THOC5 is a nuclear/cytoplasmic protein member of the spliceosome complex which potentiates C/EBP expression in adipocyte differentiation. As C/EBP family members are important regulators of myelopoiesis and THOC5 is highly expressed in neutrophil/macrophage progenitor cells we assessed the role of THOC5 in cytokine-stimulated monocytic development. M-CSF stimulated maturation of the NFS60 cell line was associated with enhanced THOC5 expression and phosphorylation. THOC5 was also shown to form a complex with C/EBPbeta. Ectopic expression of THOC5 mimicked M-CSF mediated cell maturation and enhanced protein expression of the myeloid transcription factors C/EBPbeta, C/EBPalpha, Pu-1 and also GAB2 (a PI-3 Kinase and macrophage development regulator). Increased THOC5 expression also mimicked M-CSF stimulated increases in the lipid second messenger PtdInsP(3). Inhibition of THOC5-induced increases in PtdInsP(3) levels abrogated the elevated levels of C/EBPbeta. Thus THOC5 expression can potentiate ...
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Stress responses are critical for estrogen (E2) to induce apoptosis in E2-deprived breast cancer cells. Nuclear factor-kappa B (NF-κB) is well known as a therapeutic target to prevent stress responses in chronic inflammatory diseases including cancer. However, whether E2 activates NF-κB to participate in stress-associated apoptosis in E2-deprived breast cancer cells is unclear. We demonstrated that E2 differentially modulates NF-κB activity in E2-deprived breast cancer cells according to the treatment time. Because E2 initially has significant potential to down modulate the NF-κB activation, it completely suppresses the tumor necrosis factor alpha (TNFα)-induced NF-κB activation. We found that E2 preferentially and constantly enhances the expression of transcription factor CCAAT/enhancer binding protein beta (C/EBPβ) which is responsible for suppression of NF-κB activation by E2 in MCF-7:5C cells. The mTOR signaling pathway promotes repression of NF-κB by C/EBPβ which is confirmed by ...
A recent paper in Nature Medicine showed that Down syndrome brains have reduced expression of Sorting nexin 27 (SNX27) and CCAAT/enhancer binding protein beta (C/EBP beta) and identified C/EBP beta as a transcription factor for SNX27. Down syndrome results in overexpression of miR-155, a chromosome 21-encoded microRNA that negatively regulates C/EBP beta, thereby reducing SNX27 expression. SNX27 is a brain-enriched […]. ...
CCAAT/enhancer-binding protein beta is a protein that in humans is encoded by the CEBPB gene. The protein encoded by this intronless gene is a bZIP transcription factor that can bind as a homodimer to certain DNA regulatory regions. It can also form heterodimers with the related proteins CEBP-alpha, CEBP-delta, and CEBP-gamma. The encoded protein is important in the regulation of genes involved in immune and inflammatory responses and has been shown to bind to the IL-1 response element in the IL-6 gene, as well as to regulatory regions of several acute-phase and cytokine genes. In addition, the encoded protein can bind the promoter and upstream element and stimulate the expression of the collagen type I gene. CEBP-beta is critical for normal macrophage functioning, an important immune cell sub-type; mice unable to express CEBP-beta have macrophages that cannot differentiate (specialize) and thus are unable to perform all their biological functions - including macrophage-mediated muscle repair. ...
Mouse polyclonal antibody raised against a full-length human CEBPB protein. CEBPB (AAH21931.1, 1 a.a. ~ 345 a.a) full-length human protein. (H00001051-B01P) - Products - Abnova
CCAAT/enhancer-binding protein δ (CEBPD) is expressed in hypoxic kidney tubular cells in vivo. (a) Mice were exposed to 8% O2 for 6 h using a hypoxia chamber
Binds to lipid droplets and regulates their enlargement, thereby restricting lipolysis and favoring storage. At focal contact sites between lipid droplets, promotes directional net neutral lipid transfer from the smaller to larger lipid droplets. The transfer direction may be driven by the internal pressure difference between the contacting lipid droplet pair and occurs at a lower rate than that promoted by CIDEC. Acts as a CEBPB coactivator in mammary epithelial cells to control the expression of a subset of CEBPB downstream target genes, including ID2, IGF1, PRLR, SOCS1, SOCS3, XDH, but not casein. By interacting with CEBPB, strengthens the association of CEBPB with the XDH promoter, increases histone acetylation and dissociates HDAC1 from the promoter. When overexpressed, induces apoptosis. The physiological significance of its role in apoptosis is unclear.
