生物谷報道：乙酰轉(zhuǎn)移酶Tip60調(diào)控轉(zhuǎn)錄,，涉及DNA的損傷響應(yīng)?，F(xiàn)在，它被發(fā)現(xiàn)在小鼠模型中和在人類腫瘤中都具有體內(nèi)腫瘤抑制活性。研究結(jié)果發(fā)表在最新一期的《自然》雜志上,。
人類Tip60位點(diǎn)（HTATIP）在頭部和頸部鱗狀細(xì)胞癌,、乳腺癌和淋巴癌中都經(jīng)常突變。在組織微陣列上著色的核Tip60在各種不同腫瘤中都丟失了,，而且最顯著的是在乳腺癌中也丟失了,。這項工作表明，要在初發(fā)腫瘤細(xì)胞中發(fā)起一個由致癌基因誘導(dǎo)的DNA損傷響應(yīng),，Tip60的濃度必需達(dá)到臨界水平：這一防衛(wèi)機(jī)制的失效可能與p53突變發(fā)生協(xié)同作用,，共同促進(jìn)腫瘤的發(fā)育。
 
FIGURE 1. Tip60 haplo-insufficiency accelerates Myc-induced lymphomagenesis but does not alleviate the pressure for p53 inactivation.
a, Kaplan–Meier curves showing disease-free survival of E –myc mice of the indicated genotypes. The bar graph reports disease onset in the same groups as average   s.d. (**P   0.001,*P   0.05). b,c, Genomic DNA from tumour (T) and normal (N) tail tissue from mice of the indicated genotypes was used for PCR with primers amplifying the wild-type (WT) and knockout (KO) alleles of the gene for p53 (Trp53; b) or ARF (c), as indicated. All tumours in E –mycTrp53+/–Tip60+/– mice (10/10) underwent Trp53 LOH (b and data not shown). As shown in a, these tumours developed slightly faster than in E –mycTip60+/– mice, but at the same rate as in E –mycTrp53+/– mice. Similarly, Arf LOH (c)10 and tumour onset (data not shown) were equivalent in Arf+/– and Arf+/–Tip60+/– backgrounds.

原文出處：

Nature   Volume 448 Number 7157

Tip60 is a haplo-insufficient tumour suppressor required for an oncogene-induced DNA damage response p1063
Chiara Gorrini, Massimo Squatrito, Chiara Luise, Nelofer Syed, Daniele Perna, Landon Wark, Francesca Martinato, Domenico Sardella, Alessandro Verrecchia, Samantha Bennett, Stefano Confalonieri, Matteo Cesaroni, Francesco Marchesi, Milena Gasco, Eugenio Scanziani, Maria Capra, Sabine Mai, Paolo Nuciforo, Tim Crook, John Lough & Bruno Amati

doi:10.1038/nature06055

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