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Transcription factor omics

Transcription factor omics

• The combined analysis of quantitative transcriptome and interactome data provide unique insights into protein function. Transcription factor ‘omics’.[r]

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Transcription Factor Occupancy in Differentiating Skeletal Muscle

Transcription Factor Occupancy in Differentiating Skeletal Muscle

The second question poses an interpretation dilemma. The preponderance of myogenin occupancy associating proximally with expressed genes can be explained in two ways. One is that myogenin, as a positive-acting transcription factor, occupies cis-elements around genes that need to be expressed in differentiating muscle (including those that are not differentiation-specific), and contributes to their expression. The somewhat more pessimistic explanation is that chromatin in the area of an expressed gene is more likely to be accessible, in turn increasing the likelihood of making a myogenin binding site available. Under this model myogenin will occupy any binding site that is not being obstructed by a competitor or actively repressed, but will have little to no influence on nearby gene expression, except at a relatively small (less than 10% of total occupied elements, limited to differentiation-specific genes) fraction of sites. In truth, both explanations are almost certainly valid. Based on its expression pattern, loss of function phenotype, and extensive mutagenesis analysis of select CRMs, it is clear that myogenin is crucial to the expression of muscle-specific genes and proper progress of terminal differentiation. It is also very likely that myogenin, especially due to its high abundance, can occupy most elements in the genome that are presented to it unobstructed and meet the criteria for occupancy, such as having an RRCAGSTG recognition site, or perhaps more sophisticated combinations of targeting motifs. The fundamental question, therefore, is how much does myogenin really contribute to the expression of genes that are not differentiation-specific?
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Transcription factor interplay during Drosophila haematopoiesis

Transcription factor interplay during Drosophila haematopoiesis

At the molecular level, Lz synergizes with Srp to induce crystal cell fate (Fossett et al. 2003; Waltzer et al. 2003). This functional cooperation is mediated in part by a direct interaction between both isoforms of Srp and Lz (Waltzer et al. 2003) and in part at the level of several crystal cell specific genes (including lz itself) that harbour a particular cis-regulatory module composed of at least one GATA and one RUNX binding site in close association (Ferjoux et al. 2007; Gajewski et al. 2007; Muratoglu et al. 2007) (Fig. 1B). Both type of binding sites are required for Srp/Lz- mediated transactivation in vivo, suggesting that Srp and Lz simultaneously bind their targets (Ferjoux et al. 2007). The synergy between Srp and Lz might rely on cooperative DNA binding and/or on the formation of a transactivating platform (Levine and Tjian, 2003). Alternatively, Srp may already bind these enhancers in the prohemocytes and prime them for activa- tion by Lz. It is striking that the same complex composed of a pan- haematopoietic (Srp) and a lineage-specific (Lz) transcription factor is directly involved in maintaining the expression of the lineage-specific partner and in coordinating the expression of a wide array of differentiation markers (Ferjoux et al. 2007). This probably ensures a tight coupling between crystal cell fate choice and differentiation. Interestingly, the interaction between GATA and RUNX transcription factors has been conserved through evolution (Waltzer et al. 2003). Therefore, Srp/Lz cooperation might be used as a paradigm to study how GATA/RUNX com- plexes regulate transcription and blood cell development from Drosophila to vertebrates. In human, GATA1 and RUNX1 were shown to cooperate during megakaryopoiesis ex vivo (Elagib et al. 2003; Xu et al. 2006) and deregulation of the GATA1/RUNX1 complex activity might be implicated in the development of blood cells disorders such as familial platelet disorders and acute megakaryoblastic leukaemia (Elagib and Goldfarb, 2007).
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Molecular mechanisms of OLIG2 transcription factor in brain cancer

