Research Topics
| A MoustakasSummaryAffiliation: Ludwig Institute for Cancer Research Country: Sweden Publications
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Detail Information
Publications
Mechanisms of TGF-beta signaling in regulation of cell growth and differentiationAristidis Moustakas
Ludwig Institute for Cancer Research, Uppsala, Sweden
Immunol Lett 82:85-91. 2002....
TGF-beta and the Smad signaling pathway support transcriptomic reprogramming during epithelial-mesenchymal cell transitionUlrich Valcourt
Ludwig Institute for Cancer Research, Uppsala, Sweden
Mol Biol Cell 16:1987-2002. 2005....
Induction of epithelial-mesenchymal transition by transforming growth factor βAristidis Moustakas
Ludwig Institute for Cancer Research, Science for Life Laboratory, Uppsala University, SE 751 24 Uppsala, Sweden
Semin Cancer Biol 22:446-54. 2012....- Emergence, development and diversification of the TGF-beta signalling pathway within the animal kingdomLukasz Huminiecki
Ludwig Institute for Cancer Research, Uppsala University, Uppsala, Sweden
BMC Evol Biol 9:28. 2009..Herein, we focus on the diversification of the transforming growth factor-beta (TGF-beta) pathway -- one of the fundamental and versatile metazoan signal transduction engines... 
Cloning of a novel signaling molecule, AMSH-2, that potentiates transforming growth factor beta signalingNieves Ibarrola
McKusick Nathans Institute of Genetic Medicine and Department of Biological Chemistry, Johns Hopkins University, Baltimore, MD 21205, USA
BMC Cell Biol 5:2. 2004..Signaling by these factors is mediated chiefly by the Smad family of latent transcription factors...- Ecsit-ement on the crossroads of Toll and BMP signal transductionAristidis Moustakas
Ludwig Institute for Cancer Research, SE-751 24 Uppsala, Sweden
Genes Dev 17:2855-9. 2003 - Dynamic control of TGF-beta signaling and its links to the cytoskeletonAristidis Moustakas
Ludwig Institute for Cancer Research, Uppsala University, P O Box 595, Biomedical Center, SE 751 24 Uppsala, Sweden
FEBS Lett 582:2051-65. 2008..We discuss mechanisms and models that aim at explaining the coordination between several components of the signaling network downstream of the TGF-beta signal... - Non-Smad TGF-beta signalsAristidis Moustakas
Ludwig Institute for Cancer Research, Biomedical Center, Uppsala University, Box 595, SE 751 24 Uppsala, Sweden
J Cell Sci 118:3573-84. 2005.... - TGF-beta targets PAX3 to control melanocyte differentiationAristidis Moustakas
Ludwig Institute for Cancer Research, Uppsala University, Box 595 Biomedical Center, Uppsala, Sweden
Dev Cell 15:797-9. 2008..In the presence of UV radiation, a Jnk/AP-1 pathway represses TGF-beta, which together with a UV-induced p53 pathway promotes melanocyte differentiation... - The regulation of TGFbeta signal transductionAristidis Moustakas
Ludwig Institute for Cancer Research, Uppsala University, Uppsala, Sweden
Development 136:3699-714. 2009..Signaling is modulated by negative-feedback regulation via inhibitory Smads. We review here the mechanisms of TGFbeta signal transduction in metazoans and emphasize events crucial for embryonic development... - From mono- to oligo-Smads: the heart of the matter in TGF-beta signal transductionAristidis Moustakas
Ludwig Institute for Cancer Research, SE-751 24 Uppsala, Sweden
Genes Dev 16:1867-71. 2002 - Transforming growth factor-beta induces nuclear import of Smad3 in an importin-beta1 and Ran-dependent mannerA Kurisaki
Ludwig Institute for Cancer Research, SE 751 24 Uppsala, Sweden
Mol Biol Cell 12:1079-91. 2001..The import mechanism of Smad3 shows distinct features from that of the related Smad2 and the structural basis for this difference maps to the divergent sequences of their N-terminal domains... - Smad signalling networkAristidis Moustakas
Ludwig Institute for Cancer Research, Box 595, Biomedical Center, Husargatan 3, SE-751 24 Uppsala, Sweden