Human CEBPB partial ORF ( NP_005185, 256 a.a. - 344 a.a.) recombinant protein with GST-tag at N-terminal. (H00001051-Q01) - Products - Abnova
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Fasting elicits transcriptional programs in hepatocytes leading to glucose and ketone production. This transcriptional program is regulated by many transcription factors (TFs). To understands how this complex network regulates the metabolic response to fasting we aimed at isolating the enhancers and TFs dictating it. Measuring chromatin accessibility revealed that fasting massively reorganizes liver chromatin, exposing numerous fasting-induced enhancers. By utilizing computational methods in combination with dissecting enhancers features and TF cistromes, we implicated four key TFs regulating the fasting response: glucocorticoid receptor (GR), cAMP responsive element binding protein 1 (CREB1), peroxisome proliferator activated receptor alpha (PPARA) and CCAAT/enhancer binding protein beta (CEBPB). These TFs regulate fuel production by two distinctly-operating modules, each controlling a separate metabolic pathway. The gluconeogenic module operates through assisted loading whereby GR doubles the ...
TNF-a was originally identified as a macrophage product implicated in the metabolic disturbances of chronic inflammation and malignancy. Later on, its biological actions were shown to further extend to anorexia, weight loss, and insulin resistance (7). Elevated adipose tissue expression of TNF-a mRNA has been reported in different rodent models of obesity as well as in clinical studies involving obese patients (23). TNF-a mRNA expression is positively correlated with body adiposity as well as with hyperinsulinemia, showing positive associations with fasting insulin and triglyceride concentrations. TNF-a inhibits the expression of the transcription factor CCAAT/ enhancer binding protein-a (CEBPa) and the nuclear receptor peroxisome proliferator-activated receptor (PPAR)y2 (8,12,14). Furthermore, TNF-a stimulates the nuclear factor- kB transcription factor (NFkB), which orchestrates a series of inflammatory events, including expression of adhesion molecules on the surface of both endothelial cells ...
Expression of CEBPB (C/EBP-beta, CRP2, IL6DBP, LAP, NFIL6, TCF5) in cervix, uterine tissue. Antibody staining with CAB004213 in immunohistochemistry.
Expression of CEBPB (C/EBP-beta, CRP2, IL6DBP, LAP, NFIL6, TCF5) in nasopharynx tissue. Antibody staining with CAB004213 in immunohistochemistry.
The CCAAT/enhancer-binding protein β (C/EBPβ) is a transcription factor, which was first identified as a regulator of differentiation and inflammatory processes mainly in adipose tissue and liver; however, its function in the brain was largely unknown for many years. Previous studies from our laboratory indicated that C/EBPβ is implicated in inflammatory process and brain injury, since mice lacking this gene were less susceptible to kainic acid-induced injury. We first performed cDNA microarrays analysis using hippocampal RNA isolated from C/EBPβ +/+ and C/EBPβ −/− mice. Immunocytochemical and immunohistochemical studies were done to evaluate C/EBPβ and C3 levels. Transient transfection experiments were made to analyze transcriptional regulation of C3 by C/EBPβ. To knockdown C/EBPβ and C3 expression, mouse astrocytes were infected with lentiviral particles expressing an shRNA specific for C/EBPβ or an siRNA specific for C3. Among the genes displaying
This intronless gene encodes a transcription factor that contains a basic leucine zipper (bZIP) domain and recognizes the CCAAT motif in the promoters of target genes. The encoded protein functions in homodimers and also heterodimers with CCAAT/enhancer-binding proteins beta and gamma. Activity of this protein can modulate the expression of genes involved in cell cycle regulation as well as in body weight homeostasis. The use of alternative in-frame non-AUG (CUG) and AUG start codons results in several protein isoforms with different lengths. Differential translation initiation is mediated by an out-of-frame, upstream open reading frame which is located between the CUG and the first AUG start codons. [provided by RefSeq, Sep 2014 ...
