Sun, 27 Jul 2008 08:07:14 BST CiteULike: heliopais's Yu http://www.citeulike.org/user/heliopais/author/Yu CiteULike.org en-gb Copyright © 2004-2008 citeulike.org http://www.citeulike.org/user/heliopais/article/2718410 <i>Developmental Cell, Vol. 6, No. 3. (March 2004), pp. 423-435.</i><br /><br />Runx2 is necessary and sufficient for osteoblast differentiation, yet its expression precedes the appearance of osteoblasts by 4 days. Here we show that Twist proteins transiently inhibit Runx2 function during skeletogenesis. Twist-1 and -2 are expressed in Runx2-expressing cells throughout the skeleton early during development, and osteoblast-specific gene expression occurs only after their expression decreases. Double heterozygotes for Twist-1 and Runx2 deletion have none of the skull abnormalities observed in Runx2+/- mice, a Twist-2 null background rescues the clavicle phenotype of Runx2+/- mice, and Twist-1 or -2 deficiency leads to premature osteoblast differentiation. Furthermore, Twist-1 overexpression inhibits osteoblast differentiation without affecting Runx2 expression. Twist proteins' antiosteogenic function is mediated by a novel domain, the Twist box, which interacts with the Runx2 DNA binding domain to inhibit its function. In vivo mutagenesis confirms the antiosteogenic function of the Twist box. Thus, relief of inhibition by Twist proteins is a mandatory event precluding osteoblast differentiation. A Twist Code Determines the Onset of Osteoblast Differentiation Peter Bialek Britt Kern Xiangli Yang Marijke Schrock Drazen Sosic Nancy Hong Hua Wu Kai Yu David Ornitz Eric Olson Monica Justice Gerard Karsenty doi:10.1016/S1534-5807(04)00058-9 Developmental Cell, Vol. 6, No. 3. (March 2004), pp. 423-435. 2008-04-25T13:17:16-00:00 2004 Developmental Cell 6 3 423 435 runx2 http://www.citeulike.org/user/heliopais/article/2425902 <i>Bone, Vol. 36, No. 5. (May 2005), pp. 840-853.</i><br /><br />Osteoclasts (Oc) derive from hematopoietic precursors present in the circulation and bone marrow, and they differentiate into multinucleated bone-resorbing cells in response to the dual essential signals receptor activator of NF-[kappa]B ligand (RANKL) and macrophage-colony stimulating factor (M-CSF) primarily provided by bone marrow stromal cells (BMSC) and osteoblasts (Ob). However, little is known about signals that direct Oc precursors from the circulation into bone or control their migration within the marrow. Stromal cell-derived factor-1 (SDF-1 or CXCL12) is a chemokine highly expressed by bone endothelium, BMSC, and immature Ob that is essential for the normal homing, early development, and survival of various hematopoietic progenitor cells. We investigated whether SDF-1 and its unique chemokine receptor CXCR4 were involved in regulating human Oc precursor chemotaxis, development, function, or survival. CXCR4 was highly expressed by freshly isolated human monocyte (MN) populations, in vitro generated Oc and Oc-like cells, and mature Oc isolated from human femoral bones. SDF-1 markedly stimulated the chemotactic recruitment of circulating human MN capable of generating bone-resorptive Oc, leading to a 4-fold increase in Oc formation and greater bone pit resorption after their M-CSF + RANKL induced differentiation compared to spontaneously migrating cells. SDF-1 also directly promoted early (but not later) stages of Oc development via stimulating precursor cell numbers, multinucleated cell fusion, increased cell size, and tartrate-resistant acid phosphatase (TRAP) activity in a similar, but non-additive, fashion to M-CSF + RANKL. While SDF-1 did not cause full development of bone-resorbing Oc or stimulate the resorptive function of mature Oc directly, it also did not interfere with any actions promoted by M-CSF + RANKL. In mature human Oc, SDF-1 proved equally as effective as M-CSF + RANKL for preventing Oc apoptosis induced by cytokine withdrawal. In both cases, Oc survival was accompanied by analogous rises in the mRNA ratios for anti-apoptotic Bcl-xL and Bfl-1 relative to pro-apoptotic Bax, and by marked protein suppression of the critical pro-apoptotic signal Bim. These findings demonstrate for the first time that SDF-1 chemoattracts circulating human Oc precursors capable of developing into bone-resorptive Oc, and that it can stimulate MN cell fusion and TRAP activity, mimic M-CSF + RANKL in early osteoclastogenic effects, substitute for M-CSF + RANKL in maintaining the survival of mature human Oc, and suppress Oc expression of Bim protein. Thus, high levels of SDF-1 produced by bone endothelium, BMSC, and Ob may selectively target circulating Oc precursors into bone and stimulate their marrow migration into suitable perivascular stromal sites for their early development, RANKL differentiation, and survival. Consequently, SDF-1 may be a key factor linking bone vascular cells, BMSC, Ob, and Oc in the normal homeostatic regulation of bone development and remodeling. Stromal cell-derived factor-1 binding to its chemokine receptor CXCR4 on precursor cells promotes the chemotactic recruitment, development and survival of human osteoclasts Lorinda Wright William Maloney Xuefeng Yu Libby Kindle Patricia Collin-Osdoby Philip Osdoby doi:10.1016/j.bone.2005.01.021 Bone, Vol. 36, No. 5. (May 2005), pp. 840-853. 