Role of Mxi1 in ageing organ systems and the regulation of normal and neoplastic growth

Nature

Volumn 393, Issue 6684, 1998, Pages 483-487

  Schreiber Agus, Nicole ^a   Meng, Yong ^a   Hoang, Tin ^a   Hou Jr , Harry ^a   Ghen, Ken ^a   Greenberg, Roger ^a   Cordon Cardo, Carlos ^a   Leet, Han Woong ^a   Depinho, Ronald A ^a  

^a MEMORIAL SLOAN KETTERING CANCER CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ONCOPROTEIN; REPRESSOR PROTEIN; TRANSCRIPTION FACTOR;

ANIMAL CELL; ARTICLE; CELL AGING; CELL PROLIFERATION; CELL TRANSFORMATION; CONTROLLED STUDY; GENE TRANSFER; IMMUNOHISTOCHEMISTRY; MOUSE; NONHUMAN; OPEN READING FRAME; PRIORITY JOURNAL; PROTEIN EXPRESSION; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION; SIGNAL TRANSDUCTION; SPLEEN CELL; TRANSCRIPTION REGULATION;

AGING; ANIMALS; BASIC HELIX-LOOP-HELIX TRANSCRIPTION FACTORS; CELL DIVISION; CELL TRANSFORMATION, NEOPLASTIC; DNA-BINDING PROTEINS; GENES, TUMOR SUPPRESSOR; KIDNEY; MALE; MICE; NEOPLASMS; ORGAN SPECIFICITY; PHENOTYPE; PROSTATE; TRANSCRIPTION FACTORS; TUMOR SUPPRESSOR PROTEINS;

EID: 0032482421     PISSN: 00280836     EISSN: None     Source Type: Journal    
DOI: 10.1038/31008     Document Type: Article

References (30)

1. Aycr, D. E., Kretzner, L. & Eisenman, R. N. Mad: a heterodimeric partner for Max that antagonizes Myc transcriptional activity. OB 72,211-222 (1993).
2. Hurtin, P. J. ft ai Mad3 and Mad4: novel Max-interacting transcriptional repressers that suppress cmyc dependent transformation and are expressed during neural and epidermal differentiation. EMBO 7.14,5646-5659(1995).
3. Zervos, A. S. Gyuris, J. & Brent, R. Mxil, a protein that specifically interacts with Max to bind MycMax recognition sites. Cell 72, 223-232 (1993).
4. Seh reiber-Agus, N. et al An amino-terminal domain of Mxil mediates anti-Myc oncogenic activity and interacts with a homolog of the yeast transcriptional represser SIN3. Ce//80, 777-786 (1995).
5. Ayer, D. E., Lawrence, Q. A. & Eisenman, R. N. Mad-Max transcriptional repression is mediated by ternary complex formation with mammalian homologs of yeast represser Sin3. Cell 80, 767-776 (1995).
6. Schreiber-Agus, N. & DePinho, R. A. Repression by the Mad(Mxil)-Sin3 complex. Bioessays (in the press).
7. Henriksson, M. & Luscher, B. Proteins of the Myc network: essential regulators of cell growth and differentiation. Adv. Cancer Res. 68, 109-182 (1996).
8. Edelhoff, S. et al. Mapping of two genes encoding members of a distinct subfamily of MAX interacting proteins: MAD to human chromosome 2 and mouse chromosome 6, and MXI1 to human chromosome 10 and mouse chromosome 19. Oncogene 9,665-668 (1994}.
9. Shapiro, D.M. et al. Assignment of the human MAD and MXII genes to chromosomes 2pl2-pl 3 and 10q24-q25. Gcnomics23, 282-285 (1994).
10. Wechsler, D. S. et al. Localization of the human Mxil transcription factor gene (MXIl) to chromosome 10q24-q25. Cenomics 21,669-672 (1994).
11. Adams, J. M. et al The c-myc oncogene driven by immunoglobulin enhancers induces lymphoid malignancy in transgenic mice. Nature 318, 533-538 (1985).
12. Harris, A, "W. et al Transgenic mouse models for hematopoietic tumorigenesis. Curr. Top. Microbiol Irnmunol 141, 82-93 (1988).
13. Yukawa, K. et al Strain dependency of B and T lymphoma development in immunoglobulin heavy chain enhancer (E mu)-myc transgenic mice. J. Exp. Med. 170, 711-726 (1989).
14. Raimondi, S. G. et al Cytogenetics of childhood T-ccll leukemia. Blood72,1560-1566 (1988).
15. Cowley, B. D. Jr, Chadwick, L J., Grantham, J. J. & Calvet, J. P. Elevated proto-oncogene expression in polycystic kidneys of the C57BL/6J (cpk) mouse. J. Am. Soc. Kephrol 1,1048-1053 (1991).
16. Trudel, M., D'Agati, V. & Constantint, F. C-myc as an inducer of polycystic kidney disease in transgenic mice. Kidney Int. 39, 665-671 (1991).
17. Dedeoglu, I. O. et al Spectrum of glomerulocystic kidneys: a case report and review of the literature. Ped. Path. lab. MeJ. 16,941-949 (1996).
18. Foley, K. P. et al Targeted disruption of the MYC antagonist MADl inhibits cell cycle exit during granulocyte differentiation. EMBOJ. 17, 774-785 (1998).
19. Gerlach, C et al KI-67 immunoexpression is a robust marker of proliferative eels in the rat. lab. \ Invest. 77, 697-698 (1997).
20. j 20. Hecker, E. et al International symposium: skin carcinogen esis in man and in experimental models. J. i Cancer Res. din. Oncoi 118, 321-328 (1992).
21. Serrano, M. et al Role of the IN'K4a locus in tumor suppression and cell mortality. CeJl 85, 27-37 (1996).
22. Serrano, M. et al Inhibition of ras-induced proliferation and cellular transformation by p16INK4. Science267, 249-252 (1995).
23. Pomerantz, J. et al The INK4a tumor suppressor gene product, p19ARF, interacts with MDM2 and neutralizes MDM2's inhibition of p53. Ctf/92,713-723 (1998).
24. Li, J. et al PTEN, a putative protein tyrosine phosphatase gene mutated in human brain, breast, and prostate cancer. Science 275,1943-1947 (1997).
25. Eagle, L. R. etal Mutation of the MXIl gene in prostate cancer. Nature Genet. 9,249-255 (1995).
26. Kawamata, N. etal Point mutations of the Mxil gene are rare in prostate cancers. Prostate 29,191193 (1996).
27. Gray, I. C. et al Loss of the chromosomal region 10q23-25 in prostate cancer. Cancer Res. 55, 48004803 (1995).
28. Prochownik, E. V. et al Commonly occurring loss and mutation of the MXI1 gene in prostate cancer. Genes Chromosom. Cancer (in the press).
29. Jenkins, R. B., Qian, |., Lieber, M. M. & Bostwick, D. G. Detection of c-myc oncogene amplification and chromosomal anomalies in metastatic prostatic carcinoma by fluorescence in situ hybridization. Cancer Res. 57, 524-531 (1997).
30. Thompson, T. C. et al Transgenic models for the study of prostate cancer. Cancer 71, 1165-1171 (1993).