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Having analysed data with TRANSFAC system, we may assume that the disturbed attachment of such factors as (C/EBP(CCAAT enhancer binding protein) Hoxa-3,Sp1 (serine protease inhibitor) or GATA-1, (GATA nucleotide sequence) may have an impact on IGF-1 protein synthesis, but we did not observed any significant correlation between promoter P1 polymorphism and serum IGF-1 levels ...
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TY - JOUR. T1 - Investigating protein-protein interactions in living cells using fluorescence lifetime imaging microscopy. AU - Sun, Yuansheng. AU - Day, Richard. AU - Periasamy, Ammasi. PY - 2011/9. Y1 - 2011/9. N2 - Fluorescence lifetime imaging microscopy (FLIM) is now routinely used for dynamic measurements of signaling events inside living cells, including detection of protein-protein interactions. An understanding of the basic physics of fluorescence lifetime measurements is required to use this technique. In this protocol, we describe both the time-correlated single photon counting and the frequency-domain methods for FLIM data acquisition and analysis. We describe calibration of both FLIM systems, and demonstrate how they are used to measure the quenched donor fluorescence lifetime that results from FÃ ¶rster resonance energy transfer (FRET). We then show how the FLIM-FRET methods are used to detect the dimerization of the transcription factor CCAAT/enhancer binding protein-Î ± in ...
ABSTRACT: Fluorescence lifetime imaging microscopy (FLIM) is now routinely used for dynamic measurements of signaling events inside living cells, including detection of protein-protein interactions. An understanding of the basic physics of fluorescence lifetime measurements is required to use this technique. In this protocol, we describe both the time-correlated single photon counting and the frequency-domain methods for FLIM data acquisition and analysis. We describe calibration of both FLIM systems, and demonstrate how they are used to measure the quenched donor fluorescence lifetime that results from F?rster resonance energy transfer. We then show how the FLIM-FRET methods are used to detect the dimerization of the transcription factor CCAAT enhancer binding protein-a in live mouse pituitary cell nuclei. Notably, the factors required for accurate determination and reproducibility of lifetime measurements are described. With either method, the entire protocol including specimen preparation, ...
TY - JOUR. T1 - Differentiation-induced gene expression in 3T3-L1 preadipocytes. T2 - CCAAT/enhancer binding protein interacts with and activates the promoters of two adipocyte-specific genes.. AU - Christy, R. J.. AU - Yang, V. W.. AU - Ntambi, J. M.. AU - Geiman, D. E.. AU - Landschulz, W. H.. AU - Friedman, A. D.. AU - Nakabeppu, Y.. AU - Kelly, T. J.. AU - Lane, M. D.. PY - 1989/9. Y1 - 1989/9. N2 - Previous studies have shown that differentiation of 3T3-L1 preadipocytes leads to the transcriptional activation of a group of adipose-specific genes. As an approach to defining the mechanism responsible for activating the expression of these genes, we investigated the binding of nuclear factors to the promoters of two differentiation-induced genes, the 422(aP2) and stearoyl-CoA desaturase 1 (SCD1) genes. DNase I footprinting and gel retardation analysis identified two binding regions within the promoters of each gene that interact with nuclear factors present in differentiated 3T3-L1 adipocytes. ...
In this work, we have shown that the transcription factor C/EBPβ directly regulates the expression of the C3 gene, and that this control could be relevant for the pro-inflammatory effects of this transcription factor. By microarray analysis and RT-PCR we showed that the hippocampal content of C3 transcripts was depleted in C/EBPβ −/− mice. The analysis of the C3 promoter showed that this gene was directly induced by C/EBPβ through a C/EBPβ consensus site located at −616/-599 position from the transcription start site. In accordance with these data, LPS induced the expression of C3 in glial cells, at least in part, through the induction of C/EBPβ since the repression of LPS-induction of C/EBPβ by shRNA interference blocked C3 increase. On the contrary, C/EBPβ overexpression by transient transfection induced C3 expression. Additionally, treatment of these cultures with LPS induced the levels of the pro-inflammatory factors IL-1β and COX-2, which were significantly reduced in those ...
