keyword
https://read.qxmd.com/read/21145827/characterization-of-the-transcriptional-signature-of-c-ebpbeta-isoforms-lap-lip-in-hep3b-cells-implication-of-lip-in-pro-survival-functions
#21
JOURNAL ARTICLE
Gaëlle Saint-Auret, Jean-Louis Danan, Martine Hiron, Céline Blache, Eric Sulpice, Simon Tendil, Maryvonne Daveau, Xavier Gidrol, Jean-Philippe Salier
BACKGROUND & AIMS: C/EBPbeta is an important mediator of several cellular processes, such as differentiation, proliferation, and survival of hepatic cells. However, a complete catalog of the targets of C/EBPbeta or the mechanism by which this transcription factor regulates certain liver-dependent pathways has not been clearly determined. Two major natural isoforms of this transcription factor exist: the liver-enriched activating protein (LAP) and the liver-enriched inhibitory protein (LIP), a functional LAP antagonist...
June 2011: Journal of Hepatology
https://read.qxmd.com/read/21048961/whole-blood-transcriptomics-in-cardiac-surgery-identifies-a-gene-regulatory-network-connecting-ischemia-reperfusion-with-systemic-inflammation
#22
JOURNAL ARTICLE
Orfeas Liangos, Sophie Domhan, Christian Schwager, Martin Zeier, Peter E Huber, Francesco Addabbo, Michael S Goligorsky, Lynn Hlatky, Bertrand L Jaber, Amir Abdollahi
BACKGROUND: Cardiac surgery with cardiopulmonary bypass (CS/CPB) is associated with increased risk for postoperative complications causing substantial morbidity and mortality. To identify the molecular mechanisms underlying CS/CPB-induced pathophysiology we employed an integrative systems biology approach using the whole blood transcriptome as the sentinel organ. METHODOLOGY/PRINCIPAL FINDINGS: Total RNA was isolated and globin mRNA depleted from whole blood samples prospectively collected from 10 patients at time points prior (0), 2 and 24 hours following CS/CPB...
2010: PloS One
https://read.qxmd.com/read/20818427/regulation-of-c-ebpbeta1-by-ras-in-mammary-epithelial-cells-and-the-role-of-c-ebpbeta1-in-oncogene-induced-senescence
#23
JOURNAL ARTICLE
A A Atwood, L Sealy
Overexpression of Ras(V12) in MCF10A cells, an immortalized mammary epithelial cell line, leads to transformation of these cells. We demonstrate that this is accompanied by degradation of C/EBPbeta1. C/EBPbeta is a transcription factor in which three protein isoforms exist because of alternative translation at three in-frame methionines. When C/EBPbeta1 is expressed in MCF10A-Ras(V12) cells, immunoblot analysis reveals that C/EBPbeta1 is degraded in these cells. Treatment of MCF10A-Ras(V12)-C/EBPbeta1 cells with the cdk inhibitor roscovitine leads to stabilization of C/EBPbeta1...
November 11, 2010: Oncogene
https://read.qxmd.com/read/20699097/the-c-ebpbeta-isoform-liver-inhibitory-protein-lip-induces-autophagy-in-breast-cancer-cell-lines
#24
JOURNAL ARTICLE
Maria M Abreu, Linda Sealy
Autophagy is a process involving the bulk degradation of cellular components in the cytoplasm via the lysosomal degradation pathway. Autophagy manifests a protective role in stressful conditions such as nutrient or growth factor depletion; however, extensive degradation of regulatory molecules or organelles essential for survival can lead to the demise of the cell, or autophagy-mediated cell death. The role of autophagy in cancer is complex with roles in both tumor suppression and tumor promotion proposed. Here we report that an isoform of the C/EBPbeta transcription factor, liver-enriched inhibitory protein (LIP), induces cell death in human breast cancer cells and stimulates autophagy...
