Divergence of transcription factor binding sites is considered to be an important source of regulatory evolution. The associations between transcription factor binding sites and phenotypic diversity have been investigated in many model organisms. However, the understanding of other factors that contribute to it is still limited. Recent studies have elucidated the effect of chromatin structure on molecular evolution of genomic DNA. Though the profound impact of nucleosome positions on gene regulation has been reported, their influence on transcriptional evolution is still less explored. With the availability of genome-wide nucleosome map in yeast species, it is thus desirable to investigate their impact on transcription factor binding site evolution. Here, we present a comprehensive analysis of the role of nucleosome positioning in the evolution of transcription factor binding sites. We compared the transcription factor binding site frequency in nucleosome occupied regions and nucleosome depleted regions
Didier Picard, January 2015 Current list of HBD fusion proteins_ Protein X a HBD b regulated as c Refs. transcription factor in Arabidopsis transcription factor Arabidopsis transcription factor in tobacco coactivator transcription factor 1 2 3 transcription factor transcription factor, differentiation factor transcription factor putative transcription factor in arabidposis transcription factor oncoprotein transcription factor transcription factor oncoprotein oncoprotein oncoprotein transcription factor oncoprotein, transcription factor 6 7 transcription factor transcription factor in yeast, tissue culture cells and zebra fish transcriptional repressor transcription factor transcription factor in yeast, in tissue culture cells, transgenic mice, Xenopus, Drosophila and plants transcription factor, promoter of proliferation transcription factor transcription factor 19 20, 21, i Transcription factors APETALA3 ATF6α Athb-1 GR ER e GR Bob1/OBF1 ER e CCAT (from calcium ER e 4 5 channel cav1.2) C/EBP ...
The DNA sequence that a transcription factor binds to is called a transcription factor-binding site or response element.[55]. Transcription factors interact with their binding sites using a combination of electrostatic (of which hydrogen bonds are a special case) and Van der Waals forces. Due to the nature of these chemical interactions, most transcription factors bind DNA in a sequence specific manner. However, not all bases in the transcription factor-binding site may actually interact with the transcription factor. In addition, some of these interactions may be weaker than others. Thus, transcription factors do not bind just one sequence but are capable of binding a subset of closely related sequences, each with a different strength of interaction. For example, although the consensus binding site for the TATA-binding protein (TBP) is TATAAAA, the TBP transcription factor can also bind similar sequences such as TATATAT or TATATAA. Because transcription factors can bind a set of related ...
Since the successful isolation of mouse and human embryonic stem cells (ESCs) in the past decades, massive investigations have been conducted to dissect the pluripotency network that governs the ability of these cells to differentiate into all cell types. Beside the core Oct4-Sox2-Nanog circuitry, accumulating regulators, including transcription factors, epigenetic modifiers, microRNA and signaling molecules have also been found to play important roles in preserving pluripotency. Among the various regulations that orchestrate the cellular pluripotency program, transcriptional regulation is situated in the central position and appears to be dominant over other regulatory controls. In this review, we would like to summarize the recent advancements in the accumulating findings of new transcription factors that play a critical role in controlling both pluripotency network and ESC identity.
... is a protein database which contains information on transcription factors (TFs) of silkworm.
The Oxidative Stress Responsive Transcription Factor Pap1 Confers DNA Damage Resistance on Checkpoint-Deficient Fission Yeast Cells. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
This unit describes how to use the Transcription Element Search System (TESS). This Web site predicts transcription factor binding sites (TFBS) in DNA sequence using two different kinds of models of sites, strings and positional weight matrices. The binding of transcription factors to DNA is a major part of the control of gene expression. Transcription factors exhibit sequence-specific binding; they form stronger bonds to some DNA sequences than to others. Identification of a good binding site in the promoter for a gene suggests the possibility that the corresponding factor may play a role in the regulation of that gene. However, the sequences transcription factors recognize are typically short and allow for some amount of mismatch. Because of this, binding sites for a factor can typically be found at random every few hundred to a thousand base pairs. TESS has features to help sort through and evaluate the significance of predicted sites. Curr. Protoc. Bioinform. 21:2.6.1-2.6.15. © 2008 by John ...
The transcriptional coactivator peroxisome proliferator-activated receptor-gamma coactivator-1beta (PGC-1beta) has been implicated in important metabolic processes. A mouse lacking PGC-1beta (PGC1betaKO) was generated and phenotyped using physiological, molecular, and bioinformatic approaches. PGC1betaKO mice are generally viable and metabolically healthy. Using systems biology, we identified a general defect in the expression of genes involved in mitochondrial function and, specifically, the electron transport chain. This defect correlated with reduced mitochondrial volume fraction in soleus muscle and heart, but not brown adipose tissue (BAT). Under ambient temperature conditions, PGC-1beta ablation was partially compensated by up-regulation of PGC-1alpha in BAT and white adipose tissue (WAT) that lead to increased thermogenesis, reduced body weight, and reduced fat mass. Despite their decreased fat mass, PGC1betaKO mice had hypertrophic adipocytes in WAT. The thermogenic role of PGC-1beta was
ABSTRACT: One goal of human genetics is to understand how the information for precise and dynamic gene expression programs is encoded in the genome. The interactions of transcription factors (TFs) with DNA regulatory elements clearly play an important role in determining gene expression outputs, yet the regulatory logic underlying functional transcription factor binding is poorly understood. Many studies have focused on characterizing the genomic locations of TF binding, yet it is unclear to what extent TF binding at any specific locus has functional consequences with respect to gene expression output. To evaluate the context of functional TF binding we knocked down 59 TFs and chromatin modifiers in one HapMap lymphoblastoid cell line. We then identified genes whose expression was affected by the knockdowns. We intersected the gene expression data with transcription factor binding data (based on ChIP-seq and DNase-seq) within 10 kb of the transcription start sites of expressed genes. This ...
ABSTRACT: One goal of human genetics is to understand how the information for precise and dynamic gene expression programs is encoded in the genome. The interactions of transcription factors (TFs) with DNA regulatory elements clearly play an important role in determining gene expression outputs, yet the regulatory logic underlying functional transcription factor binding is poorly understood. Many studies have focused on characterizing the genomic locations of TF binding, yet it is unclear to what extent TF binding at any specific locus has functional consequences with respect to gene expression output. To evaluate the context of functional TF binding we knocked down 59 TFs and chromatin modifiers in one HapMap lymphoblastoid cell line. We then identified genes whose expression was affected by the knockdowns. We intersected the gene expression data with transcription factor binding data (based on ChIP-seq and DNase-seq) within 10 kb of the transcription start sites of expressed genes. This ...
ABSTRACT: One goal of human genetics is to understand how the information for precise and dynamic gene expression programs is encoded in the genome. The interactions of transcription factors (TFs) with DNA regulatory elements clearly play an important role in determining gene expression outputs, yet the regulatory logic underlying functional transcription factor binding is poorly understood. Many studies have focused on characterizing the genomic locations of TF binding, yet it is unclear to what extent TF binding at any specific locus has functional consequences with respect to gene expression output. To evaluate the context of functional TF binding we knocked down 59 TFs and chromatin modifiers in one HapMap lymphoblastoid cell line. We then identified genes whose expression was affected by the knockdowns. We intersected the gene expression data with transcription factor binding data (based on ChIP-seq and DNase-seq) within 10 kb of the transcription start sites of expressed genes. This ...