In this study we have shown that the rat UDP-glucuronosyltransferase 2B1 gene is specifically activated by C/EBPα and that this activation is correlated with the binding of C/EBPα to an element residing between −91 and −99 bp upstream of the UGT2B1 gene transcription start site. Furthermore, we extend these findings to show that C/EBPα is essential for the expression of transcripts homologous to UGT2B1 in adult mouse liver.. This is the first example of the regulation of a UGT2B gene by a member of the C/EBP transcription factor family, and adds to our previous finding that the UGT2B1 gene promoter also interacts with and is activated by HNF1α (Hansen et al., 1997). Both C/EBP and HNF1 also interact with the early promoter of the albumin gene (Fig. 1) (Lichtsteiner et al., 1987). When these two factors are simultaneously overexpressed, there is a strong synergistic effect on transcription of this gene (Wu et al., 1994). It was shown that a specific C/EBPα activation domain was required ...
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Pharmacodynamic studies, including micro-ribonucleic acid (miRNA)-181 family and target gene expression, CCAAT/enhancer binding protein (C/EBP), alpha gene (CEBPA) expression, and genes involved in erythroid ...
Another study applying ChIP-seq for two different TFs (CCAAT/enhancer-binding protein α and hepatocyte nuclear factor 4 α) in the livers of five vertebrates species provides an alternative view of conservation of TF-binding events (Schmidt et al., 2010). This work demonstrated that the majority of binding events are species specific, rather than consistently localized in conserved regions. Binding to conserved sequences in one species was rarely indicative of binding to the homologous sequence in others. These differences in binding were consistently observed between human and mouse in the livers of both species, and also in the livers of aneuploid mice harbouring human chromosome 21. Binding to the human chromosome in mouse was representative of binding to the endogenous chromosome in human, rather than binding to mouse chromosomes (Wilson et al., 2008) (Fig. 4). The differences in binding between species are therefore unlikely to be due to non-equivalence in the assayed tissue. Similarly, ...
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Neutrophil-specific granule deficiency (SGD) is a rare disorder characterized by recurrent pyogenic infections, defective neutrophil chemotaxis and bactericidal activity, and lack of neutrophil secondary granule proteins. It has been linked to a defect in the transcription factor CCAAT/enhancer binding protein (CEBP) epsilon. Recently, loss-of-function mutations in SMARCD2 were identified from SGD patients. SMARCD2 is chromatin-remodeling factor, that interacts with CEBP epsilon ...
CCAAT/enhancer binding protein zeta (mouse, aa620-633) Antibody (internal region), Peptide-affinity purified goat antibody validated in WB, E (AF3888a), Abgent
TY - JOUR. T1 - A20-binding inhibitor of NF-κB (ABIN1) controls Toll-like receptor-mediated CCAAT/enhancer-binding protein β activation and protects from inflammatory disease. AU - Zhou, Jingran. AU - Wu, Ruiqiong. AU - High, Anthony A.. AU - Slaughter, Clive A.. AU - Finkelstein, David. AU - Rehg, Jerold E.. AU - Redecke, Vanessa. AU - Häcker, Hans. PY - 2011/11/1. Y1 - 2011/11/1. N2 - Toll-like receptors (TLRs) are expressed on innate immune cells and trigger inflammation upon detection of pathogens and host tissue injury. TLR-mediated proinflammatory-signaling pathways are counteracted by partially characterized anti-inflammatory mechanisms that prevent exaggerated inflammation and host tissue damage as manifested in inflammatory diseases. We biochemically identified a component of TLR-signaling pathways, A20-binding inhibitor of NF-κB (ABIN1), which recently has been linked by genome-wide association studies to the inflammatory diseases systemic lupus erythematosus and psoriasis. We ...
CCAAT/enhancer binding protein (C/EBP), epsilon, also known as CEBPE and CRP1, is a type of ccaat-enhancer-binding protein. CEBPE is its human gene and is pro-apoptotic. The protein encoded by this gene is a bZIP transcription factor which can bind as a homodimer to certain DNA regulatory regions. It can also form heterodimers with the related protein CEBP-δ. The encoded protein may be essential for terminal differentiation and functional maturation of committed granulocyte progenitor cells. Mutations in this gene have been associated with specific granule deficiency, a rare congenital disorder. Multiple variants of this gene have been described, but the full-length nature of only one has been determined. GRCh38: Ensembl release 89: ENSG00000092067 - Ensembl, May 2017 GRCm38: Ensembl release 89: ENSMUSG00000052435 - Ensembl, May 2017 "Human PubMed Reference:". "Mouse PubMed Reference:". "Entrez Gene: CEBPE CCAAT/enhancer binding protein (C/EBP), epsilon". Antonson P, Stellan B, Yamanaka R, ...