November 15, 2010: Experimental Cell Research
https://read.qxmd.com/read/20637321/c-ebp-beta-drives-expression-of-the-nutritionally-regulated-promoter-ia-of-the-acetyl-coa-carboxylase-alpha-gene-in-cattle
#25
JOURNAL ARTICLE
Xuanming Shi, Shuzhen Liu, Cornelia C Metges, Hans-Martin Seyfert
Acetyl-CoA carboxylase-alpha (ACC-alpha) is the rate-limiting enzyme for de novo fatty acid synthesis. Among the four promoters expressing the bovine gene, promoter IA (PIA) is dominantly active and nutritionally regulated in lipogenic tissues. CCAAT/enhancer binding proteins are crucially involved in regulating the activity of this promoter. We examine here, which member of this family of transcription factors is most important for promoter activation. To differentiate the individual contribution of different members of the C/EBP family transcription factors controlling the ACC-alpha gene expression in cattle, we established vectors expressing full length (FL) or N-terminally truncated (DeltaN) variants of the C/EBP factors (alpha, -beta, -delta, and -epsilon) in mammalian cells...
August 2010: Biochimica et Biophysica Acta
https://read.qxmd.com/read/20627112/s-resistin-inhibits-adipocyte-differentiation-and-increases-tnfalpha-expression-and-secretion-in-3t3-l1-cells
#26
JOURNAL ARTICLE
Carmen M Fernández, Araceli del Arco, Nilda Gallardo, Lidia Aguado, María Rodriguez, Manuel Ros, Jose M Carrascosa, Antonio Andrés, Carmen Arribas
S-resistin is a non-secretable resistin spliced variant described in white adipose tissue from Wistar rats. Since resistin has been implicated in adipogenesis regulation, here we have investigated the possible role of this new isoform in this process. For that, we have studied the adipocyte development in 3T3-L1 pre-adipocyte cell line stably expressing s-resistin and resistin. Both isoforms are able to restrain 3T3-L1 pre-adipocyte differentiation though affecting differently the expression pattern of pro-adipogenic transcription factors such CCAAT/enhancer binding proteins alpha and beta (C/EBPalpha and C/EBPbeta) and peroxisome proliferator-activated receptor gamma (PPARgamma), as well of proteins implicated in lipid metabolism such perilipin, fatty acid synthase (FAS), adipocyte lipid binding protein (ALBP/aP2) and carnitine palmitoyltransferase1 (CPT1)...
October 2010: Biochimica et Biophysica Acta
https://read.qxmd.com/read/20605485/tumor-induced-tolerance-and-immune-suppression-depend-on-the-c-ebpbeta-transcription-factor
#27
JOURNAL ARTICLE
Ilaria Marigo, Erika Bosio, Samantha Solito, Circe Mesa, Audry Fernandez, Luigi Dolcetti, Stefano Ugel, Nada Sonda, Silvio Bicciato, Erika Falisi, Fiorella Calabrese, Giuseppe Basso, Paola Zanovello, Emanuele Cozzi, Susanna Mandruzzato, Vincenzo Bronte
Tumor growth is associated with a profound alteration in myelopoiesis, leading to recruitment of immunosuppressive cells known as myeloid-derived suppressor cells (MDSCs). We showed that among factors produced by various experimental tumors, the cytokines GM-CSF, G-CSF, and IL-6 allowed a rapid generation of MDSCs from precursors present in mouse and human bone marrow (BM). BM-MDSCs induced by GM-CSF+IL-6 possessed the highest tolerogenic activity, as revealed by the ability to impair the priming of CD8(+) T cells and allow long term acceptance of pancreatic islet allografts...
June 25, 2010: Immunity
https://read.qxmd.com/read/20583135/decreased-expression-of-insulin-like-growth-factor-binding-protein-5-during-n-4-hydroxyphenyl-retinamide-induced-neuronal-differentiation-of-arpe-19-human-retinal-pigment-epithelial-cells-regulation-by-ccaat-enhancer-binding-protein
#28
JOURNAL ARTICLE
William Samuel, R Krishnan Kutty, Camasamudram Vijayasarathy, Iranzu Pascual, Todd Duncan, T Michael Redmond
Insulin-like growth factor (IGF)-binding protein-5 (IGFBP5), an important member of the IGF axis involved in regulating cell growth and differentiation, acts by modulating IGF signaling and also by IGF-independent mechanisms. We identified IGFBP5 by microarray analysis as a gene differentially regulated during N-(4-hydroxyphenyl)retinamide (4HPR)-induced neuronal differentiation of human retinal pigment epithelial (RPE) cells. IGFBP5 is expressed in human RPE cells, and its expression, mRNA as well as protein, is greatly decreased during the 4HPR-induced neuronal differentiation...