Clinical evidence suggests that antiestrogens inhibit the development of androgen-insensitive prostate cancer. Here, we show that the estrogen receptor β (ERβ) mediates inhibition by the antiestrogen ICI 182,780 (ICI) and its enhancement by estrogen. ERβ associated with gene promoters through the tumor-suppressing transcription factor KLF5 (Krüppel-like zinc finger transcription factor 5). ICI treatment increased the recruitment of the transcription coactivator CBP [CREB (adenosine 3′,5′-monophosphate response element-binding protein)-binding protein] to the promoter of FOXO1 through ERβ and KLF5, which enhanced the transcription of FOXO1. The increase in FOXO1 abundance led to anoikis in prostate cancer cells, thereby suppressing tumor growth. In contrast, estrogen induced the formation of complexes containing ERβ, KLF5, and the ubiquitin ligase WWP1 (WW domain containing E3 ubiquitin protein ligase 1), resulting in the ubiquitination and degradation of KLF5. The combined presence of ...
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Transcription factors directly control when, where, and the extent to which genes are expressed. Signal transduction pathways are responsible for either activating or inhibiting many of them. Transcription factors are also regulated by cofactors, forming complexes that can activate or inhibit transcriptional activity. Many transcription factors, such as nuclear receptors, reside in the cytoplasm and enter the nucleus upon activation (e.g., ligand binding). Posttranslational modifications and coregulating proteins provide additional layers of regulation. Transcription factors are involved in a wide variety of processes, such as development, stress responses, and immunity. Activation or inhibition of transcription factors is often dysregulated during oncogenesis. Transcription factors can also be dysregulated during developmental processes, promoting or inhibiting cellular differentiation. Analyzing the expression, regulation, activity, and sequence of transcription factor genes can help determine ...
The human transcription enhancer factor-1 (TEF-1) belongs to a family of evolutionarily conserved proteins that have a DNA binding TEA domain. TEF-1 shares a 98% homology with Drosophila scalloped (sd) in the DNA binding domain and a 50% similarity in the activation domain. We have expressed human TEF-1 in Drosophila under the hsp-70 promoter and find that it can substitute for Sd function. The transformants rescue the wingblade defects as well as the lethality of loss-of-function alleles. Observation of reporter activity in the imaginal wing discs of the enhancer-trap alleles suggests that TEF-1 is capable of promoting sd gene regulation. The functional capability of the TEF-1 product was assessed by comparing the extent of rescue by heat shock (hs)-TEF-1 with that of hs-sd. The finding that TEF-1 can function in vivo during wingblade development offers a potent genetic system for the analysis of its function and in the identification of the molecular partners of TEF-1.. ...
Background TF-TFBS-TFT triplets -Transcription factors(TF) regulate transcription factor target(TFT) through binding to transcription factor DNA binding sites(TFBS).
This paper describes a novel approach to constructing Position-Specific Weight Matrices (PWMs) based on the transcription factor binding site (TFBS) data provide by the TRANSFAC database and comparison of the newly generated PWMs with the original TRANSFAC matrices. Multiple local sequence alignment was performed on the TFBSs of each transcription factor. Several different alignment programs were tested and their matrices were compared to the original TRANSFAC matrices. One of the alignment programs, GLAM, produced comparable matrices in terms of the average ranking of true positive sites across the whole test set of sequences. ...
The mechanisms underlying the development and progression of breast cancer are not fully understood, and this is particularly challenging because of its diverse etiologies [20]. However, it is clear that changes in gene expression are essential to drive different processes that occur during tumourigenesis [21]. Transcription factors control gene expression by binding to specific DNA sequences in gene promoters and often regulate multiple target genes. Because of this ability to control different target genes, deregulation of transcription factors can drive events associated with the initiation and progression of diseases such as cancer [22]. Previous studies have shown that the Brn-3b transcription factor is elevated in ,60% of primary breast cancers [1], and when increased, it significantly enhances proliferation and anchorage-independent growth in vitro and tumour growth in vivo [2, 3]. Elevated Brn-3b also confers resistance to growth-inhibitory stimuli and increases the migratory potential ...
ELF4 is a member of the ETS family of transcription factors (TF) with transcription activating properties (Lacorazza and Nimer, 2003). ELF4 binds to DNA sequences containing the consensus 5-WGGA-3 and transactivates promoters of the hematopoietic growth factor genes CSF2, IL3, IL8, and of the bovine lysozyme gene (Miyazaki et al., 1996; Mao et al., 1999; Hedvat et al., 2004; Suico et al., 2004). ELF4 acts synergistically with RUNX1 to transactivate the IL3 promoter (Mao et al., 1999). It also transactivates the PRF1 promoter in natural killer (NK) cells (Lacorazza et al., 2002). ELF4 has important molecular functions, including protein binding, transcription activator activity, sequence-specific DNA binding, transcription factor activity. ELF4 interacts with multiple proteins, including Cyclin A/CDK2 kinase complex, FBXO4, FBXO7, PML, RUNX1, SKP2 and UBB (Miyazaki et al., 1996; Mao et al., 1999; Miyazaki et al., 2001; Liu et al., 2006; Suico et al., 2006). ELF4 has been implicated in widely ...
This function reads in transcription factor information given the selected transcription factor target gene database. The information is downloaded via the AnnotationHub package and merged, if necessary.
Breast cancer is one of the most common malignant diseases in women. Epithelial-mesenchymal transition (EMT) has been documented to play an important role in proliferation, invasion and metastasis of tumor cells as well as drug resistance. Even though the signal transducer and activator of transcription 3 (STAT3) is not a master transcription factor of EMT, STAT3 is involved in the regulation of EMT-related gene expression. However, it remains unclear whether targeted inhibitors of STAT3 affect EMT-mediated proliferation, migration, invasion and drug resistance of tumor cells. In this paper, we investigated the effects of STAT3 and its interaction with Twist, a master transcription factor, in EMT program and subsequent changes in proliferation, migration and invasion of breast cancer cells by interfering STAT3 signaling pathway with different strategies such as STAT3 inactivation and STAT3 silencing. Furthermore, we explored the role of inhibiting STAT3 phosphorylation in the EMT regulation of ...
The Turner lab has focused on the role of transcription factors in the development of peripheral sensory neurons, the spinal cord, midbrain, and habenula. Transcription factors are proteins which bind to DNA in the nucleus to switch on or off the genes which characterize specific cell types. Without the correct complement of transcription factors, cells undergo an "identity crisis" and fail to execute their correct developmental programs. Many genetic disorders in the brain and other organ systems have been linked to defective transcription factor function. Most of the Turner Lab studies have been conducted in transgenic mice in which they either "knockout" the factor of interest, or express a tracer protein in the neurons that express the factor. Studies have focused mainly on the homeodomain transcription factors Brn3a, Islet1, and Hmx1. In recent work, they have shown that without the combinatorial effects of Brn3a and Islet1, developing sensory neurons remain in a "ground state" in which ...
