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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

Cell Cycle

 
 
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Disease relevance of Cell Cycle

  • With this in mind, we performed DNA flow-cytometric measurements of ploidy and the fraction of cells in the synthesis phase of the cell cycle (S-phase fraction) on 395 specimens of node-negative breast cancer from our bank of frozen tumors, using the aliquots of pulverized frozen tissue from steroid-receptor assays [1].
  • Here we show that the tyrosine kinase activity of nuclear c-Abl is regulated in the cell cycle through a specific interaction with the retinoblastoma protein (RB) [2].
  • The cell cycle inhibitor p16INK4a is inactivated in many human tumors and in families with hereditary melanoma and pancreatic cancer [3].
  • Introduction of the RB gene into SAOS-2 osteosarcoma cells, which lack functional pRb, prevents cell cycle progression [4].
  • In contrast, mice expressing a mutant Cdk4 that cannot bind the cell-cycle inhibitor P16INK4a display pancreatic hyperplasia due to abnormal proliferation of beta-islet cells [5].
 

Psychiatry related information on Cell Cycle

 

High impact information on Cell Cycle

  • Tax exerts (a) trans-activation and -repression of transcription of different sets of cellular genes through binding to groups of transcription factors and coactivators, (b) dysregulation of cell cycle through binding to inhibitors of CDK4/6, and (c) inhibition of some tumor suppressor proteins [11].
  • Finally, we present evidence demonstrating that B cell activation via TI stimuli does not play merely a permissive role in allowing for cell cycle entry and enhanced responsiveness to other stimuli [12].
  • For example, if tumors are preferential glutamine utilizers, then TPN-enriched solutions might be employed to increase the number of cells in a phase of mitosis that makes them more susceptible to attack by cell-cycle specific chemotherapeutic agents [13].
  • Mechanisms that control timing of cell cycle and developmental events include transcriptional cascades, regulated phosphorylation and proteolysis of signal transduction proteins, transient genetic asymmetry, and intercellular communication [14].
  • Finally, PP1 promotes the exit from mitosis and maintains cells in the G1 or G2 phases of the cell cycle [15].
 

Chemical compound and disease context of Cell Cycle

 

Biological context of Cell Cycle

 

Anatomical context of Cell Cycle

 

Associations of Cell Cycle with chemical compounds

  • As in the case of cell cycle control, protein serine/threonine phosphatase plays a central role in the reentry of quiescent cells into the cycle [31].
  • Analysis of extracts of thymidine-blocked cells confirms that the complexes are cell cycle regulated [32].
  • These observations have been interpreted to indicate that estradiol and FSH can each alter the length of the specific phases of the cell cycle [33].
  • Overexpression of dominant negative c-abl disrupts cell cycle control and enhances transformation by tyrosine kinases, G proteins, and transcription factor oncogenes [34].
  • Upon regulation of expression of GPA1 by the galactose-inducible GAL1 promoter, the loss of GPA1 function was found to lead to cell-cycle arrest at the late G1 phase [35].
 

Gene context of Cell Cycle

  • Cotransfection experiments indicate that CIP1 and SV40 T antigen function in a mutually antagonistic manner to control cell cycle progression [36].
  • TGF beta inhibition of Cdk4 synthesis is linked to cell cycle arrest [37].
  • The c-Myc and E2F transcription factors are among the most potent regulators of cell cycle progression in higher eukaryotes [38].
  • Economical reutilization of coding sequences in this manner is practically without precedent in mammalian genomes, and the unitary inheritance of p16INK4a and p19ARF may underlie their dual requirement in cell cycle control [39].
  • Thus, identification of factors that interfere with and/or control the function of the RB protein is critical for understanding both cell-cycle control and oncogenesis [40].
 

