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Nol3  -  nucleolar protein 3 (apoptosis repressor...

Mus musculus

Synonyms: ARC, B430311C09Rik, MYC, NOP, Nop30, ...
 
 
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Disease relevance of Nol3

  • Using a retrovirus construct modified to express BCR-ABL and MYC genes simultaneously, we show that dominant negative MYC suppressed transformation of primary mouse bone marrow pre-B cells by BCR-ABL [1].
  • Importantly, in such p27(Kip1) deficient lymphomas an increased frequency of Myc activation is observed. p27(Kip1) deficiency was also shown to collaborate with MYC overexpression in transgenic lymphoma models [2].
  • Here we show that induction of the MYC protooncogene is required for cell transformation by vIRF, and that vIRF increases MYC transcription up to 15-fold through specific promoter interactions at an ISRE sequence called the plasmacytoma repressor factor (PRF) element [3].
  • lambda-MYC-induced mouse Burkitt lymphoma (BL) harboring the shuttle vector pUR288, which includes a lacZ reporter gene to study mutagenesis, was employed to assess genomic instability associated with MYC deregulation [4].
  • Dwarfism and dysregulated proliferation in mice overexpressing the MYC antagonist MAD1 [5].
 

Psychiatry related information on Nol3

  • Nociceptin/orphanin FQ (N/OFQ), the endogenous ligand of the NOP receptor, regulates several central functions such as pain transmission, learning and memory, fear and anxiety and feeding and locomotor activity [6].
 

High impact information on Nol3

  • Moreover, the metagene models trained with gene expression patterns evoked by ectopic production of Myc or Ras proteins in primary tissue culture cells properly predict the activity of in vivo tumor models that result from deregulation of the MYC or HRAS pathways [7].
  • Dominant negative MYC blocks transformation by ABL oncogenes [1].
  • Dominant negative MYC proteins were overexpressed in fibroblasts to determine if MYC complements ABL oncogene transformation or is essential for this process [1].
  • Transformation of hematopoietic cells by the p210bcr/abl tyrosine kinase appears to require the expression of a functional MYC protein, suggesting that simultaneous targeting of BCR-ABL and c-myc might be a rational strategy for attempting treatment of Phil-adelphia leukemia [8].
  • The J2 recombinant retrovirus expressing v-myc/v-raf (also known as MYC/RAF1) immortalized macrophages from the bone marrow of lipopolysaccharide-responsive mouse strains, producing the ANA-1 cell line from C57BL/6 mice and the INF-3A cell line from C3H/HeN mice [9].
 

Chemical compound and disease context of Nol3

  • The opioid-like neuropeptide nociceptin/orphanin FQ (N/OFQ) and its receptor (NOP) are expressed in the substantia nigra (SN), a brain area containing dopamine neurons that degenerate in Parkinson's disease [10].
  • Pharmacological blockade of the SN N/OFQ-NOP receptor system attenuated parkinsonian-like akinesia/hypokinesia in 6-hydroxydopamine hemilesioned or haloperidol-treated rats, whereas deletion of the NOP receptor gene conferred mice partial protection from haloperidol-induced motor depression [10].
 

Biological context of Nol3

  • Activation of MYC in quiescent rat and mouse fibroblasts elicited re-entry into and progression through the cell cycle, bypassing early events that would follow stimulation of the cells with serum [11].
  • The proto-oncogene MYC encodes a nuclear protein whose biochemical and physiological functions remain uncertain [11].
  • We show that in lymphocytes, MYC overexpression and p27(Kip1) deficiency independently stimulate CDK2 activity and augment the fraction of cells in S phase, in support of their distinct roles in tumorigenesis [2].
  • The protooncogene MYC has been implicated in both the proliferation and programmed cell death of lymphoid cells, and in the genesis of lymphoid tumors [12].
  • These findings are consistent with cellular MYC repression playing a role in innate immunity as well as in control of cell proliferation [3].
 