Researchers are only beginning to understand how individual variation in gene regulation can have a lasting impact on ones health and susceptibility to certain diseases. Now, an ambitious survey of the human genome has identified differences in the binding of master regulators called transcription factors to DNA that affect how genes are expressed in different people.. The study, which is published in the March 18, 2010, issue of Science, looked at two common transcription factors. HHMI medical research fellow Maya Kasowski and her colleagues in the laboratory of molecular biologist Michael Snyder at Yale University conducted the work with Jan Korbel at the European Molecular Biology Laboratory. Snyder has since joined the faculty at Stanford University.. Transcription factors account for as much as 10 percent of the coding genome in humans and other organisms. When activated, transcription factors switch on or off hundreds or thousands of genes, a cascade that programs cells to grow or divide. ...
While developmental processes such as axon pathfinding and synapse formation have been characterized in detail, comparatively less is known of the intrinsic developmental mechanisms that regulate transcription of ion channel genes in embryonic neurons. Early decisions, including motoneuron axon targeting, are orchestrated by a cohort of transcription factors that act together in a combinatorial manner. These transcription factors include Even-skipped (Eve), islet and Lim3. The perdurance of these factors in late embryonic neurons is, however, indicative that they might also regulate additional aspects of neuron development, including the acquisition of electrical properties. To test the hypothesis that a combinatorial code transcription factor is also able to influence the acquisition of electrical properties in embryonic neurons we utilized the molecular genetics of Drosophila to manipulate the expression of Eve in identified motoneurons. We show that increasing expression of this transcription factor,
While developmental processes such as axon pathfinding and synapse formation have been characterized in detail, comparatively less is known of the intrinsic developmental mechanisms that regulate transcription of ion channel genes in embryonic neurons. Early decisions, including motoneuron axon targeting, are orchestrated by a cohort of transcription factors that act together in a combinatorial manner. These transcription factors include Even-skipped (Eve), islet and Lim3. The perdurance of these factors in late embryonic neurons is, however, indicative that they might also regulate additional aspects of neuron development, including the acquisition of electrical properties. To test the hypothesis that a combinatorial code transcription factor is also able to influence the acquisition of electrical properties in embryonic neurons we utilized the molecular genetics of Drosophila to manipulate the expression of Eve in identified motoneurons. We show that increasing expression of this transcription factor,
Transcriptional coactivator for steroid receptors and nuclear receptors. Greatly increases the transcriptional activity of PPARG and thyroid hormone receptor on the uncoupling protein promoter. Can regulate key mitochondrial genes that contribute to the program of adaptive thermogenesis. Plays an essential role in metabolic reprogramming in response to dietary availability through coordination of the expression of a wide array of genes involved in glucose and fatty acid metabolism. Induces the expression of PERM1 in the skeletal muscle in an ESRRA-dependent manner. Also involved in the integration of the circadian rhythms and energy metabolism. Required for oscillatory expression of clock genes, such as ARNTL/BMAL1 and NR1D1, through the coactivation of RORA and RORC, and metabolic genes, such as PDK4 and PEPCK. Isoform 4 specifically activates the expression of IGF1 and suppresses myostatin expression in skeletal muscle leading to muscle fiber hypertrophy.
Recent development of methods for genome‐wide identification of transcription factor binding sites by chromatin immunoprecipitation (ChIP) has led to novel insights into transcriptional regulation and greater understanding of the function of individual transcription factors
Transcriptional super-enhancers drive expression of oncogenes in many cancers and are being targeted with novel transcriptional and epigenetic therapeutics (1,2,3,4). Super-enhancers are acquired in cancers through multiple mechanisms, including DNA translocation of an extant super-enhancer and focal amplification. We recently discovered a novel mechanism by which super-enhancers are nucleated in T cell acute lymphoblastic leukemias (T-ALLs) (5). In this case, a small, monoallelic insertion creates a DNA binding site for a master transcription factor protein, which binds and recruits additional factors to nucleate the super-enhancer, which in turn drives high levels of the TAL1 transcription factor. We describe here a method for unbiased identification of similar genomic insertions that nucleate potentially oncogenic regulatory elements in cancers. This approach uses data from genome-wide ChIP-Seq studies that map locations of enhancer-binding proteins to identify sequences missing from ...
It is important to note that even when all experiments are included, the best results produce clusters with only a 28% true positive rate (see Figure E.1.a in Additional data file 1). That is, most of the genes in a given cluster do not share a common, known transcription factor. There are several possible reasons for this. First, with the present state of knowledge, it is possible that genes in the same cluster do in fact share a common transcription factor that is not (yet) represented in the databases used as gold standards (YPD, SCPD and ChIP data). We note for example, that when one compares ChIP data to YPD, the false-negative rate is approximately 80% using the recommended p-value of 0.001. That is, known gene transcription factor interactions from YPD are identified only about 20% of the time by ChIP (see Table F in Additional data file 1). Hence, it is possible that our evaluation criteria all underestimate the number of co-regulated genes in a cluster. Second, gene regulation is more ...
Transcription factor and DNA molecule. Molecular model of glucocorticoid receptor (GR) transcription factor protein (purple and blue) complexed with a molecule of DNA (deoxyribonucleic acid, pink and green). Transcription factors regulate the transcription of DNA to RNA (ribonucleic acid) by the enzyme RNA polymerase. RNA is the intermediate product between a gene and its protein. When glucocorticoid binds to GR, GR enters the cells nucleus and binds to the DNA, causing an increase in the production of the apoptosis (programmed cell death) protein bax. - Stock Image A617/0259
Author Summary The main role of transcription factors is to modulate the expression levels of functionally related genes in response to environmental and cellular cues. For this process to be precise, the transcription factor needs to locate and bind specific DNA sequences in the genome and needs to bind these sites with a strength that appropriately adjusts the amount of gene expressed. Both specific protein-DNA interactions and transcription factor activity are intimately coupled, because they are both dependent upon the biochemical properties of the DNA-binding domain. Here we experimentally probe how variable these properties are using a novel in vivo selection assay. We observed that the specific binding preferences for the transcription factor MarA and its transcriptional activity can be altered over a large range with a few mutations and that selection on one function will impact the other. This work helps us to better understand the mechanism of transcriptional regulation and its evolution, and
Hi: Take a look at TRANSFAC: http://nar.oupjournals.org/cgi/content/full/29/1/281 Good luck! On 8 Jun 2001 12:10:46 +0100, Heather Peto ,hp217 at cam.ac.uk, wrote: ,Hi , ,Does anyone know how I would look up which genes are turned on/off by ,a given transciption factor? Is there a database I can search? I am ,looking to see all the proteins produced / downgraded after CREB and ,a set of other transcription factors are activated. , ,many thanks , ,Heather :) , ...
View Notes - Lec20 from BCH 110 at UC Riverside. Lecture 20 Eukaryotic Gene Regulation 2 REGULATORY TRANSCRIPTION FACTORS & ACTIVATION MECHANISMS Lodish 6th edition Chapter 7 Lodish 5th edition
...Munich (Germany) August 8 2006 -- Genomatix Software GmbH a pionee...It contains genomic TF binding sites and protein binding domains rela... We have developed our in-house TF database now for more than a decade...,MatBase,--,A,new,transcription,factor,knowledge,base,released,by,Genomatix,biological,biology news articles,biology news today,latest biology news,current biology news,biology newsletters
We present an integrated method called Chromia for the genome-wide identification of functional target loci of transcription factors. Designed to capture the characteristic patterns of transcription factor binding motif occurrences and the histone profiles associated with regulatory elements such as …
I have pursued a breadth of research that explored the functional genomic study of eukaryotic transcriptional regulation. I have utilized two model organisms, many experimental methodologies, and have developed a suite of computational resources to study the interaction of transcription factors with regulated targets. In Saccharomyces cerevisiae I worked with my collaborator Dr. Zhanzhi (Mike) Hu to characterize the whole-genome transcriptional response of 263 individual transcription factor deletions. We utilized a sophisticated error model and directed-weighted graphs to model a network of high-confidence targets for each transcription factor profiled. We then used regulatory epistasis to elucidate the true set of primary KO-regulated targets and construct a functional transcriptional regulatory network. This network was analyzed for ontological and sequence motif enrichment in order to gain insight into the biological functions represented by transcription factors studied. Functional ...
