Suppression of anchorage-independent growth by expression of the ataxia-telangiectasia group D complementing gene, ATDC.

[1]  D. Lane,et al.  T antigen is bound to a host protein in SY40-transformed cells , 1979, Nature.

[2]  J. Murnane.  Inducible gene expression by DNA rearrangements in human cells , 1986, Molecular and cellular biology.

[3]  Wen-Hwa Lee,et al.  SV40 large tumor antigen forms a specific complex with the product of the retinoblastoma susceptibility gene , 1988, Cell.

[4]  L. Kapp,et al.  Stable radioresistance in ataxia-telangiectasia cells containing DNA from normal human cells. , 1989, International journal of radiation biology.

[5]  W. Benedict,et al.  The retinoblastoma gene functions as a growth and tumor suppressor in human bladder carcinoma cells. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[6]  Y. Chen,et al.  Expression of wild-type p53 in human A673 cells suppresses tumorigenicity but not growth rate. , 1991, Oncogene.

[7]  W. Isaacs,et al.  Wild-type p53 suppresses growth of human prostate cancer cells containing mutant p53 alleles. , 1991, Cancer research.

[8]  P. Freemont,et al.  A novel zinc finger coiled-coil domain in a family of nuclear proteins. , 1992, Trends in biochemical sciences.

[9]  M. James,et al.  Cloning of a candidate gene for ataxia-telangiectasia group D. , 1992, American journal of human genetics.

[10]  L. Kapp,et al.  A critical look at the association of human genetic syndromes with sensitivity to ionizing radiation. , 1993, Seminars in cancer biology.

[11]  L. Kapp,et al.  Nucleotide sequence analysis of a candidate gene for ataxia-telangiectasia group D (ATDC). , 1994, Genomics.

[12]  Y. Hosoi,et al.  Expression of a Candidate Ataxia-telangiectasia Group D Gene in Cultured Fibroblast Cell Lines and Human Tissues. , 1994, International journal of radiation biology.

[13]  Z. Werb,et al.  Simian virus 40 transformation alters the actin cytoskeleton, expression of matrix metalloproteinases and inhibitors of metalloproteinases, and invasive behavior of normal and ataxia-telangiectasia human skin fibroblasts. , 1995, Biochemistry and cell biology = Biochimie et biologie cellulaire.

[14]  P. Brzoska,et al.  The product of the ataxia-telangiectasia group D complementing gene, ATDC, interacts with a protein kinase C substrate and inhibitor. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[15]  P. Bethwaite,et al.  Mutation at chromosome 11q23 in human non‐familial breast cancer: A microdissection microsatellite analysis , 1995, The Journal of pathology.

[16]  L. Thompson,et al.  Defects in the DNA repair and transcription gene ERCC2 in the cancer-prone disorder xeroderma pigmentosum group D. , 1995, Cancer research.

[17]  R. Sutherland,et al.  Expression of the ATDC (ataxia telangiectasia group D‐complementing) gene in A431 human squamous carcinoma cells , 1996, International journal of cancer.

[18]  P. Warne,et al.  Role of Phosphoinositide 3-OH Kinase in Cell Transformation and Control of the Actin Cytoskeleton by Ras , 1997, Cell.

[19]  K. A. Comer,et al.  Human smooth muscle α-actin gene is a transcriptional target of the p53 tumor suppressor protein , 1998, Oncogene.

[20]  K. Borden.  RING fingers and B-boxes: zinc-binding protein-protein interaction domains. , 1998, Biochemistry and cell biology = Biochimie et biologie cellulaire.

[21]  G. Landes,et al.  Combining serial analysis of gene expression and array technologies to identify genes differentially expressed in breast cancer. , 1999, Cancer research.

[22]  Altered splicing of the ATDC message in ataxia telangiectasia group D cells results in the absence of a functional protein. , 2000, Mutagenesis.

[23]  Alessandro Guffanti,et al.  The tripartite motif family identifies cell compartments , 2001, The EMBO journal.

[24]  Matthias Kretzler,et al.  Decrease and gain of gene expression are equally discriminatory markers for prostate carcinoma: a gene expression analysis on total and microdissected prostate tissue. , 2002, The American journal of pathology.