Anatomical context of Nol3

  • The protooncogene MYC can break B cell tolerance [12].
  • To test this hypothesis directly, we have used a doxycycline-inducible transgenic mouse model to overexpress MYC during different stages of mammary gland development [13].
  • Developmental stage determines the effects of MYC in the mammary epithelium [13].
  • However, we now report that the gene is a target for insertional mutagenesis in T-cell lymphomas of mice carrying a MYC oncogene, where promoter insertion results in overexpression without affecting the integrity of the coding sequence [14].
  • Because liver regeneration is an essential process for achieving liver homeostasis, therapies directed at reducing MYC expression in hepatocellular carcinoma are fraught with the theoretical possibility of injuring adjacent noncancerous liver cells, thereby restricting the liver's normal regenerative response to injury [15].
 

Associations of Nol3 with chemical compounds

  • These effects are resistant to cycloheximide but are inhibited by a dominant-negative ISRE-binding protein, indicating that vIRF acts together with a cellular cofactor at the PRF element to directly transactivate MYC [3].
  • 9. 4. In conclusion, the inhibitory effect of nociceptin/orphanin FQ on dopamine release in the striatum and retina and on noradrenaline release in the cerebral cortex is mediated via NOP receptors [16].
  • The nocifensive responses induced by substance P (i.t.) were also potentiated in NOP(-/-) mice [17].
  • The oncoprotein and DNA were measured fluorimetrically in a flow cytometer using a mouse monoclonal antibody (MYC 1-6E10) and propidium iodide [18].
  • Together, these findings indicate that presynaptic NOP receptors inhibit 5-hydroxytryptamine release in the mouse neocortex [19].
 