J Cell Sci 115:3355-6. 2002 - Smad regulation in TGF-beta signal transductionA Moustakas
Ludwig Institute for Cancer Research, Box 595, SE 751 24 Uppsala, Sweden
J Cell Sci 114:4359-69. 2001..Finally, the inhibitory Smads (I-Smads) block phosphorylation of R-Smads by the receptors and promote ubiquitination and degradation of receptor complexes, thus inhibiting signalling... - Functional consequences of tumorigenic missense mutations in the amino-terminal domain of Smad4A Moren
Ludwig Institute for Cancer Research, Box 595, S 751 24 Uppsala, Sweden
Oncogene 19:4396-404. 2000..In conclusion, mutations in the amino-terminal domain of Smad4, that are found in cancer, show loss of multiple functional properties which may contribute to tumorigenesis... - TGF-(beta) type I receptor/ALK-5 and Smad proteins mediate epithelial to mesenchymal transdifferentiation in NMuMG breast epithelial cellsE Piek
Ludwig Institute for Cancer Research, Box 595, S 75124 Uppsala, Sweden
J Cell Sci 112:4557-68. 1999..Activin A does not induce mesenchymal transformation, presumably because the number of activin receptors is limited, while BMP-7-initiated signalling cannot mediate transdifferentiation... - Id2 and Id3 define the potency of cell proliferation and differentiation responses to transforming growth factor beta and bone morphogenetic proteinMarcin Kowanetz
Ludwig Institute for Cancer Research, SE-751 24 Uppsala, Sweden
Mol Cell Biol 24:4241-54. 2004..Thus, Id genes sense Smad signals and create a permissive or refractory nuclear environment that defines decisions of cell fate and proliferation... - Smad pathway-specific transcriptional regulation of the cell cycle inhibitor p21(WAF1/Cip1)Katerina Pardali
Ludwig Institute for Cancer Research, Uppsala, Sweden
J Cell Physiol 204:260-72. 2005..Thus, p21 is a common target of all TGF-beta superfamily pathways. However, the ability of TGF-beta superfamily members to induce cell growth arrest depends on the regulation of additional gene targets... - Differential ubiquitination defines the functional status of the tumor suppressor Smad4Anita Morén
Ludwig Institute for Cancer Research, Box 595, Biomedical Center, SE 751 24 Uppsala, Sweden
J Biol Chem 278:33571-82. 2003..These data suggest that oligo-ubiquitination positively regulates Smad4 function, whereas poly-ubiquitination primarily occurs in unstable cancer mutants and leads to protein degradation... - Nuclear factor YY1 inhibits transforming growth factor beta- and bone morphogenetic protein-induced cell differentiationKeiko Kurisaki
Ludwig Institute for Cancer Research, Biomedical Center, SE 751 24 Uppsala, Sweden
Mol Cell Biol 23:4494-510. 2003..In conclusion, YY1 represses Smad transcriptional activities in a gene-specific manner and thus regulates cell differentiation induced by TGF-beta superfamily pathways... - Role of Smad proteins and transcription factor Sp1 in p21(Waf1/Cip1) regulation by transforming growth factor-betaK Pardali
Ludwig Institute for Cancer Research, Box 595, SE 751 24 Uppsala, Sweden
J Biol Chem 275:29244-56. 2000..In conclusion, Smad proteins play important roles in regulation of the p21 gene by TGF-beta, and the functional cooperation of Smad proteins with Sp1 involves the physical interaction of these two types of transcription factors... - HMGA2 and Smads co-regulate SNAIL1 expression during induction of epithelial-to-mesenchymal transitionSylvie Thuault
Ludwig Institute for Cancer Research, Box 595 Biomedical Center, Uppsala University, SE 751 24 Uppsala, Sweden
J Biol Chem 283:33437-46. 2008..The data propose that HMGA2 acts in a gene-specific manner to orchestrate the transcriptional network necessary for the EMT program... - Actions of TGF-beta as tumor suppressor and pro-metastatic factor in human cancerKaterina Pardali
