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DDIT4  -  DNA-damage-inducible transcript 4

Homo sapiens

Synonyms: DNA damage-inducible transcript 4 protein, Dig2, FLJ20500, HIF-1 responsive protein RTP801, Protein regulated in development and DNA damage response 1, ...
 
 
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Disease relevance of DDIT4

 

High impact information on DDIT4

  • Several gene products, such as BNip3, RTP801, and Noxa, were identified as HIF-1 alpha-responsive proapoptotic proteins, but the complicated hypoxic cell death pathways could not be completely explained by the few known genes [6].
  • Identification of a novel hypoxia-inducible factor 1-responsive gene, RTP801, involved in apoptosis [1].
  • However, expression of RTP801 appeared toxic for nondividing neuron-like PC12 cells and increased their sensitivity to ischemic injury and oxidative stress [1].
  • Here, we report the identification and cloning of a novel HIF-1-responsive gene, designated RTP801 [1].
  • Liposomal delivery of RTP801 cDNA to mouse lungs also resulted in massive cell death [1].
 

Biological context of DDIT4

 

Anatomical context of DDIT4

 

Associations of DDIT4 with chemical compounds

  • Overall, the data support the conclusion that REDD1 functions upstream of Tuberin and Rheb to down-regulate mTOR signaling in response to dexamethasone [7].
  • Here, we investigated the mechanism by which a DNA damaging agent, methyl methanesulfonate (MMS), induces RTP801 transcription [10].
  • RTP801 is a novel retinoic acid-responsive gene associated with myeloid differentiation [11].
  • Arsenite induces a cell stress-response gene, RTP801, through reactive oxygen species and transcription factors Elk-1 and CCAAT/enhancer-binding protein [12].
  • Such a stimulatory effect was inhibited by co-expression of superoxide dismutase or glutathione peroxidase, and was abrogated by N-acetylcysteine, implying that ROS (reactive oxygen species) were involved in transcriptional regulation of the RTP801 gene [12].
 

Other interactions of DDIT4

 

Analytical, diagnostic and therapeutic context of DDIT4

  • To assess the relevance of these observations to PD, we used immunohistochemistry to compare RTP801 expression in postmortem brains from PD and control patients [4].

References

  1. Identification of a novel hypoxia-inducible factor 1-responsive gene, RTP801, involved in apoptosis. Shoshani, T., Faerman, A., Mett, I., Zelin, E., Tenne, T., Gorodin, S., Moshel, Y., Elbaz, S., Budanov, A., Chajut, A., Kalinski, H., Kamer, I., Rozen, A., Mor, O., Keshet, E., Leshkowitz, D., Einat, P., Skaliter, R., Feinstein, E. Mol. Cell. Biol. (2002) [Pubmed]
  2. REDD1 integrates hypoxia-mediated survival signaling downstream of phosphatidylinositol 3-kinase. Schwarzer, R., Tondera, D., Arnold, W., Giese, K., Klippel, A., Kaufmann, J. Oncogene (2005) [Pubmed]
  3. Identification of amyloid beta-peptide responsive genes by cDNA microarray technology: involvement of RTP801 in amyloid beta-peptide toxicity. Kim, J.R., Lee, S.R., Chung, H.J., Kim, S., Baek, S.H., Kim, J.H., Kim, Y.S. Exp. Mol. Med. (2003) [Pubmed]
  4. RTP801 is elevated in Parkinson brain substantia nigral neurons and mediates death in cellular models of Parkinson's disease by a mechanism involving mammalian target of rapamycin inactivation. Malagelada, C., Ryu, E.J., Biswas, S.C., Jackson-Lewis, V., Greene, L.A. J. Neurosci. (2006) [Pubmed]
  5. Inhibition of oxygen-induced retinopathy in RTP801-deficient mice. Brafman, A., Mett, I., Shafir, M., Gottlieb, H., Damari, G., Gozlan-Kelner, S., Vishnevskia-Dai, V., Skaliter, R., Einat, P., Faerman, A., Feinstein, E., Shoshani, T. Invest. Ophthalmol. Vis. Sci. (2004) [Pubmed]
  6. Identification of the hypoxia-inducible factor 1 alpha-responsive HGTD-P gene as a mediator in the mitochondrial apoptotic pathway. Lee, M.J., Kim, J.Y., Suk, K., Park, J.H. Mol. Cell. Biol. (2004) [Pubmed]
  7. Dexamethasone Represses Signaling through the Mammalian Target of Rapamycin in Muscle Cells by Enhancing Expression of REDD1. Wang, H., Kubica, N., Ellisen, L.W., Jefferson, L.S., Kimball, S.R. J. Biol. Chem. (2006) [Pubmed]
  8. Sp1-dependent regulation of the RTP801 promoter and its application to hypoxia-inducible VEGF plasmid for ischemic disease. Lee, M., Bikram, M., Oh, S., Bull, D.A., Kim, S.W. Pharm. Res. (2004) [Pubmed]
  9. REDD2 gene is upregulated by modified LDL or hypoxia and mediates human macrophage cell death. Cuaz-Pérolin, C., Furman, C., Larigauderie, G., Legedz, L., Lasselin, C., Copin, C., Jaye, M., Searfoss, G., Yu, K.T., Duverger, N., Nègre-Salvayre, A., Fruchart, J.C., Rouis, M. Arterioscler. Thromb. Vasc. Biol. (2004) [Pubmed]
  10. Induction of a cell stress response gene RTP801 by DNA damaging agent methyl methanesulfonate through CCAAT/enhancer binding protein. Lin, L., Qian, Y., Shi, X., Chen, Y. Biochemistry (2005) [Pubmed]
  11. RTP801 is a novel retinoic acid-responsive gene associated with myeloid differentiation. Gery, S., Park, D.J., Vuong, P.T., Virk, R.K., Muller, C.I., Hofmann, W.K., Koeffler, H.P. Exp. Hematol. (2007) [Pubmed]
  12. Arsenite induces a cell stress-response gene, RTP801, through reactive oxygen species and transcription factors Elk-1 and CCAAT/enhancer-binding protein. Lin, L., Stringfield, T.M., Shi, X., Chen, Y. Biochem. J. (2005) [Pubmed]
  13. Growth control under stress: mTOR regulation through the REDD1-TSC pathway. Ellisen, L.W. Cell Cycle (2005) [Pubmed]
 
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