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Genome-wide analysis of p63 binding sites identifies AP-2 factors as co-regulators of epidermal differentiation 总被引:1,自引:0,他引:1
McDade SS Henry AE Pivato GP Kozarewa I Mitsopoulos C Fenwick K Assiotis I Hakas J Zvelebil M Orr N Lord CJ Patel D Ashworth A McCance DJ 《Nucleic acids research》2012,40(15):7190-7206
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DNA binding domain-independent pathways are involved in EWS/FLI1-mediated oncogenesis. 总被引:2,自引:0,他引:2
S M Welford S P Hebert B Deneen A Arvand C T Denny 《The Journal of biological chemistry》2001,276(45):41977-41984
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Lettre G Kritikou EA Jaeggi M Calixto A Fraser AG Kamath RS Ahringer J Hengartner MO 《Cell death and differentiation》2004,11(11):1198-1203
We used genome-wide RNA interference (RNAi) to identify genes that affect apoptosis in the C. elegans germ line. RNAi-mediated knockdown of 21 genes caused a moderate to strong increase in germ cell death. Genetic epistasis studies with these RNAi candidates showed that a large subset (16/21) requires p53 to activate germ cell apoptosis. Apoptosis following knockdown of the genes in the p53-dependent class also depended on a functional DNA damage response pathway, suggesting that these genes might function in DNA repair or to maintain genome integrity. As apoptotic pathways are conserved, orthologues of the worm germline apoptosis genes presented here could be involved in the maintenance of genomic stability, p53 activation, and fertility in mammals. 相似文献
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Disease mutations in RUNX1 and RUNX2 create nonfunctional, dominant-negative, or hypomorphic alleles
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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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