Molecular mechanisms of OLIG2 transcription factor in brain cancer

in apoptosis, and the body’s immune responses and inflammatory reactions, promotes osteoclast formation [71], mitogen activated protein kinase kinase 1 (MAP2K1), which controls cell proliferation, differentiation, movement, and apoptosis primarily through transcription regulation [72], mitogen activated protein kinase kinase kinase 14 (MAP3K14), which stimulates NF-kappa-B transcriptional activation and regulation via noncanonical pathways [73], mitogen activated protein kinase kinase kinase 1 (MAP3K1), which is activated by autophosphorylation, and phosphorylates other proteins with a magnesium cofactor [74]. Its increased expression in vivo promotes breast cancer survival and increases resistance of squamous cell carcinoma to photodynamic therapy [75, 76]. In the nucleus this network contains: histone deacetylase 6 (HDAC6), which is involved in transcriptional regulation, cell cycle progression, and development [77] and participates in neuroblastoma dissemination [78], hypoxia inducible factor 1, alpha subunit (HiF1A), which is involved in cancer progression, cell proliferation, and tumorigenesis [79], HIS1H4A, which may have some significance in melanoma and other cancers [80], signal transducer and activator of transcription 3 (STAT3)—a transcription factor that is involved in anti-apoptosis and tumorigenesis [81], SMAD Family Member 4 (SMAD4), which increases risk of cancer by increasing chances of cell proliferation [82], breast cancer 1, early onset (BRCA1)—aberrations
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Evolution of the activation domain in a Hox transcription factor

Evolution of the activation domain in a Hox transcription factor

ABSTRACT Linking changes in amino acid sequences to the evolution of transcription regulatory domains is often complicated by the low sequence complexity and high mutation rates of intrinsically disordered protein regions. For the Hox transcription factor Ultrabithorax (Ubx), conserved motifs distributed throughout the protein sequence enable direct comparison of specific protein regions, despite variations in the length and composition of the intervening sequences. In cell culture, the strength of transcription activation by Drosophila melanogaster Ubx correlates with the presence of a predicted helix within its activation domain. Curiously, this helix is not preserved in species more divergent than flies, suggesting the nature of transcription activation may have evolved. To determine whether this helix contributes to Drosophila Ubx function in vivo, wild-type and mu- tant proteins were ectopically expressed in the developing wing and the phenotypes evaluated. Helix mutations alter Drosophila Ubx activity in the developing wing, demonstrating its functional importance in vivo. The locations of activation domains in Ubx orthologues were identified by test- ing the ability of truncation mutants to activate transcription in yeast one-hybrid assays. In Ubx orthologues representing 540 million years of evolution, the ability to activate transcription varies substantially. The sequence and the location of the activation domains also differ. Consequently, analogous regions of Ubx orthologues change function over time, and may activate transcription in one species, but have no activity, or even inhibit transcription activation in another species. Unlike homeodomain-DNA binding, the nature of transcription activation by Ubx has substantially evolved.
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Transcription factor haploinsufficiency: when half a loaf is not enough

Transcription factor haploinsufficiency: when half a loaf is not enough

embryonic lethality occurs as a result of reduced expression of a particular protein, haploinsufficiency of tran- scription factors regulating expression of such genes would escape detection. Transcription factors regulate gene expression by binding the target gene promoter and turn the target gene “on” or “off”; in a particular cell, target gene expression is an all-or-none phe- nomenon. Transcription factor hap- loinsufficiency alters the likelihood that a promoter is activated, and this likelihood is influenced by promoter sequence–transcription factor interac- tions. While some transcription factors may interact at only one site, better def- initions of target sequences and genome databases indicate that many transcription factors probably interact at multiple sites on any one promoter. Initiation of gene transcription may require occupancy of several, if not all, binding sites. But since the number of binding sites within a cell is very small compared with the number of tran- scription factor molecules, the likeli- hood for binding site occupancy should be proportional to the concen- tration of transcription factor. Assum- ing n binding sites in a promoter and no interactions between sites, the like- lihood that all sites will be occupied is directly proportional to the transcrip- tion factor concentration to the nth power. Thus, the more promoter bind- ing sites for a transcription factor, the more sensitive gene expression will be to transcription factor concentration. In contrast, promoters that contain only a single transcription factor–tar- get site should be relatively insensitive
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Expression and developmental requirement for transcription factor Sp2

