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Gene Review

Ccng1  -  cyclin G1

Mus musculus

Synonyms: AI314029, Ccng, Cyclin-G, Cyclin-G1, cyclin G
 
 
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Disease relevance of Ccng1

  • To determine the effect of increased expression of cyclin G, retroviruses encoding cyclin G were constructed and used to infect three different murine cell lines [1].
  • Brain trauma caused by knife cut, cold injury, and kinate injection also showed CG1 accumulation in the neuronal nuclei located near the injury site [2].
  • In this study, we assessed the antitumor effects of serial portal vein infusions of matrix-targeted vectors bearing a mutant cyclin G1 (dnG1) construct in a nude mouse model of liver metastasis [3].
  • Taken together, these studies demonstrate in vivo efficacy of a high-titer antisense cyclin G1 retroviral vector in an animal model of osteosarcoma [4].
  • Histologic sections from the antisense cyclin G1 vector-treated tumors showed decreased mitotic indices and increased stroma formation within the residual tumors [4].
 

High impact information on Ccng1

 

Biological context of Ccng1

  • In agreement with previous results, we showed that these mice develop normally, and that proliferation and induction of cellular senescence in cyclin G1-deficient mouse embryo fibroblasts are indistinguishable from wild-type fibroblasts [8].
  • In contrast, in stimulated peripheral T cells, cyclin G1 mRNA is maximal in early G1 phase and declines in cell cycle progression [9].
  • Furthermore, G(2)-phase growth arrest was observed in cells irradiated at the low dose rates of 5 cGy/h and 10 cGy/h, which correlated with Trp53-mediated Ccng1/cyclin G1 up-regulation [10].
  • On the other hand, the function of cyclin G1 is not so clear despite the fact that 1-2-3 cells showed a significant increase of the cyclin G1 gene during the early stage of apoptosis [11].
  • Using a DNA binding assay, a specific p53 binding site was identified upstream from the cyclin G gene, which functioned as a p53-dependent cis-acting element in a transient transfection assay [7].
 

Anatomical context of Ccng1

  • Moreover, we showed that treatment of mice with the alkylating agent 1,4-bis[N,N'-di(ethylene)-phosphamide]piperazine (Dipin), followed by partial hepatectomy, decreased G1-S transition in cyclin G1-null hepatocytes as compared with wild type [8].
  • Cyclin G2 mRNA is differentially expressed compared to cyclin G1, the highest transcript levels seen in cerebellum, thymus, spleen, prostate, and kidney [9].
  • This prompted us to examine the roles of two negative growth-regulatory genes, cyclin G1 and cyclin G2, in the periimplantation mouse uterus [12].
  • In both a mouse p53 temperature-sensitive leukemic cell line and mouse embryonic fibroblasts (MEF) after gamma-irradiation, cyclin G mRNA was rapidly induced [7].
  • In brain, in situ hybridization studies also demonstrated cyclin G expression in a restricted group of matured neurons, particularly in the telencephalon and the thalamus [13].
 

Associations of Ccng1 with chemical compounds

  • Finally, we found a significant decrease in tumor incidence, mass, and malignancy in both male and female cyclin G1-null mice after treatment with the potent hepatocarcinogen N-diethylnitrosamine [8].
  • Pharmacological and genetic studies provide evidence that the expression of cyclin G1, not cyclin G2, is regulated by progesterone via its nuclear receptor [12].
  • Additionally, we observed that while cyclin G expression is markedly reduced upon aggregate formation in embryonic carcinoma P19 cells, retrovirus-mediated over-expression of cyclin G enhances apoptotic cell death in aggregated P19 cells, and increases the extent of apoptosis caused by retinoic acid or serum starvation of these cells [1].
  • A similar nuclear translocation of endogenous CG1 was confirmed in a primary culture of cortical neurons when a toxic level of N-methyl-D-aspartate (NMDA) was applied [2].
  • After 4 hour treatment of MNNG, populations of G2/M phase distribution and apoptotic fraction and the cyclin G mRNA level increased, while the cyclin B1 mRNA level decreased in a concentration-dependent manner [14].
 

Other interactions of Ccng1

  • This constitutive expression in mature neurons suggests that cyclin G may have a function different from other members of the cyclin group [13].
  • The mRNA expression of the p53-response genes p21, murine double minute clone 2 (mdm2), and cyclin G was increased at 2 h after irradiation but was decreased by 8 h postirradiation, relative to the 2-h time-point [15].
  • (c) Alteration of cyclin G1 and Wee-1 kinase genes may be related to the G2/M arrest induced by benzene exposure [16].
 

Analytical, diagnostic and therapeutic context of Ccng1

  • An increase in cyclin G expression after nerve injury was demonstrated by differential display PCR, carried out to compare references in expression of mRNAs between axotomized and normal hypoglossal motoneurons in the rat [13].
  • In contrast, during mitosis, cyclin G1 was undetectable by immunohistochemistry [17].
  • TUNEL staining did not exactly overlap with the CG1-positive cells, but overlapped highly with Fluoro-Jade B staining, a degeneration marker [2].
  • RESULTS: Western blot analysis revealed that the accumulation of p53 protein during the initial 24 h period following DNA damage is reduced in cyclin G1-/- cells compared to wild-type cells [18].
  • We performed chromosome mapping utilizing the fluorescence in situ hybridization (FISH) technique using both cDNA and genomic DNA for cyclin G. FISH localizes human cyclin G to the 5q32-q34 region [19].