Transcription factors (TFs) regulate gene transcription and play pivotal roles in various biological processes such as development, cell cycle progression, cell differentiation and tumor suppression. Identifying cis-regulatory elements associated with TF-encoding genes is a crucial step in understanding gene regulatory networks. To this end, we have used a comparative genomics approach to identify putative cis-regulatory elements associated with TF-encoding genes in vertebrates. We have created a database named TFCONES (T ranscription F actor Genes & Associated CO nserved N oncoding E lementS) ( http://tfcones.fugu-sg.org ) which contains all human, mouse and fugu TF-encoding genes and conserved noncoding elements (CNEs) associated with them. The CNEs were identified by gene-by-gene alignments of orthologous TF-encoding gene loci using MLAGAN. We also predicted putative transcription factor binding sites within the CNEs. A significant proportion
Background: Conventional wisdom holds that, owing to the dominance of features such as chromatin level control, the expression of a gene cannot be readily predicted from knowledge of promoter architecture. This is reflected, for example, in a weak or absent correlation between promoter divergence and expression divergence between paralogs. However, an inability to predict may reflect an inability to accurately measure or employment of the wrong parameters. Here we address this issue through integration of two exceptional resources: ENCODE data on transcription factor binding and the FANTOM5 high-resolution expression atlas. Results: Consistent with the notion that in eukaryotes most transcription factors are activating, the number of transcription factors binding a promoter is a strong predictor of expression breadth. In addition, evolutionarily young duplicates have fewer transcription factor binders and narrower expression. Nonetheless, we find several binders and cooperative sets that are ...
Conventional wisdom holds that, owing to the dominance of features such as chromatin level control, the expression of a gene cannot be readily predicted from knowledge of promoter architecture. This is reflected, for example, in a weak or absent correlation between promoter divergence and expression divergence between paralogs. However, an inability to predict may reflect an inability to accurately measure or employment of the wrong parameters. Here we address this issue through integration of two exceptional resources: ENCODE data on transcription factor binding and the FANTOM5 high-resolution expression atlas. Consistent with the notion that in eukaryotes most transcription factors are activating, the number of transcription factors binding a promoter is a strong predictor of expression breadth. In addition, evolutionarily young duplicates have fewer transcription factor binders and narrower expression. Nonetheless, we find several binders and cooperative sets that are disproportionately associated
Transcription factors are frequently the chief determinants of the composition and stability of large transcription complexes. Transcriptional regulation is mediated through the interactions of transcription factors with specific binding sites. Transcription factors help to recruit RNA polymerases to active genes for the production of RNA transcripts. Detect Transcription factors using Mercks antibodies.
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The canonical mechanism of transcription initiation in all metazoans involves recruitment of TATA-binding proteins (TBP, TLF or TBP2 in vertebrates) to the promoter, as a rate-limiting step before binding of RNA polymerase II. TBP, TLF and TBP2 have non-redundant functions, but the degree of redundancy between them is not clear; nor is it well understood whether there are TBP-independent mechanisms of transcription initiation in vivo. On p. 1340, Gert Veenstra and co-workers now show that, during early Xenopus development, there is a small group of genes whose transcription is independent of all TBP family members (denoted TBP family-insensitive or TFI genes). These genes are enriched for factors expressed in mesoderm and at Spemanns organiser and include several key transcription factors involved in mesendoderm specification. Strikingly, most TFI genes are bound by these TFI transcription factors. Gcn5, a component of the SAGA complex thought be involved in non-canonical transcription ...
Transcription factors, in a somewhat simplified definition, are proteins that regulate transcription by binding to specific sequence elements in regulatory genome regions such as promoters, enhancers etc. TFClass is a classification of eukaryotic transcription factors based on the characteristics of their DNA-binding domains. It comprises four general levels (superclass, class, family, subfamily) and two levels of instantiation (genus and molecular species). Two of them (subfamily and factor species) are optional. More detailed explanations about the classification scheme and its criteria are given here.. For further information about the latest version, kindly refer to Wingender, E., Schoeps, T., Haubrock, M., Krull, M. and Dönitz, J.: TFClass: expanding the classification of human transcription factors to their mammalian orthologs. Nucleic Acids Res. 46, D343-D347 (2018). ...
Transcription factors mediate gene regulation by site-specific binding to chromosomal operators. It is commonly assumed that the level of repression is determined solely by the equilibrium binding of a repressor to its operator. However, this assumption has not been possible to test in living cells. Here we have developed a single-molecule chase assay to measure how long an individual transcription factor molecule remains bound at a specific chromosomal operator site. We find that the lac repressor dimer stays bound on average 5 min at the native lac operator in Escherichia coli and that a stronger operator results in a slower dissociation rate but a similar association rate. Our findings do not support the simple equilibrium model. The discrepancy with this model can, for example, be accounted for by considering that transcription initiation drives the system out of equilibrium. Such effects need to be considered when predicting gene activity from transcription factor binding strengths.. ...
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TY - JOUR. T1 - Chromatin properties of regulatory DNA probed by manipulation of transcription factors. AU - Sharov, Alexei A.. AU - Nishiyama, Akira. AU - Qian, Yong. AU - Dudekula, Dawood B.. AU - Longo, Dan L.. AU - Schlessinger, David. AU - Ko, Minoru. PY - 2014/8/1. Y1 - 2014/8/1. N2 - Transcription factors (TFs) bind to DNA and regulate the transcription of nearby genes. However, only a small fraction of TF binding sites have such regulatory effects. Here we search for the predictors of functional binding sites by carrying out a systematic computational screening of a variety of contextual factors (histone modifications, nuclear lamin-bindings, and cofactor bindings). We used regression analysis to test if contextual factors are associated with upregulation or downregulation of neighboring genes following the induction or knockdown of the 9 TFs in mouse embryonic stem (ES) cells. Functional TF binding sites appeared to be either active (i.e., bound by P300, CHD7, mediator, cohesin, and ...
Transcription is a process finely regulated by different transcription factors (TFs) which bind regulatory sequences present in gene promoters and allow the precise execution of gene expression programs. Misregulation of such process can lead to different pathologies, including development/differentiation defects, uncontrolled cell growth and cancer. For these reasons it is important to understand the molecular details of the interplay that occurs between different TFs to modulate gene expression. NF-Y, the heterotrimeric complex composed by NF-YA, NF-YB and NF-YC subunits, all required for DNA binding, recognizes the consensus sequence CCAAT, present in about 30% of eukaryotic promoters, at -60/-100 bp from the Transcription Start Site (TSS). One of the most important roles of NF-Y in transcription is to interact synergistically with other TFs to activate, or to repress, gene expression. In this study we focused on the relationship occurring between NF-Y and the TFs MAX, Myc and USF1, which ...