September 2010: Journal of Cellular Physiology
https://read.qxmd.com/read/20567236/selective-deletion-of-adipocytes-but-not-preadipocytes-by-tnf-alpha-through-c-ebp-and-ppargamma-mediated-suppression-of-nf-kappab
#29
JOURNAL ARTICLE
Minori Tamai, Tsuyoshi Shimada, Nobuhiko Hiramatsu, Kunihiro Hayakawa, Maro Okamura, Yasuhiro Tagawa, Shuhei Takahashi, Shotaro Nakajima, Jian Yao, Masanori Kitamura
Tumor necrosis factor-alpha (TNF-alpha) is a key regulator of adipose tissue mass, but mechanisms underlying this effect have not been fully elucidated. We found that exposure to TNF-alpha caused a significant decrease in the number of adipocytes, but not preadipocytes. Subsequent experiments revealed that TNF-alpha selectively deleted adipocytes through induction of apoptosis. Following exposure to TNF-alpha, rapid activation of nuclear factor-kappaB (NF-kappaB) was observed only in preadipocytes, but not in adipocytes...
September 2010: Laboratory Investigation; a Journal of Technical Methods and Pathology
https://read.qxmd.com/read/20529561/identification-and-validation-of-novel-c-ebpbeta-regulated-genes-in-preadipocyte-proliferation
#30
JOURNAL ARTICLE
Mei Liu, Hai-yan Huang
BACKGROUND: CCAAT/enhancer-binding protein beta (C/EBPbeta) is required for mitotic clonal expansion (MCE) during adipogenesis. It is still unclear how C/EBPbeta regulates MCE in the earlier differentiation programs of 3T3-L1 preadipocytes. The purpose of this paper was to understand why C/EBPbeta is required for preadipocyte proliferation, and identify new target genes of C/EBPbeta with chromatin immunoprecipitation (ChIP)-on-chip. METHODS: Postconfluent growth-arrested 3T3-L1 preadipocytes were induced to differentiation using a standard differentiation protocol...
May 5, 2010: Chinese Medical Journal
https://read.qxmd.com/read/20506172/resistin-induces-expression-of-proinflammatory-cytokines-and-chemokines-in-human-articular-chondrocytes-via-transcription-and-messenger-rna-stabilization
#31
JOURNAL ARTICLE
Zhiqi Zhang, Xiaoyun Xing, Gretchen Hensley, Li-Wei Chang, Weiming Liao, Yousef Abu-Amer, Linda J Sandell
OBJECTIVE: To elucidate the effects of resistin on human articular chondrocytes and to generate a picture of their regulation at the transcriptional and posttranscriptional levels. METHODS: Human articular chondrocytes were cultured with resistin. Changes in gene expression were analyzed at various doses and times. Cells were also treated with the transcription inhibitor actinomycin D after resistin treatment or with the NF-kappaB inhibitor IKK-NBD before resistin treatment...
July 2010: Arthritis and Rheumatism
https://read.qxmd.com/read/20501671/the-ccaat-enhancer-binding-protein-beta-is-a-critical-regulator-of-steroid-induced-mitotic-expansion-of-uterine-stromal-cells-during-decidualization
#32
JOURNAL ARTICLE
Wei Wang, Quanxi Li, Indrani C Bagchi, Milan K Bagchi
During early pregnancy, the concerted actions of the maternal steroid hormones, estrogen and progesterone, promote a unique process known as decidualization, which involves extensive proliferation and differentiation of uterine stromal cells. The molecular pathways underlying this hormonally induced cellular transformation, an essential prerequisite for embryo implantation, remain poorly understood. We previously identified CCAAT/enhancer binding protein beta (C/EBPbeta) as a target of steroid regulation in the uterus...