We recently discovered that induction from the anti-inflammatory gene by cyclic AMP occurs through book cyclic AMP-dependent proteins kinase-independent systems involving activation of CCAAT/enhancer-binding proteins (C/EBP) transcription elements, notably C/EBP, from the cyclic AMP GEF EPAC1 as well as the ...
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Background The up-regulation of CCAAT/enhancer binding protein delta (CEBPD) has frequently been observed in macrophages in age-associated disorders, including rheumatoid arthritis (RA). However, the role of macrophage CEBPD in the pathogenesis of RA is unclear. Methodology and Principal Findings We found that the collagen-induced arthritis (CIA) score and the number of affected paws in Cebpd−/− mice were significantly decreased compared with the wild-type (WT) mice. The histological analysis revealed an attenuated CIA in Cebpd−/− mice, as shown by reduced pannus formation and greater integrity of joint architecture in affected paws of Cebpd−/− mice compared with WT mice. In addition, immunohistochemistry analysis revealed decreased pannus proliferation and angiogenesis in Cebpd−/− mice compared with WT mice. CEBPD activated in macrophages played a functional role in promoting the tube formation of endothelial cells and the migration and proliferation of synoviocytes. In vivo DNA
TY - JOUR. T1 - Enhancer-binding proteins with a forkhead-associated domain and the sigma(54) regulon in Myxococcus xanthus fruiting body development. AU - Jelsbak, Lars. AU - Givskov, Michael Christian. AU - Kaiser, D.. PY - 2005. Y1 - 2005. N2 - In response to starvation, Myxococcus xanthus initiates a developmental program that results in the formation of spore-filled, multicellular fruiting bodies. Many developmentally regulated genes in M. xanthus are transcribed from sigma(54) promoters, and these genes require enhancer-binding proteins. Here we report the finding of an unusual group of 12 genes encoding sigma(54)-dependent enhancer-binding proteins containing a forkhead-associated (FHA) domain as their N-terminal sensory domain. FHA domains in other proteins recognize phosphothreonine residues. An insertion mutation in one of these genes, Mx4885, caused a cell autonomous aggregation and sporulation defect. In-frame deletion mutants showed that the FHA domain is necessary for proper Mx4885 ...
Here, we investigated the mechanisms by which PPARδ agonists control expression of 14-3-3ε, a key antiinflammatory protein in endothelial cells.12 Our data not only provide evidence that PPARδ modulates expression of YWHAE gene and 14-3-3ε protein under resting conditions but also demonstrate that this nuclear receptor upregulates 14-3-3ε expression by targeting transcription via a PPRE-independent pathway involving colocalization of C/EBPβ and PPARδ on YWHAE promoter. Several lines of evidence support these conclusions. First, PPARδ agonists regulated YWHAE promoter activity in a concentration- and time-dependent manner. Concordantly, YWHAE promoter was upregulated by PPARδ overexpression, whereas specific PPARγ and PPARα ligands had no effect on YWHAE promoter under our experimental conditions. Second, PPARδ activation increased 14-3-3ε mRNA and protein expression in both primary and spontaneously transformed endothelial cell lines, whereas PPARδ knockdown depressed basal and ...
Lexpressió cortical androgen dependent del KAP està afectada en hipotiroïdisme postnatal. La síntesi puntual de T3 a partir del dia 11 postnatal, comença una resposta cortical feble de KAP que va augmentant cap als dies 15-16, que és quan es produeix un pic fisiològic de T4 i el desenvolupament puberal dels ratolins. Donat que les CCAAT/Enhancer-Binding Proteins (C/EBPs) participen en respostes mitjançades per T3 i que en el promotor del KAP existeixen quatre elements de resposta consens per a C/EBPs, hem analitzat la seva participació en la resposta androgènica de KAP mitjançada per T3. La detecció de p42C/EBPa y p35C/EBPb es troba correlacionada amb lexpressió del KAP, apareixent en extractes renal nuclears de ratolins masles control i hipotiroïdals induïts amb T3 durant els dies 7-21 postnatals, però no en els hipotiroïdals no tractats. Mitjançant transfeccions transitòries es mostrava com C/EBPa i C/EBPb eren capaces dinduir respostes màximes del promotor del KAP i que ...