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Plant development is controlled by transcription factors (TFs) which form complex gene-regulatory networks. Genome-wide TF DNA-binding studies revealed that these TFs have several thousands of binding sites in the Arabidopsis genome, and may regulate the expression of many genes directly. Given the importance of natural variation in plant developmental programs, there is a need to understand the molecular basis of this variation at the level of developmental gene regulation. However, until now, the evolutionary turnover and dynamics of TF binding sites among plant species has not yet experimentally determined. Here, we performed comparative ChIP-seq studies of the MADS-box TF SEPALLATA3 (SEP3) in inflorescences of two Arabidopsis species: A. thaliana and A. lyrata. Comparative RNA-seq analysis shows that the loss/gain of BSs is often followed by a change in gene expression ...
The three basic DNA-binding domain mutations from the associated transcription factor (Mitf), Mitfmi/mi, Mitfwh/wh and Mitfor/or, influence osteoclast differentiation with adjustable penetrance whilst impairing melanocyte advancement completely. situated on murine chromosome 6p, encodes for a simple helix-loop-helix leucine zipper (bHLH-Zip) transcription element known as Mitf (Hallsson et al., 2000). The human being MITF is definitely mutated in family members with Waardenburg symptoms type II (WS2) (Tassabehji et al., 1994). Mitf relates to its family carefully, Tfe3, TfeB and TfeC bHLH-Zip transcription elements and binds to E-box components on promoters of focus on genes such as for example so that as homodimers or 96574-01-5 manufacture as heterodimers with additional Mitf-family members, to operate a vehicle target gene manifestation (Aksan and Goding, 1998; Luchin et al., 2000; Mansky et al., 2002b; Fisher and Motyckova, 96574-01-5 manufacture 2002). Recent research established that Mitf ...
Transcription factor and ribosomal RNA (rRNA). Molecular model showing the 6 zinc fingers of transcription factor IIIA (yellow) bound to RNA (ribonucleic acid, red and blue) from a 5s ribosome sub-unit. Transcription factors are proteins that bind to specific DNA sequences, and control the movement (transcription) of genetic information from DNA to mRNA (messenger RNA) during gene expression. Ribosomes are responsible for reading the RNA strand and assembling amino acids to form the protein encoded by the gene being transcribed. - Stock Image F006/9530
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The family of repeats (FR) is a major upstream enhancer of the Epstein-Barr virus (EBV) latent C promoter (Cp) that controls transcription of six different latent nuclear proteins following interaction with the EBV nuclear protein EBNA1. Here, it was shown that Cp could also be activated by octamer-binding factor (Oct) proteins. Physical binding to the FR by the cellular transcription factors Oct-1 and Oct-2 was demonstrated by using an electrophoretic mobility-shift assay. Furthermore, Oct-1 in combination with co-regulator Bob.1, or Oct-2 alone, could drive transcription of a heterologous thymidine kinase promoter linked to the FR in both B cells and epithelial cells. Cp controlled by the FR was also activated by binding of Oct-2 to the FR. This may have direct implications for B cell-specific regulation of Cp.
Clustering of TFBSs, singly or in combination, has frequently been used as a method for computational CRM discovery. While false-positive prediction rates remain high for many studies, when CRMs are positively identified by these methods, it is assumed that the TFBSs that were used as input to the prediction algorithm are important functional regulators of the CRMs activity, as are the transcription factors that bind to these sites. Although in some cases this has been shown to be the case [e.g. [11]], more often than not the assumption is allowed to rest unchallenged. Here, we show through extensive empirical testing in vivo that many of these specific TFBSs, and/or their assumed cognate transcription factors, appear to be relatively or completely unimportant for CRM activity. This leads to the somewhat paradoxical result that although consideration of the putative TFBSs led to successful CRM discovery, the sites in many cases do not appear to be functional CRM constituents. What explains this ...
Putative chromatin remodeling complexes, such as the yeast SWI/SNF complex (for a recent review see Burns and Peterson, 1997) and its mammalian homologs (Kwon et al., 1994; Wang et al., 1996), histone acetyltransferases, such as GCN5 (Brownell et al., 1996), CBP (Bannister and Kouzarides, 1996), P300 (Ogryzko et al., 1996), P/CAF (Yang et al., 1996) and TAFII250 (Mizzen et al., 1996), and histone deacetylases (Taunton et al., 1996; Alland et al., 1997; Hassig et al., 1997) are emerging as key players in the processes of cellular differentiation and oncogenesis. These factors appear to act as effectors for a large number of sequence‐specific transcription factors such as members of the nuclear receptor superfamily (Hanstein et al., 1996, Kamei et al., 1996; Heinzel et al., 1997; Nagy et al., 1997), the myb proto‐oncogene (Dai et al., 1996), cAMP response element binding protein (Kwok et al., 1994), the proto‐oncogenes c‐jun and c‐fos (Bannister and Kouzarides, 1995; Kamei et al., 1996), ...
Following the binding of transcription factors (TF) to specific regions, chromatin remodeling including alterations in nucleosome positioning (NP) occurs. These changes in NP cause selective gene expression to determine cell function. However whether specific NP patterns upon TF binding determine the transcriptional regulation such as gene activation or suppression is unclear. Here we identified five patterns of NP around TF binding sites (TFBSs) using fixed MNase-Seq analysis. The most frequently observed NP pattern described the transcription state. The five patterns explained approximately 80% of the whole NP pattern on the genome in mouse C2C12 cells. We further performed ChIP-Seq using the input obtained from the fixed MNase-Seq. The result showed that a single trial of ChIP-Seq could visualize the NP patterns around the TFBS and predict the function of the transcriptional regulation at the same time. These findings indicate that NP can directly predict the function of TFs. ...
You have isolated a novel transcription factor. How will you determine the genes regulated by transcription factor in the whole genome? How will you determine the transcription factor binding sites in the whole genome?
Previous studies documented that 1,25-vitD treatment suppressed the induction of DC differentiation and maturation markers (CD1A, MHC class II molecules, CD83, costimulatory molecules, etc.) and suppressed the down-regulation of the monocyte marker CD14 (7, 8, 9, 10). If 1,25-vitD mainly acted through the inhibition of the differentiation and the maturation program, it would most likely act through suppressing/antagonizing the effect of transcription factors driving DC differentiation and maturation. In this way, the sets of genes regulated by differentiation and 1,25-vitD would overlap to a very large degree. Our data, however, do not support the scenario that the effect of 1,25-vitD is mostly restricted to the transcriptional regulation of "master transcription factors" or antagonism of transcription factors activated during maturation.. Our comparative analysis of the transcriptomes of monocytes, differentiating DCs, and IDCs differentiated in the presence or absence of 1,25-vitD suggest that ...
Although mutations causing monogenic disorders most frequently lie within the affected gene, sequence variation in complex disorders is more commonly found in noncoding regions. Furthermore, recent genome- wide studies have shown that common DNA sequence variants in noncoding regions are associated with normal variation in gene expression resulting in cell-specific and/or allele-specific differences. The mechanism by which such sequence variation causes changes in gene expression is largely unknown. We have addressed this by studying natural variation in the binding of key transcription factors (TFs) in the well-defined, purified cell system of erythropoiesis. We have shown that common polymorphisms frequently directly perturb the binding sites of key TFs, and detailed analysis shows how this causes considerable (∼10-fold) changes in expression from a single allele in a tissue-specific manner. We also show how a SNP, located at some distance from the recognized TF binding site, may affect ...