August 2010: Endocrinology
https://read.qxmd.com/read/20498378/calmodulin-controls-liver-proliferation-via-interactions-with-c-ebpbeta-lap-and-c-ebpbeta-lip
#33
JOURNAL ARTICLE
Daniel Orellana, Xiaoying Liu, Gou-Li Wang, Jingling Jin, Polina Iakova, Nikolai A Timchenko
A truncated isoform of C/EBPbeta, C/EBPbeta-LIP, is required for liver proliferation. This isoform is expressed at high levels in proliferating liver and in liver tumors. However, high levels of C/EBPbeta-LIP are also observed in non-proliferating livers during acute phase response (APR). In this paper we present mechanisms by which liver regulates activities of C/EBPbeta-LIP. We found that calmodulin (CaM) inhibits the ability of C/EBPbeta-LIP to promote liver proliferation during APR through direct interactions...
July 23, 2010: Journal of Biological Chemistry
https://read.qxmd.com/read/20484008/roles-for-mirna-378-378-in-adipocyte-gene-expression-and-lipogenesis
#34
JOURNAL ARTICLE
Isabelle Gerin, Guido T Bommer, Colin S McCoin, Kyle M Sousa, Venkatesh Krishnan, Ormond A MacDougald
In this study, we explored the roles of microRNAs in adipocyte differentiation and metabolism. We first knocked down Argonaute2 (Ago2), a key enzyme in the processing of micro-RNAs (miRNAs), to investigate a potential role for miRNAs in adipocyte differentiation and/or metabolism. Although we did not observe dramatic differences in adipogenesis between Ago2 knock-down and control 3T3-L1 cells, incorporation of [(14)C]glucose or acetate into triacylglycerol, and steady-state levels of triacyglycerol were all reduced, suggesting a role for miRNAs in adipocyte metabolism...
August 2010: American Journal of Physiology. Endocrinology and Metabolism
https://read.qxmd.com/read/20460753/gelsolin-an-actin-regulatory-protein-is-required-for-differentiation-of-mouse-3t3-l1-cells-into-adipocytes
#35
JOURNAL ARTICLE
Atsuko Kawaji, Yuki Ohnaka, Shigehiro Osada, Makoto Nishizuka, Masayoshi Imagawa
To elucidate molecular mechanisms of adipocyte differentiation, we previously isolated TC10-like/ TC10betaLong (TCL/TC10betaL), which was transiently expressed in the early phase of adipogenesis of 3T3-L1 cells and seemed to be a positive regulator of adipogenesis. By using TCL/TC10betaL-overexpressing NIH-3T3 cells, we also isolated gelsolin as a gene whose expression was up-regulated by TCL/TC10betaL. However, the roles of gelsolin in adipocyte differentiation are unclear. In this paper we characterized the function of gelsolin in adipogenesis in 3T3-L1 cells...
2010: Biological & Pharmaceutical Bulletin
https://read.qxmd.com/read/20459638/characterization-of-adipocyte-differentiation-from-human-mesenchymal-stem-cells-in-bone-marrow
#36
JOURNAL ARTICLE
Shu-Wen Qian, Xi Li, You-You Zhang, Hai-Yan Huang, Yuan Liu, Xia Sun, Qi-Qun Tang
BACKGROUND: Adipocyte hyperplasia is associated with obesity and arises due to adipogenic differentiation of resident multipotent stem cells in the vascular stroma of adipose tissue and remote stem cells of other organs. The mechanistic characterization of adipocyte differentiation has been researched in murine pre-adipocyte models (i.e. 3T3-L1 and 3T3-F442A), revealing that growth-arrest pre-adipocytes undergo mitotic clonal expansion and that regulation of the differentiation process relies on the sequential expression of three key transcription factors (C/EBPbeta, C/EBPalpha and PPARgamma)...