Ludwig Institute for Cancer Research, Box 595 Biomedical Center, Uppsala University, SE 751 24 Uppsala, Sweden
Biochim Biophys Acta 1775:21-62. 2007..In conclusion, TGF-beta signaling is intimately implicated in tumor development and contributes to all cardinal features of tumor cell biology... - Sustained TGF beta exposure suppresses Smad and non-Smad signalling in mammary epithelial cells, leading to EMT and inhibition of growth arrest and apoptosisA Gal
Ludwig Institute for Cancer Research, Uppsala, Sweden
Oncogene 27:1218-30. 2008..Thus, TGFbeta may modulate its own signalling to facilitate switching from tumour suppression to tumour progression... - TGFbeta induces SIK to negatively regulate type I receptor kinase signalingMarcin Kowanetz
Ludwig Institute for Cancer Research, Uppsala University, Box 595 Biomedical Center, Uppsala, Sweden
J Cell Biol 182:655-62. 2008..Loss of endogenous SIK results in enhanced gene responses of the fibrotic and cytostatic programs of TGFbeta. We thus identify in SIK a negative regulator that controls TGFbeta receptor turnover and physiological signaling... - Mechanism of TGF-beta signaling to growth arrest, apoptosis, and epithelial-mesenchymal transitionCarl Henrik Heldin
Ludwig Institute for Cancer Research, Uppsala University, BMC, Uppsala, Sweden
Curr Opin Cell Biol 21:166-76. 2009..The aim of this review is to summarize some of the recent findings on the mechanism of TGF-beta signaling to growth arrest, apoptosis, and epithelial-mesenchymal transition... - Transforming growth factor-beta employs HMGA2 to elicit epithelial-mesenchymal transitionSylvie Thuault
Ludwig Institute for Cancer Research, Uppsala University, SE 751 24 Uppsala, Sweden, and Institut National de la Sante et de la Recherche Medicale, Hopital E Herriot, Lyon Cedex, France
J Cell Biol 174:175-83. 2006..This network of signaling/transcription factors that work sequentially to establish EMT suggests that combinatorial detection of these proteins could serve as a new tool for EMT analysis in cancer patients... - TGFbeta activates mitogen- and stress-activated protein kinase-1 (MSK1) to attenuate cell deathLars P van der Heide
Department of Molecular Cell Biology, and Centre for Biomedical Genetics, Leiden University Medical Center, Postbus 9600, 2300 RC Leiden, The Netherlands
J Biol Chem 286:5003-11. 2011..Monitoring the status of MSK1 activity in cancer promises new therapeutic targets as inactivating both MSK1 and EGF signaling may (re)-sensitize cells to TGFβ-induced cell death... - TGF-beta signaling from a three-dimensional perspective: insight into selection of partnersSerhiy Souchelnytskyi
Ludwig Institute for Cancer Research, Box 595, Husargatan 3, SE 751 24, Uppsala, Sweden
Trends Cell Biol 12:304-7. 2002.... - Degradation of the tumor suppressor Smad4 by WW and HECT domain ubiquitin ligasesAnita Morén
Ludwig Institute for Cancer Research, Box 595, Biomedical Center, Uppsala University, SE 751 24 Uppsala, Sweden
J Biol Chem 280:22115-23. 2005..Such mechanisms of down-regulation of TGF-beta signaling may be critical for proper physiological response to this pathway... - The mechanism of nuclear export of Smad3 involves exportin 4 and RanAkira Kurisaki
Ludwig Institute for Cancer Research, Box 595 Biomedical Center, SE 751 24 Uppsala, Sweden
Mol Cell Biol 26:1318-32. 2006..A short peptide representing the minimal interaction domain in Smad3 effectively competes with Smad3 association to exportin 4 and blocks nuclear export of Smad3 in vivo. We thus delineate a novel nuclear export pathway for Smad3... - Signaling networks guiding epithelial-mesenchymal transitions during embryogenesis and cancer progressionAristidis Moustakas
Ludwig Institute for Cancer Research, Uppsala University, Box 595 Biomedical Center, SE 751 24 Uppsala, Sweden