Definition of nf-e2 transcription factor, p45 subunit in the Definitions.net dictionary. Meaning of nf-e2 transcription factor, p45 subunit. What does nf-e2 transcription factor, p45 subunit mean? Information and translations of nf-e2 transcription factor, p45 subunit in the most comprehensive dictionary definitions resource on the web.
The researchers identified the hierarchical tree of coherent gene groups and transcription-factor networks that determine the patterns of genes expressed during brain development. They found that some "master transcription factors" at the top level of the hierarchy regulated the expression of a significant number of gene groups.. The scientists findings can be used for selection of transcription factors that could be targeted in the treatment of specific mental disorders.. "We live in the unique time when huge amounts of data related to genes, DNA, RNA, proteins, and other biological objects have been extracted and stored," said lead author Igor Tsigelny, a research scientist with SDSC as well as with UC San Diegos Moores Cancer Center and its Department of Neurosciences.. "I can compare this time to a situation when the iron ore would be extracted from the soil and stored as piles on the ground. All we need is to transform the data to knowledge, as ore to steel. Only the supercomputers and ...
New York University biologists captured highly transient interactions between transcription factors-proteins that control gene expression-and target genes in the genome and showed that these typically missed interactions have important practical implications. In a new study published in Nature Communications, the researchers developed a method to capture transient interactions of NLP7, a master transcription factor involved in nitrogen use in plants, revealing that the majority of a plants response to nitrogen is controlled by these short-lived regulatory interactions.. "Our approaches to capturing transient transcription factor-target interactions genome-wide can be applied to validate dynamic interactions of transcription factors for any pathway of interest in agriculture or medicine," said Gloria Coruzzi, Carroll & Milton Petrie Professor in NYUs Department of Biology and Center for Genomics and Systems Biology and the papers senior author.. Dynamic interactions between regulatory proteins ...
View Notes - Lecture 4 Regulation of Transcription Factor Activity by Extracellular Signals from IPHY 3060 at Colorado. IPHY 2060 Lecture 4: Regulation of Transcription Factor Activity by
Molecular biology is a rapidly evolving field that has led to the development of increasingly sophisticated technologies to improve our capacity to study cellular processes in much finer detail. Transcription is the first step in protein expression and the major point of regulation of the components that determine the characteristics, fate and functions of cells. The study of transcriptional regulation has been greatly facilitated by the development of reporter genes and transcription factor expression vectors, which have become versatile tools for manipulating promoters, as well as transcription factors in order to examine their function. The understanding of promoter complexity and transcription factor structure offers an insight into the mechanisms of transcriptional control and their impact on cell behaviour. This review focuses on some of the many applications of molecular cut-and-paste tools for the manipulation of promoters and transcription factors leading to the understanding of crucial aspects
We present an individual agent-based model of transcription factor binding to DNA. We explicitly represent every single transcription factor and every sing
CD4 T cells can adopt one of two opposing fates: a helper T cell (Th) specialized in supporting pathogen clearance, or a regulatory T cell (Treg) that attenuates immune responses. IL-17A-producing inflammatory Th17 cells stand out among Th cells, possessing a high level of inherent plasticity in response to altered environments. The underlying mechanisms controlling such flexibility are largely unknown. In this regard, we have identified the AP-1 family of transcription factors (TFs) as key regulators of Th17 cell identity. Our previous work revealed the pioneering role of BATF in supporting global enhancer accessibility and flexibility in CD4 T cells, and here, we describe an antagonistic AP-1 TF, JunB, that limits Th17 plasticity. Indeed, we find that CD4 T cells deficient in JunB exhibit dysregulated effector cytokine and TF expression signatures, and lack disease potential in a mouse model of autoimmunity. In particular, JunB serves to restrain inappropriate Treg and Th1 differentiation. ...
There are at least 16 genes within the common overlapping region. A few of these genes are expressed in the central nervous system and/or likely to be dosage sensitive, or reported to be associated with disease by animal studies. These genes could be candidate genes for patients with deletion or duplication in this region.. The transcription factor gene (SP1) is most likely to be dosage sensitive (haploinsufficiency score: 0.81%) [DECIPHER]. The protein encoded by the SP1 gene is a zinc finger transcription factor that binds to GC-rich motifs of many promoters and is then involved in a variety of cellular processes such as cell growth, apoptosis, differentiation and immune responses, DNA damage response, and chromatin remodeling (provided by RefSeq, Nov 2014). The SP7 gene (haploinsufficiency score: 14.4%) encodes a bone specific transcription factor (osterix) which regulates osteogenesis and bone formation during embryonic development [8]. Niger et al. [9] reported that the activity of osterix ...
Interacting selectively and non-covalently with a activating transcription factor and also with the basal transcription machinery in order to increase the frequency, rate or extent of transcription. Cofactors generally do not bind DNA, but rather mediate …
Researchers] display estimates of the predicted transcription factors in five genomes in Table 1, ranging from about 300 in E. coli to over 3000 in humans. These constitute between 6% (in E. coli and yeast) and 8% (in human) of the encoded proteins in these organisms. van Nimwegens [ref 24 PMID 12957540] earlier observation that larger genomes tend to have more transcription factors per gene is in accordance with the trend seen in eukaryotes (Table 1)." See notes beneath ...
Nashun B, Hill PW, Hajkova P, 2015, Reprogramming of cell fate: epigenetic memory and the erasure of memories past., EMBO Journal, Vol: 34, Pages: 1296-1308, ISSN: 0261-4189 Cell identity is a reflection of a cell type-specific gene expression profile, and consequently, cell type-specific transcription factor networks are considered to be at the heart of a given cellular phenotype. Although generally stable, cell identity can be reprogrammed in vitro by forced changes to the transcriptional network, the most dramatic example of which was shown by the induction of pluripotency in somatic cells by the ectopic expression of defined transcription factors alone. Although changes to cell fate can be achieved in this way, the efficiency of such conversion remains very low, in large part due to specific chromatin signatures constituting an epigenetic barrier to the transcription factor-mediated reprogramming processes. Here we discuss the two-way relationship between transcription factor binding and ...
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Inter-individual genetic variation is a major cause of diversity in phenotypes and disease susceptibility. Although sequence variants in gene promoters and protein-coding regions provide obvious prioritization of disease-causing variants, most (88%) genome-wide association study (GWAS) loci are in non-coding DNA, suggesting regulatory functions1. Prioritization of functional intergenic variants remains challenging, owing in part to an incomplete understanding of how regulation is achieved at the nucleotide level in different cell types and environmental contexts2,3,4,5,6,7,8,9,10,11. Recent studies have described important roles for lineage-determining transcription factors (LDTFs), also referred to as pioneer factors or master regulators, in selecting cell-type-specific enhancers12,13,14,15, but the sequence determinants that guide their binding are poorly understood. Previous findings in macrophages and B cells suggest a hierarchical model of regulatory function6, in which a relatively small ...
Active Motif offers a large number of recombinant transcription factor proteins that can be used in a variety of assays to study transcriptional regulation and DNA binding.