Choi B.H., Park G.T., Rho H.M. (1999). Interaction of hepatitis B viral X protein and CCAAT/enhancer-binding protein alpha synergistically activates the hepatitis B viral enhancer II/pregenomic promoter.. J. Biol. Chem. 274: 2858 - 2865. PubMed DOI:10.1074/jbc.274.5.2858 ...
Plasmid p-eGFP-beta 2 CP from Dr. John Coopers lab contains the insert capping protein beta 2 subunit and is published in J Cell Biol. 1998 Dec 28. 143(7):1919-30. This plasmid is available through Addgene.
mammary gland and aided in the elucidation of the mechanisms of the response to diet. The aim of this study was to evaluate the effect of different forage diets (grazing vs. hay) near the time of ewe parturition on the relationship between the fatty acid profile and gene expression in the mammary gland of the Churra Tensina sheep breed. Results: In this study, the forage type affected the C18:2 cis-9 trans-11 (CLA) and long-chain saturated fatty acid (LCFA) content, with higher percentages during grazing than during hay feeding. This may suggest that these FAs act as regulatory factors for the transcriptional control of the carnitine palmitoyltransferase 1B (CPT1B) gene, which was more highly expressed in the grazing group (GRE). The most highly expressed gene in the mammary gland at the fifth week of lactation is CAAT/ enhancer- binding protein beta (CEBPB), possibly due to its role in milk fat synthesis in the mammary gland. More stable housekeeping genes in the ovine mammary gland that would ...
Chronic pain is increasingly recognized as an important comorbidity of HIV-infected patients, however, the exact molecular mechanisms of HIV-related pain are still elusive. CCAAT/enhancer binding proteins (C/EBPs) are expressed in various tissues, including the central nervous system. C/EBPβ, one of C/EBPs is involved in the progression of HIV/AIDS, but the exact role of C/EBPβ and its upstream factors are not clear in HIV pain state. Here, we used a neuropathic pain model of perineural HIV envelope glycoprotein gp120 application onto the rat sciatic nerve to test the role of phosphorylated C/EBPβ (pC/EBPβ) and its upstream pathway in the spinal cord dorsal horn (SCDH ...
Targeting MUC1-C with silencing or an inhibitor downregulates p-HER2 activation in HER2-overexpressing breast cancer cells. Moreover, MUC1-C has been linked to regulation of downstream RTK signaling, such as the PI3K→AKT and MEK→ERK pathways. MUC1-C is also imported into the nucleus by importin-β, where it interacts with transcription factors and contributes to their transactivating function. In this regard, MUC1-C associates with NF-κB p65 and induces activation of the ZEB1 gene by a NF-κB-mediated mechanism. In turn, MUC1-C binds to ZEB1 and suppresses miR-200c expression with the resulting induction of EMT. In addition, MUC1-C interacts with the CCAAT/enhancer-binding protein β (C/EBPβ) on the ALDH1A1 gene promoter and induces C/EBPβ-mediated ALDH1A1 expression. The available evidence thus links MUC1-C to the induction of EMT and ALDH activity, both characteristics of breast cancer stem-like cell populations. Overexpression of MUC1, as found in breast cancer cells, is also ...
CIK cells could promote Raji and BJAB cells apoptosis (t = 3.634, P < 0.05; t = 3.976, P < 0.05), and increase the expression of miR-155 in Raji by (6.87 ± 0.19) fold (t = 2.787, P < 0.05), meanwhile, in BJAB cells by (5.06 ± 0.25) fold (t = 3.513, P < 0.05). Moreover, miR-155 inhibitor might block this process (t = 3.842, P < 0.05; t = 4.016, P < 0.05). Furthermore, miR-155 mimics induced Raji and BJAB cells apoptosis (t = 4.239, P < 0.05; t = 3.477, P < 0.05). MiR-155 targeted at the site of CEBPB 3-UTR, and CIK cells could decrease the luciferase activity of Raji cells by (42.89 ± 2.06)% (t = 3.281, P < 0.05); meanwhile, in BJAB cells by (37.02 ± 1.98)% (t = 4.933, P < 0.05). ...