Expression and developmental requirement for transcription factor Sp2

Sp4 expression are detected within the entire central nervous system as well as other neural structures including, the retina, trigeminal ganglia, spinal ganglia and developing cranial nerves. In addition to the nervous system, Sp4 expression is also found at high levels in the hypothalamus, the nasal epithelium, and vomeronasal organ, and low levels of Sp4 are found in several mesenchymal tissues, such as the liver, testes, ovaries, and developing teeth (Supp et al, 1996;). An additional report has detected Sp4 expression as early as E8.5 in the ventricular segment of the developing heart tube and remains expressed in the ventricular muscle and in components of the cardiac conduction system (Nguyen-Tran et al., 2000). The mouse Sp4 promoter has been isolated and characterized (Song et al., 2000). The Sp4 promoter is GC-rich, lacks a TATA box, and contains two CAAT boxes. In addition, it carries putative binding sites for Sp-family members as well as sites for the binding of the MAZ protein. MAZ, also called Zf87, or its mouse homolog Pur-1 is a zinc-"finger" protein and acts as a transcription factor (Bossone et al., 1992; Kennedy and Rutter., 1992; Pryc et al., 1992). Interestingly, Sp1 or MAZ, but not Sp3, have been shown to suppress expression of the Sp4 promoter in a dose-dependent fashion (Song et al., 2000).
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DNA-Mediated Oxidation of Transcription Factor p53

DNA-Mediated Oxidation of Transcription Factor p53

Transcription factor p53 was initially thought to be an oncogene, due to its marked upregulation in numerous human cancers. It was however determined that p53 is a transcription factor whose mutation leads to a predisposition to cancer. Therefore, p53 is a tumor suppressor and not itself an oncogene. Human transcription factor p53 transduces a variety of cellular stresses into transcriptional responses. The pivotal role which p53 plays in human cells classifies this protein as a tumor suppressor. Intracellularly, p53 has a short half life due to its negative regulator murine double minute 2 (MDM2), which is an E3 ubiquitin ligase that sequesters p53 and targets it for proteolytic degradation through multiubiquitination. When some cellular stress signal is sensed, such as oxidative stress, hypoxia, or oncogene activation, p53 is activated and escapes MDM2 control. This increases intracellular p53 levels leading to the regulation of p53 target genes or other protein-protein interactions. Overall, many of the pathways in which p53 is involved revolve around decisions of cellular fate, including responses like apoptosis, senescence, cell cycle arrest, or DNA repair (Figure 1.3). 31-36
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Nac1 interacts with the POZ-domain transcription factor, Miz1.

Nac1 interacts with the POZ-domain transcription factor, Miz1.

Abbreviations: BEN, B-cell translocation gene 3 associated nuclear protein, E5R and Nac1; BMB, 1,4-bismaleimidobutane; BTB, bric-` a-brac, tramtrack and broad complex; FASN, fatty acid synthase; FLAG-Nac1 2 − 514 , FLAG-tagged Nac1; Gadd45GIP1, growth arrest and DNA-damage-inducible 45- γ interacting protein; GFP-Miz1 2 − 794 , green fluorescent protein-tagged full-length Miz1; HA, haemagglutinin; HA-Miz1 2 − 794 , HA-tagged Miz1; mCherry-Nac1 2 − 794 , mCherry-tagged full-length Nac1; Miz1, Myc-interacting zinc-finger protein 1; Nac1, nucleus accumbens 1; POZ, poxvirus and zinc finger; POZ-TF, POZ-domain transcription factor; siRNA, small interfering RNA.
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Therapeutic applications of transcription factor decoy oligonucleotides

Therapeutic applications of transcription factor decoy oligonucleotides

occasionally found in multiple iterations. Although this protein-DNA interaction is quite sequence-specific, the binding sites for a single transcription factor may vary by several base pairs when found in the promoter regions of different genes; in this case, a common motif, or consensus binding site, can be described. Often a number of different transcription factor binding sites are located in the regions both upstream and downstream from a given transcription initiation site. The binding of these different factors, and the subsequent interactions of these proteins with each other, as well as with RNA polymerases or their cofactors, yield a complex set of conditions that determines the relative transcriptional activity at different times and under varying conditions in different cell types. The transcription factor decoy approach Because transcription factors can recognize their relatively short […]
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Variable structure motifs for transcription factor binding sites

Variable structure motifs for transcription factor binding sites

Berger and Bulyk have described a protocol [68] using universal protein binding microarrays to precisely deter- mine the sequence binding preferences of transcription factors in vitro. Data for many transcription factors are available in their UniProbe database [69]. In light of this, motif search may become less relevant for those transcription factors assayed using this protocol. Never- theless, we do not expect a comprehensive database of transcription factor binding preferences for all organ- isms to be available in the near future. Also the protocol has some limitations: it does not cater for transcription factors with long binding sites; neither can it accurately reproduce features of the in vivo system such as post- translational modifications and interactions with co-
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Variable structure motifs for transcription factor binding sites