CD4(+) T lymphocytes orchestrate adaptive immune responses by differentiating into various subsets of effector T cells such as T-helper 1 (Th1), Th2, Th17, and regulatory T cells. These subsets have been generally described by master transcription factors that dictate the expression of cytokines and receptors, which ultimately define lymphocyte effector functions. However, the view of T-lymphocyte subsets as stable and terminally differentiated lineages has been challenged by increasing evidence of functional plasticity within CD4(+) T-cell subsets, which implies flexible programming of effector functions depending on time and space of T-cell activation. An outstanding question with broad basic and traslational implications relates to the mechanisms, besides transcriptional regulation, which define the plasticity of effector functions. In this study, we discuss the emerging role of regulatory non-coding RNAs in T-cell differentiation and plasticity. Not only microRNAs have been proven to be ...
Lets return to the example of transcription factor binding to DNA. As already noted, if a DNA sequence serves as an enhancer or promoter, it will bind a specific set of transcription factors. If a scientist then observes transcription factors binding to DNA, it is reasonable to conclude that these binding sites play a role in regulating gene expression. Though not certain, this conclusion is probabilistic. Despite the uncertainty associated with it, the conclusion is still reasonable because a vast body of data demonstrates that transcription factors bind to specific DNA sequences that regulate gene expression. Yes, another explanation for why these transcription factors bind to DNA may exist. Confirmatory experiments can reduce this uncertainty ...
Hypoxia-inducible factor-1 (HIF1) is a master transcription factor that orchestrates the adaptation of tumor cells to hypoxia by activating the expression of a broad range of genes promoting neoangiogenesis, tumor growth, glycolysis, metastasis, and resistance to treatments. Accumulating evidence now suggests that this adaptation depends on the stabilization or the increased synthesis of the HIF1A subunit. To have a better understanding of HIF1A regulation, we focused our attention on the environmental carcinogen cadmium (Cd). Our data now challenge these hypotheses and reveal unique and opposing activities of Cd on HIF1A expression and activity. Instead of a mere action on synthesis, Cd increases by itself the stability of HIF1A protein under normoxia; independently of proteasome impairment, oxidative damage or endoplasmic reticulum stress. However, little if any HIF1A is able to translocate to the nucleus of Cd-treated cells where it activates barely HIF1 transcriptional function. ...
The NFkB family of transcription factors regulates multiple cellular processes including inflammation, immunity, and stress responses. The IkB family of inhibitors sequester these transcription factors in the cytosol. A variety of ligands such as inflammatory cytokines, growth factors, and antigens from pathogens activate the NFkB pathway, stimulating IkB protein phosphorylation and subsequent degradation. Newly released NFkB transcription factors form active complexes and translocate into the nucleus to induce expression of their target genes. Hundreds of NFkB target genes have been identified using experimental techniques such as expression studies, chromatin immunoprecipitation, and bioinformatic analyses of predicted transcription factor binding sites. These NFkB target genes include cytokines as well as genes involved in biological processes such as inflammation, immune responses, development and differentiation, and apoptosis. Dysregulation of NFkB signal transduction is associated with ...
The interactions between sequence-specific transcription factors (TFs) and their DNA binding sites are an integral part of the gene regulatory networks within cells. My group developed highly parallel in vivo microarray technology, termed protein
We wanted to test the idea that stress causes a loss of brain synapses in humans," said senior author Ronald Duman, the Elizabeth Mears and House Jameson Professor of Psychiatry and professor of neurobiology and of pharmacology. "We show that circuits normally involved in emotion, as well as cognition, are disrupted when this single transcription factor is activated.". The research team analyzed tissue of depressed and non-depressed patients donated from a brain bank and looked for different patterns of gene activation. The brains of patients who had been depressed exhibited lower levels of expression in genes that are required for the function and structure of brain synapses. Lead author and postdoctoral researcher H.J. Kang discovered that at least five of these genes could be regulated by a single transcription factor called GATA1. When the transcription factor was activated, rodents exhibited depressive-like symptoms, suggesting GATA1 plays a role not only in the loss of connections between ...
These tracks complement each other and together can shed much light on regulatory DNA. The histone marks are informative at a high level, but they have a resolution of just ~200 bases and do not provide much in the way of functional detail. The DNase hypersensitivity assay is higher in resolution at the DNA level and can be done on a large number of cell types since its just a single assay. At the functional level, DNase hypersensitivity suggests that a region is very likely to be regulatory in nature, but provides little information beyond that. The transcription factor ChIP assay has a high resolution at the DNA level and, due to the very specific nature of the transcription factors, is often informative with respect to functional detail. However, since each transcription factor must be assayed separately, the information is only available for a limited number of transcription factors on a limited number of cell lines. Though each assay has its strengths and weaknesses, the fact that all of ...
We demonstrate a computational approach for achieving systematic understanding of transcription factor functions based on gene regulation network.
We demonstrate a computational approach for achieving systematic understanding of transcription factor functions based on gene regulation network.
This gene encodes a member of the GATA family of zinc-finger transcription factors that are named for the consensus nucleotide sequence they bind in the promoter regions of target genes. The encoded protein plays an essential role in regulating transcription of genes involved in the development and proliferation of hematopoietic and endocrine cell lineages. Alternative splicing results in multiple transcript variants.[provided by RefSeq, Mar 2009 ...
TF not in the TRANSFAC database. What now? - posted in Bioinformatics and Biostatistics: Hi, Oddly enough I cannot find the important and highly topical transcription factor in the TRANSFAC database. I want to perform TFBS prediction and want to make sure NANOG is included in the results. I have run a few gene promoters which are experimentally proven to be targeted by NANOG through some of the TRANSFAC prediction programs, but NANOG does not show up. Any suggestions onhow to proceed....
Here, we report that a complex enhancer, encoded by the distant Tce1 activator of transcription factor Gata3, is necessary for T cell development and is critical for the generation of ETP and for CD4 development, as demonstrated by CRISPR/Cas-mediated genome editing. This analysis also illuminated the mechanism of action of Tce1 during T cell development and identified several transcription factors that are responsible for engaging this enhancer activity in T cells.. Many studies have shown that GATA3 is required at multiple stages for normal T cell development (1, 2). Its abundance varies significantly between stages and is tightly controlled (5-11, 74). Although several transcription factors have been proposed as upstream regulators of Gata3 by demonstration that they bind near the Gata3 1a and/or 1b promoters (39, 40, 50, 75, 76), a functional requirement for any of those binding sites has not been confirmed by in vivo mutagenesis. Furthermore, the data shown here and previously clearly ...
The regulation of gene expression is a fundamental process within every cell that often allows exquisite control over a genes activity (for review see [1]). Altering transcription rates is an effective strategy for regulating gene activity. It is well established that transcription of a given gene is dependent upon a promoter sequence located within a few hundred base pairs of the transcriptional start site. Promoter activity is modulated by sequence-specific transcription factors that physically interact either with the protein complexes that make up the core transcriptional machinery or with the promoter sequence itself.. In eukaryotes, the activity of a promoter can be modified by transcription factors binding to DNA sequences (frequently termed cis-regulatory modules or enhancers) that are located from hundreds to hundreds of thousands of base pairs away from the promoter. These regulatory modules can either increase or decrease the rate of transcription for a target gene, depending on the ...