2008-02-25T15:58:21-00:00 2005 Bone 36 5 840 853 cxcl12 http://www.citeulike.org/user/heliopais/article/1701800 <i>Genomics Proteomics Bioinformatics, Vol. 5, No. 2. (May 2007), pp. 131-142.</i><br /><br />In the post-genomic era, identification of specific regulatory motifs or transcription factor binding sites (TFBSs) in non-coding DNA sequences, which is essential to elucidate transcriptional regulatory networks, has emerged as an obstacle that frustrates many researchers. Consequently, numerous motif discovery tools and correlated databases have been applied to solving this problem. However, these existing methods, based on different computational algorithms, show diverse motif prediction efficiency in non-coding DNA sequences. Therefore, understanding the similarities and differences of computational algorithms and enriching the motif discovery literatures are important for users to choose the most appropriate one among the online available tools. Moreover, there still lacks credible criterion to assess motif discovery tools and instructions for researchers to choose the best according to their own projects. Thus integration of the related resources might be a good approach to improve accuracy of the application. Recent studies integrate regulatory motif discovery tools with experimental methods to offer a complementary approach for researchers, and also provide a much-needed model for current researches on transcriptional regulatory networks. Here we present a comparative analysis of regulatory motif discovery tools for TFBSs. Comparative analysis of regulatory motif discovery tools for transcription factor binding sites. W Wei XD Yu doi:10.1016/S1672-0229(07)60023-0 Genomics Proteomics Bioinformatics, Vol. 5, No. 2. (May 2007), pp. 131-142. 2007-09-27T14:55:57-00:00 2007 Genomics Proteomics Bioinformatics 1672-0229 5 2 131 142 binding_site_prediction transcription_factor http://www.citeulike.org/user/heliopais/article/498727 <i>Cell Metab, Vol. 3, No. 2. (February 2006), pp. 87-98.</i><br /><br />Current understanding of microRNA (miRNA) biology is limited, and antisense oligonucleotide (ASO) inhibition of miRNAs is a powerful technique for their functionalization. To uncover the role of the liver-specific miR-122 in the adult liver, we inhibited it in mice with a 2'-O-methoxyethyl phosphorothioate ASO. miR-122 inhibition in normal mice resulted in reduced plasma cholesterol levels, increased hepatic fatty-acid oxidation, and a decrease in hepatic fatty-acid and cholesterol synthesis rates. Activation of the central metabolic sensor AMPK was also increased. miR-122 inhibition in a diet-induced obesity mouse model resulted in decreased plasma cholesterol levels and a significant improvement in liver steatosis, accompanied by reductions in several lipogenic genes. These results implicate miR-122 as a key regulator of cholesterol and fatty-acid metabolism in the adult liver and suggest that miR-122 may be an attractive therapeutic target for metabolic disease. miR-122 regulation of lipid metabolism revealed by in vivo antisense targeting. C Esau S Davis SF Murray XX Yu SK Pandey M Pear L Watts SL Booten M Graham R McKay A Subramaniam S Propp BA Lollo S Freier CF Bennett S Bhanot BP Monia doi:10.1016/j.cmet.2006.01.005 Cell Metab, Vol. 3, No. 2. (February 2006), pp. 87-98. 2006-02-08T11:00:11-00:00 2006 Cell Metab 1550-4131 3 2 87 98 antimicrorna microrna microrna_microarray http://www.citeulike.org/user/heliopais/article/2105952 <i>Nature Genetics, Vol. 40, No. 1. (9 December 2007), pp. 43-50.