Cancer Sci 98:1512-20. 2007..Here we present some of the current mechanisms that mediate the process of EMT and discuss their relevance to cancer progression... - Notch signaling is necessary for epithelial growth arrest by TGF-betaHideki Niimi
Ludwig Institute for Cancer Research, Biomedical Center, Uppsala University, SE 751 24 Uppsala, Sweden
J Cell Biol 176:695-707. 2007..We establish an intimate involvement of Notch signaling in the epithelial cytostatic response to TGF-beta... - A SNAIL1-SMAD3/4 transcriptional repressor complex promotes TGF-beta mediated epithelial-mesenchymal transitionTheresa Vincent
Ludwig Institute for Cancer Research, Stockholm Branch, 17177 Stockholm, Sweden
Nat Cell Biol 11:943-50. 2009..We propose that activation of a SNAIL1-SMAD3/4 transcriptional complex represents a mechanism of gene repression during EMT... - Immortalized keratinocytes derived from patients with epidermolytic ichthyosis reproduce the disease phenotype: a useful in vitro model for testing new treatmentsJ C Chamcheu
Department of Medical Sciences, Dermatology and Venereology, University Hospital, Uppsala University, SE 751 85 Uppsala, Sweden
Br J Dermatol 164:263-72. 2011..While the aetiology of EI is known, model systems are needed for pathophysiological studies and development of novel therapies... - PARP-1 attenuates Smad-mediated transcriptionPeter Lönn
Ludwig Institute for Cancer Research, Uppsala University, Box 595 Biomedical Center, SE 751 24 Uppsala, Sweden
Mol Cell 40:521-32. 2010..Thus, our results identify ADP-ribosylation of Smad proteins by PARP-1 as a key step in controlling the strength and duration of Smad-mediated transcription... - Functional role of Meox2 during the epithelial cytostatic response to TGF-betaUlrich Valcourt
Ludwig Institute for Cancer Research, Uppsala University, Box 595, Biomedical Center, SE 751 24 Uppsala, Sweden
Mol Oncol 1:55-71. 2007..Thus, Meox2 is primarily involved in the TGF-beta tumor suppressor pathway... - Regulating the stability of TGFbeta receptors and SmadsPeter Lönn
Ludwig Institute for Cancer Research, Uppsala University, Box 595, Biomedical Center, SE 751 24 Uppsala, Sweden
Cell Res 19:21-35. 2009..We highlight links between these mechanisms and human diseases, such as tissue fibrosis and cancer... - Hyaluronan fragments induce endothelial cell differentiation in a CD44- and CXCL1/GRO1-dependent mannerYoshinori Takahashi
Ludwig Institute for Cancer Research, Box 595, Biomedical Center, Uppsala University, S 751 24 Uppsala, Sweden
J Biol Chem 280:24195-204. 2005..Our data show that hyaluronan fragments and FGF-2 affect endothelial cell morphogenesis by the induction of overlapping but also by distinct sets of genes... - A new twist in Smad signalingCarl-Henrik Heldin
Ludwig Institute for Cancer Research, Uppsala University, Box 595, SE-751 24 Uppsala, Sweden
Dev Cell 10:685-6. 2006..New findings demonstrate that transcriptional intermediary factor 1gamma (TIF1gamma) also can bind to R-Smads, as an alternative to Smad4, and mediate different transcriptional effects... - Transforming growth factor beta promotes complexes between Smad proteins and the CCCTC-binding factor on the H19 imprinting control region chromatinRosita Bergstrom
Ludwig Institute for Cancer Research, Uppsala University, SE 751 24 Uppsala, Sweden
J Biol Chem 285:19727-37. 2010..Because the CTCF-Smad complex is not essential for the chromatin insulator function of the H19 ICR, we propose that it can play a role in chromatin cross-talk organized by the H19 ICR... - Mechanism of a transcriptional cross talk between transforming growth factor-beta-regulated Smad3 and Smad4 proteins and orphan nuclear receptor hepatocyte nuclear factor-4Wan Chih Chou
Department of Basic Sciences, University of Crete Medical School and Institute of Molecular Biology and Biotechnology, Foundation of Research and Technology of Hellas, Heraklion GR 71110, Greece