2010: BMC Developmental Biology
https://read.qxmd.com/read/20452968/ccaat-enhancer-binding-protein-beta-dna-binding-is-auto-inhibited-by-multiple-elements-that-also-mediate-association-with-p300-creb-binding-protein-cbp
#37
JOURNAL ARTICLE
Sook Lee, Maria Miller, Jon D Shuman, Peter F Johnson
Signaling through Ras GTPases controls the activity of many transcription factors including CCAAT/enhancer-binding protein (C/EBPbeta), which regulates oncogenic H-Ras(V12)-induced senescence and growth arrest. Here we report that C/EBPbeta (LAP) DNA binding is inhibited by N-terminal sequences and derepressed by oncogenic Ras signaling. Sequence and mutational analyses showed that auto-repression involves two LXXLF (phiXXphiphi)-like motifs (LX1 and LX2) and a third element, auto-inhibitory domain (AID), located within conserved region CR5...
July 9, 2010: Journal of Biological Chemistry
https://read.qxmd.com/read/20446924/chip-chromatin-immunoprecipitation-analysis-demonstrates-co-ordinated-binding-of-two-transcription-factors-to-the-promoter-of-the-p53-tumour-suppressor-gene
#38
JOURNAL ARTICLE
Amanda Polson, Paula Takahashi, David Reisman
p53 is a tumour-suppressor protein that plays a role in many cellular processes, including regulation of the cell cycle, DNA repair, transcriptional regulation of genes, chromosomal segregation, cell senescence and apoptosis. The protein's role as a transcription factor has shown that deregulated transcription, whether increased or decreased, has the potential to contribute to the formation of human cancers. It was previously reported that binding of two transcription factors, C/EBPbeta and RBP-Jkappa, to a regulatory site on the p53 promoter regulates its activity, in vitro, in a cell cycle-dependent manner...
September 2010: Cell Biology International
https://read.qxmd.com/read/20444945/interaction-of-adenosine-3-5-cyclic-monophosphate-and-tumor-necrosis-factor-alpha-on-serum-amyloid-a3-expression-in-mouse-granulosa-cells-dependence-on-ccaat-enhancing-binding-protein-beta-isoform
#39
JOURNAL ARTICLE
Deok-Soo Son, Paul F Terranova, Katherine F Roby
TNFalpha is an inflammatory-related cytokine that has inhibitory effects on gonadotropin- and cAMP-stimulated steroidogenesis and folliculogenesis. Because ovulation is an inflammatory reaction and TNF specifically induces serum amyloid A3 (SAA3) in mouse granulosa cells, the effect of cAMP on TNF-induced SAA3 promoter activity, mRNA and protein was investigated. Granulosa cells from immature mice were cultured with TNF and/or cAMP. TNF increased SAA3 promoter activity, mRNA, and protein, which were further increased by cAMP...
July 2010: Endocrinology
https://read.qxmd.com/read/20385540/ici-182-780-induces-p-cadherin-overexpression-in-breast-cancer-cells-through-chromatin-remodelling-at-the-promoter-level-a-role-for-c-ebpbeta-in-cdh3-gene-activation
#40
JOURNAL ARTICLE
André Albergaria, Ana Sofia Ribeiro, Sandra Pinho, Fernanda Milanezi, Vítor Carneiro, Bárbara Sousa, Sónia Sousa, Carla Oliveira, José Carlos Machado, Raquel Seruca, Joana Paredes, Fernando Schmitt
CDH3/P-cadherin is a classical cadherin. Overexpression of which has been associated with proliferative lesions of high histological grade, decreased cell polarity and poor survival of patients with breast cancer. In vitro studies showed that it can be up-regulated by ICI 182,780, suggesting that the lack of ERalpha signalling is responsible for the aberrant P-cadherin overexpression and for its role in inducing breast cancer cell invasion and migration. However, the mechanism by which ER-signalling inhibition leads to P-cadherin expression is still unknown...
July 1, 2010: Human Molecular Genetics
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