GATA 3, 0.1 mg. The genes for all 4 subunits of the T-cell antigen receptor (alpha, beta, gamma and delta) are controlled by distinct enhancers and their enhancer-binding proteins.
The study expands on work reported in 2001 in the journal Molecular Cell announcing that a team led by Buck had found that a small piece of an important regulatory protein called C/EBP beta was responsible for fibrous tissue growth, or excessive scar tissue following injury or illness. When normal scarring goes awry, excessive build-up of fibrous tissue can produce disfiguring scars or clog vital internal organs and lead to serious complications. Buck and colleagues developed a mutated protein that stopped this excessive fibrous tissue growth ...
TY - JOUR. T1 - Role of glucocorticoid receptor and CCAAT/enhancer-binding protein α in the feed-forward induction of 11β-hydroxysteroid dehydrogenase type 1 expression by cortisol in human amnion fibroblasts. AU - Yang, Zhen. AU - Guo, Chunming. AU - Zhu, Ping. AU - Li, Wenjiao. AU - Myatt, Leslie. AU - Sun, Kang. PY - 2007/11/1. Y1 - 2007/11/1. N2 - The amount of cortisol available to its receptors is increased by the pre-receptor enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) which converts cortisone to cortisol. We examined the molecular mechanisms of the feedback effect of cortisol on 11β-HSD1 mRNA expression in human amnion fibroblasts. Our data showed that cortisol-induced 11β-HSD1 mRNA expression dose dependently in amnion fibroblasts, which could be completely blocked both by the mRNA transcription inhibitor 5,6-dichlorobenzimidazole riboside and by the glucocorticoid receptor (GR) antagonist RU486, and partially blocked by global inhibition of CCAAT/enhancer-binding ...
The basic leucine zipper transcription factor ATF5 is overexpressed in many tumor types and interference with its expression or function inhibits cancer cell survival. As a potential therapeutic approach to exploit these findings, we created dominant-negative (DN) ATF5 forms lacking DNA-binding ability that retain the ATF5 leucine zipper, and thus associate with and sequester ATF5s requisite leucine zipper-binding partners. Preclinical studies with DN-ATF5, including a cell-penetrating form, show in vitro and in vivo efficacy in compromising cancer cell survival. However, DN-ATF5s targets, and particularly those required for tumor cell survival, have been unknown. We report that cells lacking ATF5 succumb to DN-ATF5, indicating that ATF5 itself is not DN-ATF5s obligate target. Unbiased pull-down assays coupled with mass spectrometry and immunoblotting revealed that DN-ATF5 associates in cells with the basic leucine zipper proteins CEBPB and CEBPD and coiled-coil protein CCDC6. Consistent with ...
Insulin can inhibit the stimulatory effect of glucocorticoid hormones on the transcription of genes coding for enzymes involved in glucose metabolism. We reported earlier that insulin inhibits the glucocorticoid-stimulated transcription of the gene coding for liver 6-phosphofructo-2-kinase (PFK-2). To elucidate the mechanism of these hormonal effects, we have studied the regulatory regions of the PFK-2 gene in transfection experiments. We found that both glucocorticoids and insulin act via the glucocorticoid response unit (GRU) located in the first intron. Footprinting experiments showed that the GRU binds not only the glucocorticoid receptor (GR), but also ubiquitous [nuclear factor I (NF-I)] and liver-enriched [hepatocyte nuclear factor (HNF)-3, HNF-6, CAAT/enhancer binding protein (C/EBP)] transcription factors. Site-directed mutational analysis of the GRU revealed that these factors modulate glucocorticoid action but that none of them seems to be individually involved in the inhibitory ...
Adapter protein involved in invadopodia and podosome formation and extracellular matrix degradation. Binds matrix metalloproteinases (ADAMs), NADPH oxidases (NOXs) and phosphoinositides. Acts as an organizer protein that allows NOX1- or NOX3-dependent reactive oxygen species (ROS) generation and ROS localization. Plays a role in mitotic clonal expansion during the immediate early stage of adipocyte differentiation (By similarity).