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Novel Regulatory Factors Interacting with the Promoter of the Gene Encoding the mRNA Cap Binding Protein (eIF4E) and Their Function in Growth Regulation 总被引:1,自引:0,他引:1
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Kelly A. Johnston Michael Polymenis Shanping Wang John Branda Emmett V. Schmidt 《Molecular and cellular biology》1998,18(10):5621-5633
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Michael A. Weiss 《The Journal of biological chemistry》2009,284(29):19159-19163
Insulin plays a central role in the regulation of vertebrate metabolism. The hormone, the post-translational product of a single-chain precursor, is a globular protein containing two chains, A (21 residues) and B (30 residues). Recent advances in human genetics have identified dominant mutations in the insulin gene causing permanent neonatal-onset DM2 (1–4). The mutations are predicted to block folding of the precursor in the ER of pancreatic β-cells. Although expression of the wild-type allele would in other circumstances be sufficient to maintain homeostasis, studies of a corresponding mouse model (5–7) suggest that the misfolded variant perturbs wild-type biosynthesis (8, 9). Impaired β-cell secretion is associated with ER stress, distorted organelle architecture, and cell death (10). These findings have renewed interest in insulin biosynthesis (11–13) and the structural basis of disulfide pairing (14–19). Protein evolution is constrained not only by structure and function but also by susceptibility to toxic misfolding.Insulin plays a central role in the regulation of vertebrate metabolism. The hormone, the post-translational product of a single-chain precursor, is a globular protein containing two chains, A (21 residues) and B (30 residues). Recent advances in human genetics have identified dominant mutations in the insulin gene causing permanent neonatal-onset DM2 (1–4). The mutations are predicted to block folding of the precursor in the ER of pancreatic β-cells. Although expression of the wild-type allele would in other circumstances be sufficient to maintain homeostasis, studies of a corresponding mouse model (5–7) suggest that the misfolded variant perturbs wild-type biosynthesis (8, 9). Impaired β-cell secretion is associated with ER stress, distorted organelle architecture, and cell death (10). These findings have renewed interest in insulin biosynthesis (11–13) and the structural basis of disulfide pairing (14–19). Protein evolution is constrained not only by structure and function but also by susceptibility to toxic misfolding. 相似文献
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ETO, a Target of t(8;21) in Acute Leukemia, Interacts with the N-CoR and mSin3 Corepressors 总被引:22,自引:7,他引:22
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Bart Lutterbach Jennifer J. Westendorf Bryan Linggi Andrea Patten Mariko Moniwa James R. Davie Khanh D. Huynh Vivian J. Bardwell Robert M. Lavinsky Michael G. Rosenfeld Christopher Glass Edward Seto Scott W. Hiebert 《Molecular and cellular biology》1998,18(12):7176-7184
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Chen-Yin Ou Jeong Hoon Kim Catherine K. Yang Michael R. Stallcup 《The Journal of biological chemistry》2009,284(31):20629-20637
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