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Roze siah part 125
Roze siah part 125







roze siah part 125

Science 330(6012):1834–1838įilipek A, Jastrzebska B, Nowotny M, Kwiatkowska K, Hetman M, Surmacz L, Wyroba E, Kuznicki J (2002) Ca 2+-dependent translocation of the calcyclin-binding protein in neurons and neuroblastoma NB-2a cells. Nature 448(7150):151–156įamulski JK, Trivedi N, Howell D, Yang Y, Tong Y, Gilbertson R, Solecki DJ (2010) Siah regulation of Pard3A controls neuronal cell adhesion during germinal zone exit. Curr Biol 13(11):960–966ĭietzl G, Chen D, Schnorrer F, Su KC, Barinova Y, Fellner M, Gasser B, Kinsey K, Oppel S, Scheiblauer S, Couto A, Marra V, Keleman K, Dickson BJ (2007) A genome-wide transgenic RNAi library for conditional gene inactivation in Drosophila. Genetics 189(3):861–870Ĭliffe A, Hamada F, Bienz M (2003) A role of Dishevelled in relocating Axin to the plasma membrane during wingless signaling. Proc Nat Acad Sci USA 91(24):11689–11693Ĭasad ME, Abraham D, Kim IM, Frangakis S, Dong B, Lin N, Wolf MJ, Rockman HA (2011) Cardiomyopathy is associated with ribosomal protein gene haplo-insufficiency in Drosophila melanogaster. PLoS ONE 6(4):e18497Ĭarthew RW, Neufeld TP, Rubin GM (1994) Identification of genes that interact with the sina gene in Drosophila eye development. Biochim Biophys Acta 1789(4):343–353Ĭammarato A, Ahrens CH, Alayari NN, Qeli E, Rucker J, Reedy MC, Zmasek CM, Gucek M, Cole RN, Van Eyk JE, Bodmer R, O’Rourke B, Bernstein SI, Foster DB (2011) A mighty small heart: the cardiac proteome of adult Drosophila melanogaster. Biochemistry 44(27):9462–9471īryantsev AL, Cripps RM (2009) Cardiac gene regulatory networks in Drosophila. J Cell Biochem 98(3):555–566īhattacharya S, Lee YT, Michowski W, Jastrzebska B, Filipek A, Kuznicki J, Chazin WJ (2005) The modular structure of SIP facilitates its role in stabilizing multiprotein assemblies. Hum Mol Genet 16(23):2933–2943Īu KW, Kou CY, Woo AY, Chim SS, Fung KP, Cheng CH, Waye MM, Tsui SK (2006) Calcyclin binding protein promotes DNA synthesis and differentiation in rat neonatal cardiomyocytes. Alterations in Armadillo signaling during development lead to important changes in the size and function of the adult heart.Īllikian MJ, Bhabha G, Dospoy P, Heydemann A, Ryder P, Earley JU, Wolf MJ, Rockman HA, McNally EM (2007) Reduced life span with heart and muscle dysfunction in Drosophila sarcoglycan mutants. In summary, we show that deletion of CG3226, which has homology to mammalian SIP, causes cardiomyopathy in adult Drosophila. While, increasing Armadillo signaling in the heart did not have an effect on adult heart function, decreasing Armadillo signaling in the fly heart caused the significant reduction in heart chamber size. To investigate the effects of altering β-catenin/Armadillo signaling in the adult fly, we measured heart function in flies expressing either constitutively active Armadillo or transgenic constructs that block Armadillo signaling, specifically in the heart.

roze siah part 125

Mammalian SIP functions as an adaptor protein involved in one of the β-catenin degradation complexes.

roze siah part 125

CG3226 is an uncharacterized gene in Drosophila possessing homology to the mammalian Siah-interacting protein (SIP) gene.

roze siah part 125

Using a number of strategies including customized smaller deletions, screening of mutant alleles, and transgenic rescue, we identified CG3226 as the causative gene for this deficiency. Using optical coherence tomography to phenotype cardiac function in awake adult Drosophila, we identified Df(1)Exel6240 as having cardiomyopathy. To identify novel genes that cause cardiomyopathy, we performed a deficiency screen in adult Drosophila. Drosophila is a useful model organism in which the genetics of human diseases, including recent advances in identification of the genetics of heart development and disease in the fly, can be studied.









Roze siah part 125