</i><br /><br />The c-Myc oncogenic transcription factor (Myc) is pathologically activated in many human malignancies. Myc is known to directly upregulate a pro-tumorigenic group of microRNAs (miRNAs) known as the miR-17-92 cluster. Through the analysis of human and mouse models of B cell lymphoma, we show here that Myc regulates a much broader set of miRNAs than previously anticipated. Unexpectedly, the predominant consequence of activation of Myc is widespread repression of miRNA expression. Chromatin immunoprecipitation reveals that much of this repression is likely to be a direct result of Myc binding to miRNA promoters. We further show that enforced expression of repressed miRNAs diminishes the tumorigenic potential of lymphoma cells. These results demonstrate that extensive reprogramming of the miRNA transcriptome by Myc contributes to tumorigenesis. Widespread microRNA repression by Myc contributes to tumorigenesis. Tsung-Cheng Chang Duonan Yu Yun-Sil Lee Erik Wentzel Dan Arking Kristin West Chi Dang Andrei Thomas-Tikhonenko Joshua Mendell doi:10.1038/ng.2007.30 Nature Genetics, Vol. 40, No. 1. (9 December 2007), pp. 43-50. 2007-12-13T17:58:50-00:00 2007 Nature Genetics 1546-1718 40 1 43 50 cancer microrna myc http://www.citeulike.org/user/heliopais/article/1283686 <i>Trends in Genetics, Vol. 23, No. 8. (3 May 2007), pp. 372-375.</i><br /><br />MicroRNAs (miRNAs) modulate expression of their target genes in various tissues and at different developmental stages, but it is unclear whether they drive cross-species variation in gene expression. By comparing data from mammal and fly species we found that the cross-species expression variation of miRNA targets is significantly lower than that of other genes. This implies that miRNAs can affect gene expression by reducing stochastic noise, buffering cross-species variation and constraining evolutionary gene expression variation. MicroRNA regulation and interspecific variation of gene expression. Qinghua Cui Zhenbao Yu Enrico Purisima Edwin Wang doi:10.1016/j.tig.2007.04.003 Trends in Genetics, Vol. 23, No. 8. (3 May 2007), pp. 372-375. 2007-05-08T13:41:17-00:00 2007 Trends in Genetics 0168-9525 23 8 372 375 Elsevier microrna http://www.citeulike.org/user/heliopais/article/1071095 <i>Nucleic Acids Research, Vol. 35, No. 1. (January 2007), pp. 152-164.</i> Global analysis of microRNA target gene expression reveals that miRNA targets are lower expressed in mature mouse and Drosophila tissues than in the embryos Yu Zhenbao Jian Zhaofeng Shen Shi-Hsiang Purisima Enrico Wang Edwin doi:10.1093/nar/gkl1032 Nucleic Acids Research, Vol. 35, No. 1. (January 2007), pp. 152-164. 2007-01-27T15:10:30-00:00 2007 Nucleic Acids Research 0305-1048 35 1 152 164 Oxford University Press microrna http://www.citeulike.org/user/heliopais/article/63188 <i>Bioinformatics, Vol. 20, No. 18., 3594.</i> Advances to Bayesian network inference for generating causal networks from observational biological data Jing Yu Anne Smith Paul Wang Alexander Hartemink doi:10.1093/bioinformatics/bth448 Bioinformatics, Vol. 20, No. 18., 3594. 2004-12-28T18:22:26-00:00 Bioinformatics 1367-4803 20 18 3594 Oxford University Press genetic_regulatory_network http://www.citeulike.org/user/heliopais/article/976207 <i>Biochem Biophys Res Commun (27 November 2006)</i><br /><br />Over the past few years, microRNAs (miRNAs) have emerged as a new prominent class of gene regulatory factors that negatively regulate expression of approximately one-third of the genes in animal genomes at post-transcriptional level. However, it is still unclear why some genes are regulated by miRNAs but others are not, i.e. what principles govern miRNA regulation in animal genomes. In this study, we systematically analyzed the relationship between transcription factors (TFs) and miRNAs in gene regulation. We found that the genes with more TF-binding sites have a higher probability of being targeted by miRNAs and have more miRNA-binding sites on average. This observation reveals that the genes with higher cis-regulation complexity are more coordinately regulated by TFs at the transcriptional level and by miRNAs at the post-transcriptional level. This is a potentially novel discovery of mechanism for coordinated regulation of gene expression. Gene ontology analysis further demonstrated that such coordinated regulation is more popular in the developmental genes. MicroRNAs preferentially target the genes with high transcriptional regulation complexity. Qinghua Cui Zhenbao Yu Youlian Pan Enrico O Purisima Edwin Wang doi:10.1016/j.bbrc.2006.11.080 Biochem Biophys Res Commun (27 November 2006) 2006-12-06T12:21:27-00:00 2006 Biochem Biophys Res Commun 0006-291X microrna http://www.citeulike.org/user/heliopais/article/1380942 <i>BMC Bioinformatics, Vol. 8 (11 June 2007), 194.</i> Transcript-level annotation of Affymetrix probesets improves the interpretation of gene expression data Hui Yu Feng Wang Kang Tu Lu Xie Yuan-Yuan Li Yi-Xue Li doi:10.1186/1471-2105-8-194 BMC Bioinformatics, Vol. 8 (11 June 2007), 194. 2007-06-12T09:43:05-00:00 2007 BMC Bioinformatics 1471-2105 8 194 microarray probesets