Variable structure motifs for transcription factor binding sites

Background: Classically, models of DNA-transcription factor binding sites (TFBSs) have been based on relatively few known instances and have treated them as sites of fixed length using position weight matrices (PWMs). Various extensions to this model have been proposed, most of which take account of dependencies between the bases in the binding sites. However, some transcription factors are known to exhibit some flexibility and bind to DNA in more than one possible physical configuration. In some cases this variation is known to affect the function of binding sites. With the increasing volume of ChIP-seq data available it is now possible to investigate models that incorporate this flexibility. Previous work on variable length models has been constrained by: a focus on specific zinc finger proteins in yeast using restrictive models; a reliance on hand-crafted models for just one transcription factor at a time; and a lack of evaluation on realistically sized data sets.
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Transcription factor mutations as a cause of familial myeloid neoplasms

Transcription factor mutations as a cause of familial myeloid neoplasms

Next-generation sequencing has revealed that germline mutations predisposing to MDS/AML are considerably more common than previously thought. Analyses of these mutations in genes encod- ing transcription factors continue to unveil mechanistic insights that may provide new avenues for innovating much-sought-after molecularly targeted therapies. The transcription factors described herein exhibit varying degrees of mechanistic overlap. A factor can regulate expression of the other, and multiple factors expressed at the same time and in the same cell can function collectively in het- eromeric complexes at target genes. Genetic networks established and maintained by these factors are still being discovered. While it is relatively straightforward to conduct transcriptional profiling to tabulate gene expression changes resulting from a given tran- scription factor perturbation, now even at the single-cell level, it is highly challenging to integrate this rudimentary information with other -omic data sets to yield a lucid view of the regulatory networks. Furthermore, new approaches are required to decipher functionally critical circuits within the networks and elucidate how altering the expression and activity of components within these circuits impacts cell function. It would not be surprising if MDS/ AML resulting from germline mutations of transcription factor– encoding genes involves a multitude of perturbations of network components to yield a spectrum of disease phenotypes with impli- cations for precision medicine therapeutics.
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Activated transcription factor nuclear factor kappa B is present in the atherosclerotic lesion

Activated transcription factor nuclear factor kappa B is present in the atherosclerotic lesion

Nuclear factor-kappa B (NF- k B)/Rel transcription factors play an important role in the inducible regulation of a vari- ety of genes involved in the inflammatory and proliferative responses of cells. The present study was designed to eluci- date the implication of NF- k B/Rel in the pathogenesis of atherosclerosis. Activation of the dimeric NF- k B complex is regulated at a posttranslational level and requires the re- lease of the inhibitor protein I k B. The newly developed mAb a -p65mAb recognizes the I k B binding region on the p65 (RelA) DNA binding subunit and therefore selectively reacts with p65 in activated NF- k B. Using immunofluores- cence and immunohistochemical techniques, activated NF- k B was detected in the fibrotic-thickened intima/media and atheromatous areas of the atherosclerotic lesion. Activation of NF- k B was identified in smooth muscle cells, macro- phages, and endothelial cells. Little or no activated NF- k B was detected in vessels lacking atherosclerosis. Electro- phoretic mobility shift assays and colocalization of acti- vated NF- k B with NF- k B target gene expression suggest functional implications for this transcription factor in the atherosclerotic lesion. This study demonstrates the presence of activated NF- k B in human atherosclerotic tissue for the first time. Atherosclerosis, characterized by features of chronic inflammation and proliferative processes, may be a paradigm for the involvement of NF- k B/Rel in chronic inflammatory disease. ( J. Clin. Invest. 1996. 97:1715–1722.) Key words: smooth muscle cells • macrophages • endothelial
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Spliced Leader RNA Gene Transcription in Trypanosoma brucei Requires Transcription Factor TFIIH

Spliced Leader RNA Gene Transcription in Trypanosoma brucei Requires Transcription Factor TFIIH

