in our reporter assays. In addition to phosphorylation, cAMP also may inhibit SREBP cleavage, as suggested in a recent report (43). However, our present results have shown that levels ...
Sigma-Aldrich offers abstracts and full-text articles by [Yukari Nakamura, Eiichi Hinoi, Takeshi Takarada, Yoshifumi Takahata, Tomomi Yamamoto, Hiroyuki Fujita, Saya Takada, Syota Hashizume, Yukio Yoneda].
ZNF619, 0.1 ml. Zinc-finger proteins contain DNA-binding domains and have a wide variety of functions, most of which encompass some form of transcriptional activation or repression.
By differential hybridization, we identified a number of genes in Saccharomyces cerevisiae that are activated by addition of cyclic AMP (cAMP) to cAMP-depleted cells. A majority, but not all, of these genes encode ribosomal proteins. While expression of these genes is also induced by addition of the appropriate nutrient to cells starved for a nitrogen source or for a sulfur source, the pathway for nutrient activation of ribosomal protein gene transcription is distinct from that of cAMP activation: (i) cAMP-mediated transcriptional activation was blocked by prior addition of an inhibitor of protein synthesis whereas nutrient-mediated activation was not, and (ii) cAMP-mediated induction of expression occurred through transcriptional activation whereas nutrient-mediated induction was predominantly a posttranscriptional response. Transcriptional activation of the ribosomal protein gene RPL16A by cAMP is mediated through a upstream activation sequence element consisting of a pair of RAP1 binding ...
The Keap1-Nrf2-ARE signaling pathway elicits an adaptive response for cell survival after endogenous and exogenous stresses, such as inflammation and carcinogens, respectively. Keap1 inhibits the transcriptional activation activity of Nrf2 (p45 nuclear factor erythroid-derived 2-related factor 2) in unstressed cells by facilitating its degradation. Through transcriptional analyses in Keap1- or Nrf2-disrupted mice, we identified interactions between the Keap1-Nrf2-ARE and the Notch1 signaling pathways. We found that Nrf2 recognized a functional antioxidant response element (ARE) in the promoter of Notch1. Notch1 regulates processes such as proliferation and cell fate decisions. We report a functional role for this cross talk between the two pathways and show that disruption of Nrf2 impeded liver regeneration after partial hepatectomy and was rescued by reestablishment of Notch1 signaling.. ...
Stimulation of pancreatic β-cells with glucose activates the protein kinases B-Raf and extracellular signal-regulated protein kinase that participate in glucose sensing. Inhibition of both kinases results in impairment of glucose-regulated gene transcription. To analyze the signaling pathway controlled by B-Raf, we expressed a conditionally active form of B-Raf in INS-1 insulinoma cells. Here, we show that stimulation of B-Raf strongly activated the transcription factor AP-1 which is accompanied by increased c-Jun and c-Fos promoter activities, an upregulation of c-Jun and c-Fos biosynthesis, and elevated transcriptional activation potentials of c-Jun and c-Fos ...
By means of the fluorescent differential display method, we isolated novel mouse and human genes, Drctnnb1a and DRCTNNB1A, the expression levels of which were inversely correlated to the amount of β-catenin present in cells. Recent reports have identified a number of mammalian genes including c-myc (6) , cyclin D1 (7) , matrilysin (8) , WISP (9) , c-jun, fra-1, uPAR, ZO-1 (10) , and NBL4 (11) that are regulated by stabilization and activation of β-catenin. In Xenopus or Drosophila, target genes for Wnt signaling include the nodal-related 3 gene, Xnr3 (17) , a member of the transforming growth factor-β superfamily, and homeobox genes engrailed (18) , goosecoid, siamois (17) , twin (19) , ultrabithorax (20) , and fibronectin (21) . Among those reported molecules, all but ZO-1 appeared to be up-regulated byβ -catenin through transactivation of Tcf/Lef transcription factors. Hence, DRCTNNB1A is only the second gene to be identified as down-regulated by the accumulation of β-catenin. ...