Analytical, diagnostic and therapeutic context of Nol3

References

  1. Dominant negative MYC blocks transformation by ABL oncogenes. Sawyers, C.L., Callahan, W., Witte, O.N. Cell (1992) [Pubmed]
  2. Loss of p27(Kip1) but not p21(Cip1) decreases survival and synergizes with MYC in murine lymphomagenesis. Martins, C.P., Berns, A. EMBO J. (2002) [Pubmed]
  3. Three unrelated viral transforming proteins (vIRF, EBNA2, and E1A) induce the MYC oncogene through the interferon-responsive PRF element by using different transcription coadaptors. Jayachandra, S., Low, K.G., Thlick, A.E., Yu, J., Ling, P.D., Chang, Y., Moore, P.S. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
  4. Genomic instability in mouse Burkitt lymphoma is dominated by illegitimate genetic recombinations, not point mutations. Rockwood, L.D., Torrey, T.A., Kim, J.S., Coleman, A.E., Kovalchuk, A.L., Xiang, S., Ried, T., Morse, H.C., Janz, S. Oncogene (2002) [Pubmed]
  5. Dwarfism and dysregulated proliferation in mice overexpressing the MYC antagonist MAD1. Quéva, C., McArthur, G.A., Ramos, L.S., Eisenman, R.N. Cell Growth Differ. (1999) [Pubmed]
  6. Blockade of nociceptin/orphanin FQ-NOP receptor signalling produces antidepressant-like effects: pharmacological and genetic evidences from the mouse forced swimming test. Gavioli, E.C., Marzola, G., Guerrini, R., Bertorelli, R., Zucchini, S., De Lima, T.C., Rae, G.A., Salvadori, S., Regoli, D., Calo, G. Eur. J. Neurosci. (2003) [Pubmed]
  7. Gene expression phenotypic models that predict the activity of oncogenic pathways. Huang, E., Ishida, S., Pittman, J., Dressman, H., Bild, A., Kloos, M., D'Amico, M., Pestell, R.G., West, M., Nevins, J.R. Nat. Genet. (2003) [Pubmed]
  8. Leukemia treatment in severe combined immunodeficiency mice by antisense oligodeoxynucleotides targeting cooperating oncogenes. Skorski, T., Nieborowska-Skorska, M., Campbell, K., Iozzo, R.V., Zon, G., Darzynkiewicz, Z., Calabretta, B. J. Exp. Med. (1995) [Pubmed]
  9. Heterogeneity of hematopoietic cells immortalized by v-myc/v-raf recombinant retrovirus infection of bone marrow or fetal liver. Cox, G.W., Mathieson, B.J., Gandino, L., Blasi, E., Radzioch, D., Varesio, L. J. Natl. Cancer Inst. (1989) [Pubmed]
  10. Blockade of nociceptin/orphanin FQ transmission attenuates symptoms and neurodegeneration associated with Parkinson's disease. Marti, M., Mela, F., Fantin, M., Zucchini, S., Brown, J.M., Witta, J., Di Benedetto, M., Buzas, B., Reinscheid, R.K., Salvadori, S., Guerrini, R., Romualdi, P., Candeletti, S., Simonato, M., Cox, B.M., Morari, M. J. Neurosci. (2005) [Pubmed]
  11. The MYC protein activates transcription of the alpha-prothymosin gene. Eilers, M., Schirm, S., Bishop, J.M. EMBO J. (1991) [Pubmed]
  12. The protooncogene MYC can break B cell tolerance. Refaeli, Y., Field, K.A., Turner, B.C., Trumpp, A., Bishop, J.M. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  13. Developmental stage determines the effects of MYC in the mammary epithelium. Blakely, C.M., Sintasath, L., D'Cruz, C.M., Hahn, K.T., Dugan, K.D., Belka, G.K., Chodosh, L.A. Development (2005) [Pubmed]
  14. Proviral insertion indicates a dominant oncogenic role for Runx1/AML-1 in T-cell lymphoma. Wotton, S., Stewart, M., Blyth, K., Vaillant, F., Kilbey, A., Neil, J.C., Cameron, E.R. Cancer Res. (2002) [Pubmed]
  15. Conditional deletion of c-myc does not impair liver regeneration. Li, F., Xiang, Y., Potter, J., Dinavahi, R., Dang, C.V., Lee, L.A. Cancer Res. (2006) [Pubmed]
  16. Inhibition of striatal and retinal dopamine release via nociceptin/orphanin FQ receptors. Flau, K., Redmer, A., Liedtke, S., Kathmann, M., Schlicker, E. Br. J. Pharmacol. (2002) [Pubmed]
  17. In vivo pain-inhibitory role of nociceptin/orphanin FQ in spinal cord. Inoue, M., Kawashima, T., Takeshima, H., Calo, G., Inoue, A., Nakata, Y., Ueda, H. J. Pharmacol. Exp. Ther. (2003) [Pubmed]
  18. Flow cytometric quantitation of DNA and c-myc oncoprotein in archival biopsies of uterine cervix neoplasia. Hendy-Ibbs, P., Cox, H., Evan, G.I., Watson, J.V. Br. J. Cancer (1987) [Pubmed]
  19. Pharmacological profile of nociceptin/orphanin FQ receptors regulating 5-hydroxytryptamine release in the mouse neocortex. Mela, F., Marti, M., Ulazzi, L., Vaccari, E., Zucchini, S., Trapella, C., Salvadori, S., Beani, L., Bianchi, C., Morari, M. Eur. J. Neurosci. (2004) [Pubmed]
  20. Normal sensitivity to acute pain, but increased inflammatory hyperalgesia in mice lacking the nociceptin precursor polypeptide or the nociceptin receptor. Depner, U.B., Reinscheid, R.K., Takeshima, H., Brune, K., Zeilhofer, H.U. Eur. J. Neurosci. (2003) [Pubmed]
  21. The Pole3 bidirectional unit is regulated by MYC and E2Fs. Bolognese, F., Forni, C., Caretti, G., Frontini, M., Minuzzo, M., Mantovani, R. Gene (2006) [Pubmed]
  22. The NOP (ORL1) receptor antagonist Compound B stimulates mesolimbic dopamine release and is rewarding in mice by a non-NOP-receptor-mediated mechanism. Koizumi, M., Sakoori, K., Midorikawa, N., Murphy, N.P. Br. J. Pharmacol. (2004) [Pubmed]
  23. Oncogenes modulate cell sensitivity to apoptosis induced by glucose deprivation. Kansara, M., Berridge, M.V. Anticancer Res. (2004) [Pubmed]
 
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