共查询到20条相似文献,搜索用时 15 毫秒
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Biophysical characterization of interactions between the core binding factor alpha and beta subunits and DNA 总被引:1,自引:0,他引:1
Tang YY Crute BE Kelley JJ Huang X Yan J Shi J Hartman KL Laue TM Speck NA Bushweller JH 《FEBS letters》2000,470(2):167-172
Core binding factors (CBFs) play key roles in several developmental pathways and in human disease. CBFs consist of a DNA binding CBFalpha subunit and a non-DNA binding CBFbeta subunit that increases the affinity of CBFalpha for DNA. We performed sedimentation equilibrium analyses to unequivocally establish the stoichiometry of the CBFalpha:beta:DNA complex. Dissociation constants for all four equilibria involving the CBFalpha Runt domain, CBFbeta, and DNA were defined. Conformational changes associated with interactions between CBFalpha, CBFbeta, and DNA were monitored by nuclear magnetic resonance and circular dichroism spectroscopy. The data suggest that CBFbeta 'locks in' a high affinity DNA binding conformation of the CBFalpha Runt domain. 相似文献
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Disease mutations in RUNX1 and RUNX2 create nonfunctional, dominant-negative, or hypomorphic alleles 下载免费PDF全文
Matheny CJ Speck ME Cushing PR Zhou Y Corpora T Regan M Newman M Roudaia L Speck CL Gu TL Griffey SM Bushweller JH Speck NA 《The EMBO journal》2007,26(4):1163-1175
Monoallelic RUNX1 mutations cause familial platelet disorder with predisposition for acute myelogenous leukemia (FPD/AML). Sporadic mono- and biallelic mutations are found at high frequencies in AML M0, in radiation-associated and therapy-related myelodysplastic syndrome and AML, and in isolated cases of AML M2, M5a, M3 relapse, and chronic myelogenous leukemia in blast phase. Mutations in RUNX2 cause the inherited skeletal disorder cleidocranial dysplasia (CCD). Most hematopoietic missense mutations in Runx1 involve DNA-contacting residues in the Runt domain, whereas the majority of CCD mutations in Runx2 are predicted to impair CBFbeta binding or the Runt domain structure. We introduced different classes of missense mutations into Runx1 and characterized their effects on DNA and CBFbeta binding by the Runt domain, and on Runx1 function in vivo. Mutations involving DNA-contacting residues severely inactivate Runx1 function, whereas mutations that affect CBFbeta binding but not DNA binding result in hypomorphic alleles. We conclude that hypomorphic RUNX2 alleles can cause CCD, whereas hematopoietic disease requires more severely inactivating RUNX1 mutations. 相似文献
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Gutiérrez J Sierra J Medina R Puchi M Imschenetzky M van Wijnen A Lian J Stein G Stein J Montecino M 《Biochemistry》2000,39(44):13565-13574
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Structure and backbone dynamics of Apo-CBFbeta in solution 总被引:1,自引:0,他引:1
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Filamin A-bound PEBP2beta/CBFbeta is retained in the cytoplasm and prevented from functioning as a partner of the Runx1 transcription factor 下载免费PDF全文
Yoshida N Ogata T Tanabe K Li S Nakazato M Kohu K Takafuta T Shapiro S Ohta Y Satake M Watanabe T 《Molecular and cellular biology》2005,25(3):1003-1012
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