Involved in transcriptional regulation. Modulates TGF-beta-mediated transcription via association with SMAD proteins, MYOD1-mediated transcription via association with PABPN1, RB1-mediated transcriptional repression, and retinoid-X receptor (RXR)- and vitamin D receptor (VDR)-dependent gene transcription in a cell line-specific manner probably involving coactivators NCOA1 and GRIP1. Is involved in NOTCH1-mediated transcriptional activation. Binds to multimerized forms of Notch intracellular domain (NICD) and is proposed to recruit transcriptional coactivators such as MAML1 to form an intermediate preactivation complex which associates with DNA-bound CBF-1/RBPJ to form a transcriptional activation complex by releasing SNW1 and redundant NOTCH1 NICD. Proposed to be involved in transcriptional activation by EBV EBNA2 of CBF-1/RBPJ-repressed promoters. Is recruited by HIV-1 Tat to Tat:P-TEFb:TAR RNA complexes and is involved in Tat transcription by recruitment of MYC, MEN1 and TRRAP to the HIV ...
We have examined the involvement of components of the interleukin-1 (IL-1) signaling pathway in the transactivation of gene expression by the p65 subunit of NF-kappaB. Transient transfection of cells with plasmids encoding wild-type MyD88, IL-1 receptor-associated kinase 1 (IRAK-1), and TRAF-6 drove p65-mediated transactivation. In addition, dominant negative forms of MyD88, IRAK-1, and TRAF-6 inhibited the IL-1-induced response. In cells lacking MyD88 or IRAK-1, no effect of IL-1 was observed. Together, these results indicate that MyD88, IRAK-1, and TRAF-6 are important downstream regulators of IL-1-mediated p65 transactivation. We have previously shown that the low-molecular-weight G protein Rac1 is involved in this response. Constitutively active RacV12-mediated transactivation was not inhibited by dominant negative MyD88, while dominant negative RacN17 inhibited the MyD88-driven response, placing Rac1 downstream of MyD88 on this pathway. Dominant negative RacN17 inhibited wild-type IRAK-1- ...
Mouse anti Human glucocorticoid receptor antibody, clone 8E9 recognizes the human glucocorticoid receptor (GR), also known as Nuclear rece
DESCRIPTION (provided by applicant): Estrogen receptor-1 (ER) and progesterone receptor (PR) are ligand-induced transcription factors. Accessory proteins, termed coactivators modulate the transcriptional activation of these factors. It has been shown that coactivators enhance transcription of the target genes and play important roles in diverse pathological processes, such as cancers, inherited genetic diseases, metabolic disorders, and inflammation. Earlier work by our laboratory identified E6-associated protein (E6-AP) as a coactivator of steroid hormone receptors. In an attempt to identify E6-AP-interacting protein(s), we have cloned WW-domain binding protein-2 (WBP-2) and have shown that WBP-2 selectively coactivates the transactivation functions of ER and PR. WBP-2 is a novel polyproline rich (PPXY) motif containing protein. The PPXY motif of WBP-2 has been shown to be involved in transcriptional activation pathways. The PPXY motif interacts with WW-domain containing proteins and form PPXY ...
Chrysin greatly increased UGT1A1 expression in immortalized cell lines, such as Caco-2 and HepG2 cells, in previous reports (Galijatovic et al., 2000, 2001; Walle et al., 2000). Our studies confirmed the large induction observed in HepG2 cells. However, only a few reports have focused on the mechanism by which chrysin induces drug-metabolizing enzymes. Zhang et al. (2003) found that the induction of CYP1A1 reporter activity by chrysin was mediated through AhR activation and subsequent binding to dioxin-responsive elements present in the gene in HepG2 cells. In a separate study, Sugatani et al. (2004) found that the UGT1A1 response to chrysin was alleviated the most when the AhRE within the gtPBREM was mutated in transactivation experiments conducted in HepG2 cells. UGT1A1 and CYP2B6 gene reporter activation by chrysin and 3-MC was compared in HepG2 cells in the present study. CYP2B6 was not responsive to chrysin, but it was responsive to PB, a PXR and CAR activator, when the PBREM was ...