Mol Biol Cell 14:1279-94. 2003..Furthermore, the specificity of this interaction for certain target promoters may play an important role in various hepatocyte functions, which are regulated by TGFbeta and the Smads... - LIM-kinase 2 and cofilin phosphorylation mediate actin cytoskeleton reorganization induced by transforming growth factor-betaLina Vardouli
Department of Biochemistry, School of Medicine, University of Crete, GR 71110, Heraklion, Greece
J Biol Chem 280:11448-57. 2005..Our data define a novel pathway emanating from the TGF-beta type I receptor and leading to regulation of actin assembly, via the kinase LIMK2... - Engagement of activin and bone morphogenetic protein signaling pathway Smad proteins in the induction of inhibin B production in ovarian granulosa cellsJonas Bondestam
Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, P O Box 63 Haartmaninkatu 8, 00014, Helsinki, Finland
Mol Cell Endocrinol 195:79-88. 2002.... - Functions of transforming growth factor-beta family type I receptors and Smad proteins in the hypertrophic maturation and osteoblastic differentiation of chondrocytesUlrich Valcourt
Institut de Biologie et Chimie des Proteines, UMR 5086 CNRS Université Claude Bernard Lyon 1, 7 passage du Vercors, 69367 Lyon Cedex 07, France
J Biol Chem 277:33545-58. 2002.... - Tgf-beta3-induced palatal fusion is mediated by Alk-5/Smad pathwayMarek Dudas
Developmental Biology Program, Department of Pathology of University of Southern California, Childrens Hospital Los Angeles, Los Angeles, CA 90027, USA
Dev Biol 266:96-108. 2004..Based on these observations, we conclude that the Smad2-dependent Alk-5 signaling pathway is dominant in palatal fusion driven by Tgf-beta3... - The role of Sp1 family members, the proximal GC-rich motifs, and the upstream enhancer region in the regulation of the human cell cycle inhibitor p21WAF-1/Cip1 gene promoterGeorge Koutsodontis
Department of Basic Sciences, University of Crete Medical School and Institute of Molecular Biology and Biotechnology, Foundation of Research and Technology of Hellas, Herakleion GR 71110, Greece
Biochemistry 41:12771-84. 2002.... - Elucidation of Smad requirement in transforming growth factor-beta type I receptor-induced responsesSusumu Itoh
Division of Cellular Biochemistry, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands
J Biol Chem 278:3751-61. 2003..However, the TGF-beta-induced epithelial to mesenchymal transdifferentiation was found to require an intact L45 loop and is likely to be dependent on the Smad pathways... - PPARalpha inhibits TGF-beta-induced beta5 integrin transcription in vascular smooth muscle cells by interacting with Smad4Ulrich Kintscher
Department of Medicine, Division of Endocrinology, Diabetes and Hypertension, University of California, Los Angeles, School of Medicine, Los Angeles, Calif 90095, USA
Circ Res 91:e35-44. 2002..The full text of this article is available at http://www.circresaha.org... - The nuts and bolts of IRF structureAristidis Moustakas
Nat Struct Biol 10:874-6. 2003 - Growth differentiation factor-9 induces Smad2 activation and inhibin B production in cultured human granulosa-luteal cellsNoora Kaivo-oja
Program for Developmental and Reproductive Biology, Biomedicum Helsinki, and Department of Bacteriology, Haartman Institute, University of Helsinki, 00014 Helsinki, Finland
J Clin Endocrinol Metab 88:755-62. 2003.... - Doxorubicin requires the sequential activation of caspase-2, protein kinase Cdelta, and c-Jun NH2-terminal kinase to induce apoptosisTheocharis Panaretakis
Department of Oncology and Pathology, Cancer Centrum Karolinska, Karolinska Hospital and Institute, S-171 76 Stockholm, Sweden
Mol Biol Cell 16:3821-31. 2005..The data thus support a sequential model involving caspase-2, PKCdelta, and JNK signaling in response to doxorubicin, leading to the activation of Bak and execution of apoptosis...