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Author |
Keshet, Y.; Seger, R. |
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Title |
The MAP kinase signaling cascades: a system of hundreds of components regulates a diverse array of physiological functions |
Type |
Journal Article |
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Year |
2010 |
Publication |
Methods in Molecular Biology (Clifton, N.J.) |
Abbreviated Journal |
Methods Mol Biol |
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Volume |
661 |
Issue |
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Pages |
3-38 |
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Keywords |
Animals; Extracellular Signal-Regulated MAP Kinases/metabolism; Humans; JNK Mitogen-Activated Protein Kinases/metabolism; *MAP Kinase Signaling System; p38 Mitogen-Activated Protein Kinases/metabolism |
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Abstract |
Sequential activation of kinases within the mitogen-activated protein (MAP) kinase (MAPK) cascades is a common, and evolutionary-conserved mechanism of signal transduction. Four MAPK cascades have been identified in the last 20 years and those are usually named according to the MAPK components that are the central building blocks of each of the cascades. These are the extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-Terminal kinase (JNK), p38, and ERK5 cascades. Each of these cascades consists of a core module of three tiers of protein kinases termed MAPK, MAPKK, and MAP3K, and often two additional tiers, the upstream MAP4K and the downstream MAPKAPK, which can complete five tiers of each cascade in certain cell lines or stimulations. The transmission of the signal via each cascade is mediated by sequential phosphorylation and activation of the components in the sequential tiers. These cascades cooperate in transmitting various extracellular signals and thus control a large number of distinct and even opposing cellular processes such as proliferation, differentiation, survival, development, stress response, and apoptosis. One way by which the specificity of each cascade is regulated is through the existence of several distinct components in each tier of the different cascades. About 70 genes, which are each translated to several alternatively spliced isoforms, encode the entire MAPK system, and allow the wide array of cascade's functions. These components, their regulation, as well as their involvement together with other mechanisms in the determination of signaling specificity by the MAPK cascade is described in this review. Mis-regulation of the MAPKs signals usually leads to diseases such as cancer and diabetes; therefore, studying the mechanisms of specificity-determination may lead to better understanding of these signaling-related diseases. |
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Address |
Department of Biological Regulation, The Weizmann Institute of Science, Rehovot, Israel |
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ISSN |
1064-3745 |
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WP5 In vitro |
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Notes |
PMID:20811974 |
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CBM.UAM @ ccobaleda @ |
Serial |
66 |
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Author |
Borst, L.; Wesolowska, A.; Joshi, T.; Borup, R.; Nielsen, F.C.; Andersen, M.K.; Jonsson, O.G.; Wehner, P.S.; Wesenberg, F.; Frost, B.M.; Gupta, R.; Schmiegelow, K. |
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Title |
Genome-wide analysis of cytogenetic aberrations in ETV6/RUNX1-positive childhood acute lymphoblastic leukaemia |
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Journal Article |
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Year |
2012 |
Publication |
British Journal of Haematology |
Abbreviated Journal |
Br J Haematol |
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Abstract |
The chromosomal translocation t(12;21) resulting in the ETV6/RUNX1 fusion gene is the most frequent structural cytogenetic abnormality among patients with childhood acute lymphoblastic leukaemia (ALL). We investigated 62 ETV6/RUNX1-positive childhood ALL patients by single nucleotide polymorphism array to explore acquired copy number alterations (CNAs) at diagnosis. The mean number of CNAs was 2.82 (range 0-14). Concordance with available G-band karyotyping and comparative genomic hybridization was 93%. Based on three major protein-protein complexes disrupted by these CNAs, patients could be categorized into four distinct subgroups, defined by different underlying biological mechanisms relevant to the aetiology of childhood ALL. When recurrent CNAs were evaluated by an oncogenetic tree analysis classifying their sequential order, the most common genetic aberrations (deletions of 6q, 9p, 13q and X, and gains of 10 and 21) seemed independent of each other. Finally, we identified the most common regions with recurrent gains and losses, which comprise microRNA clusters with known oncogenic or tumour-suppressive roles. The present study sheds further light on the genetic diversity of ETV6/RUNX1-positive childhood ALL, which may be important for understanding poor responses among this otherwise highly curable subset of ALL and lead to novel targeted treatment strategies. |
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Address |
Clinic for Paediatric and Adolescent Medicine, The Juliane Marie Centre, The University Hospital Rigshospitalet, Copenhagen |
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ISSN |
0007-1048 |
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WP6 In vivo |
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PMID:22404039 |
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no |
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Call Number |
CBM.UAM @ ccobaleda @ |
Serial |
167 |
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Author |
Schmiegelow, K.; Lausten Thomsen, U.; Baruchel, A.; Pacheco, C.E.; Pieters, R.; Pombo-de-Oliveira, M.S.; Andersen, E.W.; Rostgaard, K.; Hjalgrim, H.; Pui, C.-H. |
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Title |
High concordance of subtypes of childhood acute lymphoblastic leukemia within families: lessons from sibships with multiple cases of leukemia |
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Journal Article |
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Year |
2012 |
Publication |
Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K |
Abbreviated Journal |
Leukemia |
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Volume |
26 |
Issue |
4 |
Pages |
675-681 |
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Abstract |
Polymorphic genes have been linked to the risk of acute lymphoblastic leukemia (ALL). Surrogate markers for a low burden of early childhood infections are also related to increased risk for developing childhood ALL. It remains uncertain, whether siblings of children with ALL have an increased risk of developing ALL. This international collaboration identified 54 sibships with two (N=51) or more (N=3) cases of childhood ALL (ages <18 years). The 5-year event-free survival for 61 patients diagnosed after 1 January 1990 was 0.83+/-0.05. Ages at diagnosis (Spearman correlation coefficient, r(S)=0.41, P=0.002) were significantly correlated, but not WBCs (r(S)=0.23, P=0.11). In 18 sibships with successful karyotyping in both cases, six were concordant for high-hyperdiploidy (N=3), t(12;21) [ETV6/RUNX1] (N=1), MLL rearrangement (N=1) or t(1;19)(q23/p13) (N=1). Eleven sibships were ALL-subtype concordant, being T-cell ALL (T-ALL) (N=5, of a total of six sibships, where the first-born had T-ALL) or B-lineage ALL belonging to the same cytogenetic subset (N=6), a finding that differs significantly from the expected chance distribution (kappa: 0.58; P<0.0001). These data indicate strong genetic and/or environmental risk factors for childhood ALL that are restricted to specific ALL subtypes, which must be taken into account, when performing epidemiological studies to reveal etiological factors. |
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1] Pediatric Clinics, The Juliane Marie Centre, The University Hospital Rigshospitalet, Copenhagen, Denmark [2] The Faculty of Medicine, Institute of Gynecology, Obstetrics and Pediatrics, The University of Copenhagen, Copenhagen, Denmark |
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ISSN |
0887-6924 |
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Notes |
PMID:22005784 |
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no |
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Call Number |
CBM.UAM @ ccobaleda @ |
Serial |
185 |
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Author |
Mullighan, C.G. |
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Title |
Genomic profiling of B-progenitor acute lymphoblastic leukemia |
Type |
Journal Article |
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Year |
2011 |
Publication |
Best Practice & Research. Clinical Haematology |
Abbreviated Journal |
Best Pract Res Clin Haematol |
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Volume |
24 |
Issue |
4 |
Pages |
489-503 |
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Keywords |
Animals; B-Cell-Specific Activator Protein/genetics; B-Lymphocytes/cytology/*metabolism; CREB-Binding Protein/genetics; Child; Child, Preschool; *Chromosome Aberrations; Fusion Proteins, bcr-abl/genetics; Gene Expression Profiling/*methods; Gene Expression Regulation, Neoplastic; Genomics/*methods; Humans; Ikaros Transcription Factor/genetics; Janus Kinase 1/genetics; Janus Kinase 2/genetics; Mice; *Mutation; Precursor Cell Lymphoblastic Leukemia-Lymphoma/diagnosis/*genetics/pathology; Receptors, Cytokine/genetics; Recurrence |
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Abstract |
Childhood acute lymphoblastic leukemia (ALL) is comprised of multiple subtypes defined by recurring chromosomal alterations that are important events in leukemogenesis and are widely used in diagnosis and risk stratification, yet fail to fully explain the biology of this disease. In the last 5 years, genome-wide profiling of gene expression, structural DNA alterations and sequence variations has yielded important insights into the nature of submicroscopic genetic alterations that define novel subgroups of acute lymphoblastic leukemia and cooperate with known cytogenetic alterations in leukemogenesis. Importantly, several of these alterations are important determinants of risk of relapse and are potential targets for therapeutic intervention. Here, these advances and future directions in the genomic analysis of ALL are discussed. |
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Department of Pathology, St Jude Children's Research Hospital, Memphis, TN 38105, USA. Charles.mullighan@stjude.org |
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ISSN |
1521-6926 |
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Notes |
PMID:22127311 |
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CBM.UAM @ ccobaleda @ |
Serial |
186 |
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Author |
Wu, L.Q.; Dickman, J.D. |
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Title |
Neural Correlates of a Magnetic Sense |
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Journal Article |
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Year |
2012 |
Publication |
Science (New York, N.Y.) |
Abbreviated Journal |
Science |
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Abstract |
Many animals rely on the Earth's magnetic field for spatial orientation and navigation. However, how the brain receives and interprets magnetic field information is unknown. Support for the existence of magnetic receptors in the vertebrate retina, beak, nose, and inner ear has been proposed and immediate gene expression markers have identified several brain regions activated by magnetic stimulation, but the central neural mechanisms underlying magnetoreception remain unknown. Here, we describe neuronal responses in the pigeon's brainstem that show how single cells encode magnetic field direction, intensity, and polarity-qualities that are necessary to derive an internal model representing directional heading and geosurface location. Our findings demonstrate a neural substrate for a vertebrate magnetic sense. |
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Address |
Department of Neuroscience, Baylor College of Medicine, Houston, TX 77024, USA |
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English |
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ISSN |
0036-8075 |
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Area |
WP6 In vivo |
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Notes |
PMID:22539554 |
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Call Number |
CBM.UAM @ ccobaleda @ |
Serial |
187 |
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