Analytical, diagnostic and therapeutic context of Cell Cycle

References

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  2. A C-terminal protein-binding domain in the retinoblastoma protein regulates nuclear c-Abl tyrosine kinase in the cell cycle. Welch, P.J., Wang, J.Y. Cell (1993) [Pubmed]
  3. Role of the INK4a locus in tumor suppression and cell mortality. Serrano, M., Lee, H., Chin, L., Cordon-Cardo, C., Beach, D., DePinho, R.A. Cell (1996) [Pubmed]
  4. Regulation of retinoblastoma protein functions by ectopic expression of human cyclins. Hinds, P.W., Mittnacht, S., Dulic, V., Arnold, A., Reed, S.I., Weinberg, R.A. Cell (1992) [Pubmed]
  5. Loss of Cdk4 expression causes insulin-deficient diabetes and Cdk4 activation results in beta-islet cell hyperplasia. Rane, S.G., Dubus, P., Mettus, R.V., Galbreath, E.J., Boden, G., Reddy, E.P., Barbacid, M. Nat. Genet. (1999) [Pubmed]
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  15. Functional diversity of protein phosphatase-1, a cellular economizer and reset button. Ceulemans, H., Bollen, M. Physiol. Rev. (2004) [Pubmed]
  16. Cell-cycle regulatory sequences in a hamster histone promoter and their interactions with cellular factors. Artishevsky, A., Wooden, S., Sharma, A., Resendez, E., Lee, A.S. Nature (1987) [Pubmed]
  17. Suppression of breast cancer by chemical modulation of vulnerable zinc fingers in estrogen receptor. Wang, L.H., Yang, X.Y., Zhang, X., Mihalic, K., Fan, Y.X., Xiao, W., Howard, O.M., Appella, E., Maynard, A.T., Farrar, W.L. Nat. Med. (2004) [Pubmed]
  18. HMG-CoA reductase mediates the biological effects of retinoic acid on human neuroblastoma cells: lovastatin specifically targets P-glycoprotein-expressing cells. Dimitroulakos, J., Yeger, H. Nat. Med. (1996) [Pubmed]
  19. Lymphoma models for B cell activation and tolerance. III. Cell cycle dependence for negative signalling of WEHI-231 B lymphoma cells by anti-mu. Scott, D.W., Livnat, D., Pennell, C.A., Keng, P. J. Exp. Med. (1986) [Pubmed]
  20. The renal papilla is a niche for adult kidney stem cells. Oliver, J.A., Maarouf, O., Cheema, F.H., Martens, T.P., Al-Awqati, Q. J. Clin. Invest. (2004) [Pubmed]
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  22. Ordering S phase and M phase in the cell cycle. Nurse, P. Cell (1994) [Pubmed]
  23. The 70 kDa S6 kinase complexes with and is activated by the Rho family G proteins Cdc42 and Rac1. Chou, M.M., Blenis, J. Cell (1996) [Pubmed]
  24. Association of BRCA1 with Rad51 in mitotic and meiotic cells. Scully, R., Chen, J., Plug, A., Xiao, Y., Weaver, D., Feunteun, J., Ashley, T., Livingston, D.M. Cell (1997) [Pubmed]
  25. E2F-1 functions in mice to promote apoptosis and suppress proliferation. Field, S.J., Tsai, F.Y., Kuo, F., Zubiaga, A.M., Kaelin, W.G., Livingston, D.M., Orkin, S.H., Greenberg, M.E. Cell (1996) [Pubmed]
  26. salvador Promotes both cell cycle exit and apoptosis in Drosophila and is mutated in human cancer cell lines. Tapon, N., Harvey, K.F., Bell, D.W., Wahrer, D.C., Schiripo, T.A., Haber, D.A., Hariharan, I.K. Cell (2002) [Pubmed]
  27. p53-dependent inhibition of cyclin-dependent kinase activities in human fibroblasts during radiation-induced G1 arrest. Dulić, V., Kaufmann, W.K., Wilson, S.J., Tlsty, T.D., Lees, E., Harper, J.W., Elledge, S.J., Reed, S.I. Cell (1994) [Pubmed]
  28. Evidence that the leukocyte-common antigen is required for antigen-induced T lymphocyte proliferation. Pingel, J.T., Thomas, M.L. Cell (1989) [Pubmed]
  29. Catabolism of thymidine during the lymphocyte cell cycle. Usher, D.C., Reiter, H. Cell (1977) [Pubmed]
  30. Abnormal TNF activity in Timp3-/- mice leads to chronic hepatic inflammation and failure of liver regeneration. Mohammed, F.F., Smookler, D.S., Taylor, S.E., Fingleton, B., Kassiri, Z., Sanchez, O.H., English, J.L., Matrisian, L.M., Au, B., Yeh, W.C., Khokha, R. Nat. Genet. (2004) [Pubmed]
  31. Protein serine/threonine phosphatases: structure, regulation, and functions in cell growth. Mumby, M.C., Walter, G. Physiol. Rev. (1993) [Pubmed]
  32. Cell cycle regulation of the E2F transcription factor involves an interaction with cyclin A. Mudryj, M., Devoto, S.H., Hiebert, S.W., Hunter, T., Pines, J., Nevins, J.R. Cell (1991) [Pubmed]
  33. Hormonal regulation of ovarian cellular proliferation. Rao, M.C., Midgley, A.R., Richards, J.S. Cell (1978) [Pubmed]
  34. The nuclear tyrosine kinase c-Abl negatively regulates cell growth. Sawyers, C.L., McLaughlin, J., Goga, A., Havlik, M., Witte, O. Cell (1994) [Pubmed]
  35. GPA1, a haploid-specific essential gene, encodes a yeast homolog of mammalian G protein which may be involved in mating factor signal transduction. Miyajima, I., Nakafuku, M., Nakayama, N., Brenner, C., Miyajima, A., Kaibuchi, K., Arai, K., Kaziro, Y., Matsumoto, K. Cell (1987) [Pubmed]
  36. The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases. Harper, J.W., Adami, G.R., Wei, N., Keyomarsi, K., Elledge, S.J. Cell (1993) [Pubmed]
  37. TGF beta inhibition of Cdk4 synthesis is linked to cell cycle arrest. Ewen, M.E., Sluss, H.K., Whitehouse, L.L., Livingston, D.M. Cell (1993) [Pubmed]
  38. The novel ATM-related protein TRRAP is an essential cofactor for the c-Myc and E2F oncoproteins. McMahon, S.B., Van Buskirk, H.A., Dugan, K.A., Copeland, T.D., Cole, M.D. Cell (1998) [Pubmed]
  39. Alternative reading frames of the INK4a tumor suppressor gene encode two unrelated proteins capable of inducing cell cycle arrest. Quelle, D.E., Zindy, F., Ashmun, R.A., Sherr, C.J. Cell (1995) [Pubmed]
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  43. A human BRCA2 complex containing a structural DNA binding component influences cell cycle progression. Marmorstein, L.Y., Kinev, A.V., Chan, G.K., Bochar, D.A., Beniya, H., Epstein, J.A., Yen, T.J., Shiekhattar, R. Cell (2001) [Pubmed]
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  45. Activation of a cell-cycle-regulated histone gene by the oncogenic transcription factor IRF-2. Vaughan, P.S., Aziz, F., van Wijnen, A.J., Wu, S., Harada, H., Taniguchi, T., Soprano, K.J., Stein, J.L., Stein, G.S. Nature (1995) [Pubmed]
 
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