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Gene Review

Nedd9  -  neural precursor cell expressed,...

Mus musculus

Synonyms: CAS-L, CRK-associated substrate-related protein, Cas-L, CasL, Casl, ...
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Disease relevance of Nedd9


High impact information on Nedd9

  • Deletion of a putative myocyte-specific enhancer factor 1 (MEF-1) binding site, containing a canonical E-box motif, had no effects on muscle-specific transcription, indicating that this site is not required for the activity of the enhancer [4].
  • In contrast to reports involving cotransfection of 10T1/2 cells with plasmids expressing the myogenic determination factor MyoD, we show that the skeletal myocyte activity of multimerized MEF1 sites is 30-fold lower than that of the 206-bp enhancer [5].
  • Mutations at three sites have larger effects in muscle than nonmuscle cells; an A/T-rich site mutation has a pronounced effect in both striated muscle types, mutations at the MEF1 (Right E-box) site are relatively specific to expression in skeletal muscle, and mutations at the CArG site are relatively specific to expression in cardiac muscle [5].
  • Mannosamine treatment, which down-regulates cell-surface uPAR, decreased MEF-2 migration by 40% without significantly affecting MEF-1 migration [6].
  • A myocyte specific protein complex, MEF1, binds the MCK-R site [7].

Biological context of Nedd9

  • One sequence located at approximately -940 base pairs corresponds to the motif called MEF1 which has been shown in other muscle genes to bind the myogenic regulatory factors of which MyoD is one example [8].
  • This may be due to an 18% nucleotide difference between the MEF-1 and Sabin 2 strains, resulting in 72 amino acid substitutions and leading to antigenic dissimilarity [9].
  • These data suggest that bHLH gene expression is not required for the early steps of osteogenesis; moreover, inhibition of bHLH protein binding to a MEF1-type E box might be an integral part of osteogenic commitment [10].

Associations of Nedd9 with chemical compounds

  • Promoter-reporter studies also demonstrated inhibition of MEF-1 driven CAT expression by dexamethasone under differentiation-permissive conditions in RI-2J cells [10].
  • MEF-1 oligonucleotide, the E-box sequence from the muscle creatine kinase enhancer, demonstrated no changes in binding with nuclear extracts from moderately differentiated (W-20) or relatively mature (ROS 17/2.8) cells under any conditions tested [10].

Other interactions of Nedd9

  • However, in poorly differentiated RI-2J cells, which do not express osteogenic markers unless treated with dexamethasone, induction of differentiation was reflected in transient inhibition of binding to MEF-1 [10].


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  6. Embryonic fibroblasts that are genetically deficient in low density lipoprotein receptor-related protein demonstrate increased activity of the urokinase receptor system and accelerated migration on vitronectin. Weaver, A.M., Hussaini, I.M., Mazar, A., Henkin, J., Gonias, S.L. J. Biol. Chem. (1997) [Pubmed]
  7. Muscle gene E-box control elements. Evidence for quantitatively different transcriptional activities and the binding of distinct regulatory factors. Apone, S., Hauschka, S.D. J. Biol. Chem. (1995) [Pubmed]
  8. A possible regulatory role for conserved promoter motifs in an adult-specific muscle myosin gene from mouse. Takeda, S., North, D.L., Lakich, M.M., Russell, S.D., Whalen, R.G. J. Biol. Chem. (1992) [Pubmed]
  9. Evaluation of immunogenicity and protective properties of inactivated poliovirus vaccines: a new surrogate method for predicting vaccine efficacy. Dragunsky, E.M., Ivanov, A.P., Wells, V.R., Ivshina, A.V., Rezapkin, G.V., Abe, S., Potapova, S.G., Enterline, J.C., Hashizume, S., Chumakov, K.M. J. Infect. Dis. (2004) [Pubmed]
  10. HLH transcription factor activity in osteogenic cells. Kazhdan, I., Rickard, D., Leboy, P.S. J. Cell. Biochem. (1997) [Pubmed]
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