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There are no specific protocols for Human Glucocorticoid Receptor alpha peptide (ab39764). Please download our general protocols booklet
CoAA contains two copies of RNA recognition motifs (RRM) and an intrinsic transactivation domain rich in repetitive tyrosines and glutamines (YxxQ domain). Previously, CoAA has been shown to be a transcriptional coactivator that stimulates transcriptional activation and regulates alternative splicing. A pattern and profile search revealed that the YxxQ domain in CoAA shared significant pattern homology with the oncogenic EWS activation domains (EAD) in TET family proteins, including, TLS/FUS, EWS and TAFII 68. It was further demonstrated that CoAAs YxxQ domain and EWS EAD also shared functional similarities. Based on these findings, this work investigated the aberration of CoAA in cancers and its pathophysiological significance. The results showed that the CoAA gene was amplified in a high percentage of inflammation-related human cancers with recurrent loss of the 5 regulatory element upstream of its promoter. This genomic aberration resulted in CoAA protein overexpression, which in turn, ...
CoAA contains two copies of RNA recognition motifs (RRM) and an intrinsic transactivation domain rich in repetitive tyrosines and glutamines (YxxQ domain). Previously, CoAA has been shown to be a transcriptional coactivator that stimulates transcriptional activation and regulates alternative splicing. A pattern and profile search revealed that the YxxQ domain in CoAA shared significant pattern homology with the oncogenic EWS activation domains (EAD) in TET family proteins, including, TLS/FUS, EWS and TAFII 68. It was further demonstrated that CoAAs YxxQ domain and EWS EAD also shared functional similarities. Based on these findings, this work investigated the aberration of CoAA in cancers and its pathophysiological significance. The results showed that the CoAA gene was amplified in a high percentage of inflammation-related human cancers with recurrent loss of the 5 regulatory element upstream of its promoter. This genomic aberration resulted in CoAA protein overexpression, which in turn, ...
Chromatin organization is highly dynamic and regulates transcription. Upon transcriptional activation, chromatin is remodeled and referred to as "open," but quantitative and dynamic data of this decompaction process are lacking. Here, we have developed a quantitative high resolution-microscopy assay in living yeast cells to visualize and quantify chromatin dynamics using the GAL7-10-1 locus as a model system. Upon transcriptional activation ...
Activation of transcription is the ultimate endpoint for many signal transduction and developmental pathways, and understanding the mechanism of activation is a...
MADRID, Jan. 28, 2014 /PRNewswire/ -- Adrian Bird wins the Frontiers of Knowledge Award for mapping gene activation and introducing new prospects to cure...
STAT4 and DNMT3A play opposing roles in regulating Th1 gene expression, and one mechanism for STAT4-dependent gene programming is in establishing a derepressed genetic state susceptible to transactivation by additional fate-determining transcription factors ...
Scientists have made a medical breakthrough which may help bring new insights on how genes are activated. Roughly 3 metres of DNA is tightly folded into the nucleus of every cell in our body. This folding allows some genes to be expressed, or activated, while excluding others.
Binding of transcriptional activators to a promoter is a prerequisite process in transcriptional activation. It is well established that the efficiency of activator binding to a promoter is determined by the affinity of direct interactions between the DNA-binding domain of an activator and its specific target sequences. However, I describe here that activator binding to a promoter is augmented in vivo by the effects of two other determinants that have not been generally appreciated: (i) the number of activator binding sites present in a promoter and (ii) the potency of activation domains of activators. Multiple sites within a promoter can cooperatively recruit cognate factors regardless of whether they contain an effective activation domain. This cooperativity can result in the synergistic activation of transcription. The second effect is the enhancement of activator binding to a promoter by the presence of activation domains. In this case, activation domains are not simply tethered to the ...
Transgenic techniques offer a valuable tool for determining gene functions. Although various promoters are available for use in gene overexpression, gene knockdown, and identification of transgenic individuals, there is nevertheless a lack of versatile promoters for such studies, and this dearth acts as a bottleneck, especially with regard to nonmodel organisms. Here, we succeeded in identifying a novel strong and ubiquitous promoter/enhancer in the silkworm. We identified a unique silkworm strain whose reporter gene showed strong and ubiquitous expression during the establishment of enhancer trap strains. In this strain, the transposon was inserted into the 5′UTR of hsp90, a housekeeping gene that is abundantly expressed in a range of tissues. To determine whether the promoter/enhancer of hsp90 could be used to induce strong gene expression, a 2.9-kb upstream genomic fragment of hsp90 was isolated (hsp90P2.9k), and its transcriptional activation activity was examined. Strikingly, hsp90P2.9k ...