Trypanosomatid parasites share a gene expression mode which differs greatly from that of their human and insect hosts. In these unicellular eukaryotes, protein-coding genes are transcribed polycistronically and individual mRNAs are processed from precursors by spliced leader (SL) trans splicing and polyadenylation. In trans splicing, the SL RNA is consumed through a transfer of its 5 ⴕ -terminal part to the 5 ⴕ end of mRNAs. Since all mRNAs are trans spliced, the parasites depend on strong and continuous SL RNA synthesis mediated by RNA polymerase II. As essential factors for SL RNA gene transcription in Trypanosoma brucei, the general transcription factor (GTF) IIB and a complex, consisting of the TATA-binding protein–related protein 4, the small nuclear RNA-activating protein complex, and TFIIA, were recently identified. Although T. brucei TFIIA and TFIIB are extremely divergent to their counterparts in other eukaryotes, their characterization suggested that trypanosomatids do form a class II transcription preinitiation complex at the SL RNA gene promoter and harbor orthologues of other known GTFs. TFIIH is a GTF which functions in transcription initiation, DNA repair, and cell cycle control. Here, we investigated whether a T. brucei TFIIH is important for SL RNA gene transcription and found that silencing the expression of the highly conserved TFIIH subunit XPD in T. brucei affected SL RNA gene synthesis in vivo, and depletion of this protein from extract abolished SL RNA gene transcription in vitro. Since we also identified orthologues of the TFIIH subunits XPB, p52/TFB2, and p44/SSL1 copurifying with TbXPD, we concluded that the parasite harbors a TFIIH which is indispensable for SL RNA gene transcription.
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Characterisation of a cellular transcription factor which co-ordinates cell cycle events with transcription

Characterisation of a cellular transcription factor which co-ordinates cell cycle events with transcription

Much work has centred on the control of viral promoters in embryonic stem (ES) cells and in the F9 embryonal carcinoma (EC) cell line as a means for defining cellular transcription factors regulated during differentiation. F9 EC cells are pluripotential stem cells derived from an explanted teratocarcinoma (Bemstine et a/., 1973). They can be induced to differentiate using, cAMP and retinoic acid (RA), to form several cell types similar to those in the developing mouse embryo. Treatment with RA gives rise to primitive endoderm whereas cAMP and retinoic acid together produce parietal endoderm (Strickland and Mahdavi, 1978;Strickland et a/., 1980). Some viral promoters are inefficiently transcribed in EC cells which could result from a lack of positively acting factors or from the presence of specific repressors, though it is possible that both models are applicable. For example the SV40 and polyoma virus enhancers are poorly transcribed in EC cells but more efficiently in PE cells. This in part can be explained by the cellular transcription factor PEAl (murine AP-1) which regulates expression of the polyoma enhancer and is abundant in differentiated cells but low in EC cells (Kryske et a/., 1987).
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When is a transcription factor a NAP?

When is a transcription factor a NAP?

Finally, although FIS (the Factor for Inversion Stimula- tion) is viewed as a NAP, it can function as a conventional transcription factor by recruiting RNA polymerase via protein-protein contacts to initiate transcription [19]. These examples show the challenge in identifying clear distinctions between NAPs and transcription factors. This distinction becomes even more blurred because NAPs are sometimes equivalent to functional domains within transcription factors: NtrC is a prominent example. NtrC is the response regulator partner of the cytosolic NtrB sensor kinase and it activates transcription at s 54 -dependent pro- moters in response to nitrogen stress [20]. These interactions require NtrC to bind to a well-defined enhancer sequence upstream of the target promoter. The DNA-binding domain of NtrC is closely related to the NAP FIS, leading to the proposal, supported by phylogenetic evidence, that FIS evolved from an NtrC-like transcription factor [21]. The fis gene probably arrived in E. coli at the same time as dusB (formerly yhdG ), with which it now forms a dusB-fis operon. The DusB protein is related to NifR3 in Rhodobacter , Rhizobium and the nifR3 gene is co-transcribed in those bacteria with ntrB and ntrC . It has been proposed that dusB/yhdG and fis evolved following horizontal gene transfer of the nifR3 ntrB ntrC nitrogen metabolism operon followed by deletion of all but the fis sequences from ntrC [21]. Here we consider the case of BldC, a recently characterized DNA-binding protein from the Gram-positive bacterium Streptomyces . Streptomycetes are filamentous bacteria that differentiate by producing spore-bearing reproductive structures called aerial hyphae [22,23]. The transition from vegetative to reproductive growth is controlled by the bld (bald) loci, which were identified in classical mutagenic screens. Mutations in bld genes prevent the formation of aerial hyphae, either by blocking entry into development (typically mutations in activators) or by inducing precocious sporulation in the vegetative mycelium (typically mutations in repressors) [24–26]. One of the classic bld genes, bldC , encodes a 68-residue DNA-binding protein related to the DNA-binding domain of MerR-family transcription factors. Recent transcriptional, biochemical and structural analyses have revealed the effect of BldC on global gene expression, how it binds DNA, its wider relationship to previously characterized transcription factors and NAPs, and the diverse modes of DNA binding found among BldC-related proteins. These observations raise further interesting questions about the distinction between NAPs and tran- scription factors, and the evolution of one from the other.
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Transcription factor ETV1 is essential for rapid conduction in the heart