References

  1. A role of cyclin G in the process of apoptosis. Okamoto, K., Prives, C. Oncogene (1999) [Pubmed]
  2. The p53-independent nuclear translocation of cyclin G1 in degenerating neurons by ischemic and traumatic insults. Maeda, M., Ampo, K., Kiryu-Seo, S., Konishi, H., Ohba, N., Kadono, C., Kiyama, H. Exp. Neurol. (2005) [Pubmed]
  3. Inhibition of metastatic tumor growth in nude mice by portal vein infusions of matrix-targeted retroviral vectors bearing a cytocidal cyclin G1 construct. Gordon, E.M., Liu, P.X., Chen, Z.H., Liu, L., Whitley, M.D., Gee, C., Groshen, S., Hinton, D.R., Beart, R.W., Hall, F.L. Cancer Res. (2000) [Pubmed]
  4. Retroviral vector-mediated transfer of an antisense cyclin G1 construct inhibits osteosarcoma tumor growth in nude mice. Chen, D.S., Zhu, N.L., Hung, G., Skotzko, M.J., Hinton, D.R., Tolo, V., Hall, F.L., Anderson, W.F., Gordon, E.M. Hum. Gene Ther. (1997) [Pubmed]
  5. Cyclin G recruits PP2A to dephosphorylate Mdm2. Okamoto, K., Li, H., Jensen, M.R., Zhang, T., Taya, Y., Thorgeirsson, S.S., Prives, C. Mol. Cell (2002) [Pubmed]
  6. Ets1 is required for p53 transcriptional activity in UV-induced apoptosis in embryonic stem cells. Xu, D., Wilson, T.J., Chan, D., De Luca, E., Zhou, J., Hertzog, P.J., Kola, I. EMBO J. (2002) [Pubmed]
  7. Cyclin G is a transcriptional target of the p53 tumor suppressor protein. Okamoto, K., Beach, D. EMBO J. (1994) [Pubmed]
  8. Reduced hepatic tumor incidence in cyclin G1-deficient mice. Jensen, M.R., Factor, V.M., Fantozzi, A., Helin, K., Huh, C.G., Thorgeirsson, S.S. Hepatology (2003) [Pubmed]
  9. Cyclin G1 and cyclin G2 comprise a new family of cyclins with contrasting tissue-specific and cell cycle-regulated expression. Horne, M.C., Goolsby, G.L., Donaldson, K.L., Tran, D., Neubauer, M., Wahl, A.F. J. Biol. Chem. (1996) [Pubmed]
  10. Dose and dose-rate effects of low-dose ionizing radiation on activation of Trp53 in immortalized murine cells. Sugihara, T., Magae, J., Wadhwa, R., Kaul, S.C., Kawakami, Y., Matsumoto, T., Tanaka, K. Radiat. Res. (2004) [Pubmed]
  11. The mechanisms of death of an erythroleukemic cell line by p53: involvement of the microtubule and mitochondria. Kato, M.V. Leuk. Lymphoma (1999) [Pubmed]
  12. Cyclin G1 and cyclin G2 are expressed in the periimplantation mouse uterus in a cell-specific and progesterone-dependent manner: evidence for aberrant regulation with Hoxa-10 deficiency. Yue, L., Daikoku, T., Hou, X., Li, M., Wang, H., Nojima, H., Dey, S.K., Das, S.K. Endocrinology (2005) [Pubmed]
  13. p53-independent cyclin G expression in a group of mature neurons and its enhanced expression during nerve regeneration. Morita, N., Kiryu, S., Kiyama, H. J. Neurosci. (1996) [Pubmed]
  14. Cell cycle was disturbed in the MNNG-induced initiation stage during in vitro two-stage transformation of Balb/3T3 cells. Fang, M.Z., Mar, W.C., Cho, M.H. Toxicology (2001) [Pubmed]
  15. The infant mouse as a in vivo model for the detection and study of DNA damage-induced changes in the liver. Reynolds, R., Witherspoon, S., Fox, T. Mol. Carcinog. (2004) [Pubmed]
  16. Mechanisms of benzene-induced hematotoxicity and leukemogenicity: cDNA microarray analyses using mouse bone marrow tissue. Yoon, B.I., Li, G.X., Kitada, K., Kawasaki, Y., Igarashi, K., Kodama, Y., Inoue, T., Kobayashi, K., Kanno, J., Kim, D.Y., Inoue, T., Hirabayashi, Y. Environ. Health Perspect. (2003) [Pubmed]
  17. Regulation of cyclin G1 during murine hepatic regeneration following Dipin-induced DNA damage. Jensen, M.R., Factor, V.M., Thorgeirsson, S.S. Hepatology (1998) [Pubmed]
  18. Cyclin G1 associates with MDM2 and regulates accumulation and degradation of p53 protein. Kimura, S.H., Nojima, H. Genes Cells (2002) [Pubmed]
  19. Structure and chromosomal assignment of the human cyclin G gene. Endo, Y., Fujita, T., Tamura, K., Tsuruga, H., Nojima, H. Genomics (1996) [Pubmed]
 
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