Kaghad M, Bonnet H, Yang A, Creancier L, Biscan J C, Valent A, Minty A, Chalon P, Lelias J M, Dumont X, Ferrara P, McKeon F, Caput D
Sanofi Recherche, Labege, France.
Cell. 1997 Aug 22;90(4):809-19. doi: 10.1016/s0092-8674(00)80540-1.
We describe a gene encoding p73, a protein that shares considerable homology with the tumor suppressor p53. p73 maps to 1p36, a region frequently deleted in neuroblastoma and other tumors and thought to contain multiple tumor suppressor genes. Our analysis of neuroblastoma cell lines with 1p and p73 loss of heterozygosity failed to detect coding sequence mutations in remaining p73 alleles. However, the demonstration that p73 is monoallelically expressed supports the notion that it is a candidate gene in neuroblastoma. p73 also has the potential to activate p53 target genes and to interact with p53. We propose that the disregulation of p73 contributes to tumorigenesis and that p53-related proteins operate in a network of developmental and cell cycle controls.
我们描述了一种编码p73的基因，p73是一种与肿瘤抑制蛋白p53具有相当同源性的蛋白质。p73定位于1p36，该区域在神经母细胞瘤和其他肿瘤中经常缺失，并且被认为含有多个肿瘤抑制基因。我们对1p和p73杂合性缺失的神经母细胞瘤细胞系进行分析，未能在剩余的p73等位基因中检测到编码序列突变。然而，p73单等位基因表达的证明支持了它是神经母细胞瘤候选基因的观点。p73还具有激活p53靶基因并与p53相互作用的潜力。我们提出，p73的失调促成肿瘤发生，并且p53相关蛋白在发育和细胞周期控制网络中发挥作用。