Transcription factor ETV1 is essential for rapid conduction in the heart

maintaining normal cardiac rhythm and optimal cardiac output. Conduction defects in these tissues produce a disproportionate burden of arrhythmic disease and are major predictors of mortality in heart failure patients. Despite the clinical importance, little is known about the gene regulatory network that dictates the fast conduction phenotype. Here, we have used signal transduction and transcriptional profiling screens to identify a genetic pathway that converges on the NRG1-responsive transcription factor ETV1 as a critical regulator of fast conduction physiology for PAM and VCS cardiomyocytes. Etv1 was highly expressed in murine PAM and VCS cardiomyocytes, where it regulates expression of Nkx2-5, Gja5, and Scn5a, key cardiac genes required for rapid conduction. Mice deficient in Etv1 exhibited marked cardiac conduction defects coupled with developmental abnormalities of the VCS. Loss of Etv1 resulted in a complete disruption of the normal sodium current heterogeneity that exists between atrial, VCS, and ventricular myocytes. Lastly, a phenome-wide
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Transcription factor MITF regulates cardiac growth and hypertrophy

Transcription factor MITF regulates cardiac growth and hypertrophy

High levels of microphthalmia transcription factor (MITF) expression have been described in several cell types, including melanocytes, mast cells, and osteoclasts. MITF plays a pivotal role in the regulation of specific genes in these cells. Although its mRNA has been found to be present in relatively high levels in the heart, its cardiac role has never been explored. Here we show that a specific heart isoform of MITF is expressed in cardiomyocytes and can be induced by b-adrenergic stimulation but not by paired box gene 3 (PAX3), the regulator of the melanocyte MITF isoform. In 2 mouse strains with different MITF mutations, heart weight/body weight ratio was decreased as was the hypertrophic response to b-adrenergic stimulation. These mice also demonstrated a tendency to sudden death following b-
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Phosphorylation and dimerisation of transcription factor ATF-1

Phosphorylation and dimerisation of transcription factor ATF-1

T he m am m alian transcription factor CREB is thought to activate cA M P-inducible genes in a variety of differentiated cell types and is probably involved in o th e r sig n a llin g p a th w a y s . U n d iffe re n tia te d F9 embryonal carcinoma (UF9) cells are refractory to cAMP and becom e cAMP-responsive following differentiation to endoderm like cells. It has been proposed that UF9 cells contain a negative regulator(s) o f the cAM P- response that might act through direct interaction with CREB. W e have used a protein blotting assay and labelled CREB to probe for CREB-binding proteins in nuclear extracts from F9 cells and to exam ine their abundance during differentiation. W e find that ATF1 (a protein that is highly homologous to CREB) and a novel polypeptide(s) of - 1 0 0 kDa (CBP100) are the major CREB-binding proteins in extracts from UF9 cells. As expected A T F l is detected due to leucine zipper- dependent heterodim erisation with CREB. In contrast CBP100 interacts with CREB independently o f the leucine zipper. T he total am ount of A T F l and the am ount of A T F l that is complexed with CREB are substantially reduced following differentiation. In addition, A T F l mRNA levels are lower in differentiated F9 cells indicating that a pretranslational m echanism contributes to the decreased A T F l protein levels observed. CBP100 levels are also reduced or CBP100 is m odified upon differentiation. W e discuss the potential roles of A T F l and CBP100 in regulating CREB a c tiv ity d urin g d iffe re n tia tio n o f F9 em b ryo n a l carcinom a cells.
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