Genes with promoter regions [-2kb,2kb] around transcription start site containing the motif GGGAGGRR which matches annotation for MAZ: MYC-associated zinc finger protein (purine-binding transcription factor). Source Broad Institute. Link http://www.broadi…
basic helix-loop-helix (bHLH) transcription factor belonging to the class A family; acts as a general negative regulator of cell proliferation; binds specifically to oligomers of E-box motifs; forms heterodimers with other bHLH proteins of both class A and class B, e.g. E2A, TAL1, myogenin and MyoD; implicated in myogenesis, hematopoiesis and neurogenesis ...
Thank you very much for your suggestion. It is easy to registrate on gene-regulation.com. But when I browse the TRANSFAC database, it links to http://www.biobase-international.com/. For a free trial, it must finish a registration form. It is hard to pass this registration form. It is like this http://www.biobase-international.com/pages/index.php?id=456. In JARSPAR I can not find the factors which I interested no profiles in JASPAR satisfies search criteria 2008/5/29 lichunjiang ,lichunjiang at sibs.ac.cn,: , , , Really? I registrated for gene-regulation.com a couple of years ago, it is , quite easy.�It does not make sense that you can not register. Or you , should just write to the service to fix the problem. , , Actually, , it is free to use a reduced version. For the full professional version, , you need to pay. , , Besides Transfac, I recommend another , database: JARSPAR available at http://jaspar.genereg.net/.�It is , totally free to use. , Hope this help. , Good luck! , , , ,, It seems ...
Transforming growth factor β (TGF-β) signaling pathway is a major pathway in cellular processes such as cell growth, apoptosis, and cellular homeostasis. The signaling pathway activated by 17β-estadiol (E2) appeared to inhibit the TGF-β signaling pathway by cross-talk with the TGF-β components in estrogen receptor (ER) positive cells. In this study, we examined the inhibitory effects of endocrine disrupting chemicals (EDCs), including 4-nonylphenol (NP), 4-otylphenol (OP), bisphenol A (BPA), and benzophenon-1 (BP-1), in the TGF-β signaling pathway in BG-1 ovarian cancer cells expressing estrogen receptors (ERs). The transcriptional and translational levels of TGF-β related genes were examined by reverse transcription-PCR (RT-PCR), Western blot analysis, and xenograft mouse models of ovarian cancer cells. As a result, treatment with NP, OP, and BPA induced the expressions of SnoN, a TGF-β pathway inhibitor, and c-Fos, a TGF-β target transcription factor. Treatment with NP, BPA, and BP-1 ...
The regulation of a gene depends on the binding of transcription factors to specific sites located in the regulatory region of the gene. The generation of these binding sites and of cooperativity between them are essential building blocks in the evolution ...
NAM, ATAF, and CUC2 (NAC) proteins are encoded by one of the largest plant-specific transcription factor gene families. The functions of many NAC proteins relate to different aspects of lignocellulosi
... is available now at: http://transfac.gbf.de. On the TRANSFAC server, you will find also the sequence analysis programs PatSearch MatInspector SaGa FastM and Thure Etzolds SRS5 with a large collection of databases. TRANSFAC is a database about eukaryotic transcription factors and their binding sites. It consists of six cross-linked tables: SITE CELL FACTOR CLASS MATRIX GENE It is also cross-linked with TRRD (Transcription Regulatory Region Database) and COMPEL from the ICG, Novosibirsk (N. A. Kolchanov, A. E. Kel). It contains numerous cross-references to external databases such EMBL, SWISSPROT, PIR, FLYBASE, EPD, and PROSITE. For further details see Wingender et al., Nucleic Acids Res. 25:265-268, 1997. NEW FEATURES are: - Additional FACTOR and SITE entries, - cross-references to PDB, - comprehensive linkage of FACTOR entries with a proposed transcription factor classification sytem (http://transfac.gbf.de/TRANSFAC/cl/cl.html). The TRANSFAC database comes along with several ...
These oligonucleotides contain consensus DNA-binding sites for individual transcription factors and have 5´ OH blunt ends, allowing labeling to high specific activity with T4 PNK.
Motivation: Traditional and high-throughput techniques for determining transcription factor (TF) binding specificities are generating large volumes of data of uneven quality, which are scattered across individual databases. Results: FootprintDB integrates some of the most comprehensive freely available libraries of curated DNA binding sites and systematically annotates the binding interfaces of the corresponding TFs. The first release contains 2422 unique TF sequences, 10 112 DNA binding sites and 3662 DNA motifs. A survey of the included data sources, organisms and TF families was performed together with proprietary database TRANSFAC, finding that footprintDB has a similar coverage of multicellular organisms, while also containing bacterial regulatory data. A search engine has been designed that drives the prediction of DNA motifs for input TFs, or conversely of TF sequences that might recognize input regulatory sequences, by comparison with database entries. Such predictions can also be ...
bHLH transcription factors have common roles in inducing neuronal differentiation, but distinct roles in neuronal subtype specification, functions that are contingent on developmental context (Parras et al., 2002; Nakada et al., 2004a; Powell et al., 2004; Reeves and Posakony, 2005). To determine Atoh1-specific targets, we first identified transcripts specific to the Atoh1 lineage and not common to the neighboring dorsal Neurog1 lineage. Significantly, we identified five new Atoh1-specific targets and their responsive enhancers using a combination of microarray expression data, ChIP-seq experiments, and enhancer-reporter assays.. Previously, known direct targets of Atoh1 in vivo in the developing neural tube or cerebellum included the homeodomain transcription factors, Barhl1 and Barhl2 (Saba et al., 2005; Kawauchi and Saito, 2008), the Sonic hedgehog transcriptional effector, Gli2 (Flora et al., 2009), and Atoh1 itself (Helms et al., 2000). The direct Atoh1 targets identified here have diverse ...
Sensors made from custom DNA molecules could be used to personalize cancer treatments and monitor the quality of stem cells, according to an international team of researchers led by scientists at UC Santa Barbara and the University of Rome Tor Vergata.. The new nanosensors can quickly detect a broad class of proteins called transcription factors, which serve as the master control switches of life. The research is described in an article published in Journal of the American Chemical Society.. "The fate of our cells is controlled by thousands of different proteins, called transcription factors," said Alexis Vallée-Bélisle, a postdoctoral researcher in UCSBs Department of Chemistry and Biochemistry, who led the study. "The role of these proteins is to read the genome and translate it into instructions for the synthesis of the various molecules that compose and control the cell. Transcription factors act a little bit like the settings of our cells, just like the settings on our phones or ...
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Define transcription factor: any of various proteins that bind to DNA and play a role in the regulation of gene expression by promoting transcription
You describe your approach to mapping transcription regulatory networks as gene-centered. What does that mean?. Most people trying to understand transcription at a global scale are doing ChIP-chromatin-immunoprecipitation. Thats a transcription factor-centered approach, or protein-to-gene: you pull down a factor, and identify a bunch of DNA fragments by PCR sequencing or microarray (ChIP-chip). Its beautiful, but it does have its limitations. If you have a transcription factor with a restricted expression pattern-maybe its expressed at very low levels or only in one or two cells of the worm-then ChIP isnt technically feasible yet. And there arent enough good antibodies to do this on a genome-wide scale, which partly explains the paucity of data for 99% of transcription factors in the human genome.. So we go the other away around. We start with a piece of DNA, and identify the transcription factors that can bind to it- what we call a transcription factor binding profile-using the yeast ...