DNA damage-inducible transcript 3
From Wikipedia, the free encyclopedia
DNA-damage-inducible transcript 3, also known as DDIT3, is a human gene.[1]
[edit] References
[edit] Further reading
- Ramji DP, Foka P (2002). "CCAAT/enhancer-binding proteins: structure, function and regulation.". Biochem. J. 365 (Pt 3): 561–75. doi: . PMID 12006103.
- Oyadomari S, Mori M (2004). "Roles of CHOP/GADD153 in endoplasmic reticulum stress.". Cell Death Differ. 11 (4): 381–9. doi: . PMID 14685163.
- Aman P, Ron D, Mandahl N, et al. (1993). "Rearrangement of the transcription factor gene CHOP in myxoid liposarcomas with t(12;16)(q13;p11).". Genes Chromosomes Cancer 5 (4): 278–85. PMID 1283316.
- Park JS, Luethy JD, Wang MG, et al. (1992). "Isolation, characterization and chromosomal localization of the human GADD153 gene.". Gene 116 (2): 259–67. PMID 1339368.
- Ron D, Habener JF (1992). "CHOP, a novel developmentally regulated nuclear protein that dimerizes with transcription factors C/EBP and LAP and functions as a dominant-negative inhibitor of gene transcription.". Genes Dev. 6 (3): 439–53. PMID 1547942.
- Papathanasiou MA, Kerr NC, Robbins JH, et al. (1991). "Induction by ionizing radiation of the gadd45 gene in cultured human cells: lack of mediation by protein kinase C.". Mol. Cell. Biol. 11 (2): 1009–16. PMID 1990262.
- Eneroth M, Mandahl N, Heim S, et al. (1990). "Localization of the chromosomal breakpoints of the t(12;16) in liposarcoma to subbands 12q13.3 and 16p11.2.". Cancer Genet. Cytogenet. 48 (1): 101–7. PMID 2372777.
- Rabbitts TH, Forster A, Larson R, Nathan P (1993). "Fusion of the dominant negative transcription regulator CHOP with a novel gene FUS by translocation t(12;16) in malignant liposarcoma.". Nat. Genet. 4 (2): 175–80. doi: . PMID 7503811.
- Crozat A, Aman P, Mandahl N, Ron D (1993). "Fusion of CHOP to a novel RNA-binding protein in human myxoid liposarcoma.". Nature 363 (6430): 640–4. doi: . PMID 8510758.
- Chen BP, Wolfgang CD, Hai T (1996). "Analysis of ATF3, a transcription factor induced by physiological stresses and modulated by gadd153/Chop10.". Mol. Cell. Biol. 16 (3): 1157–68. PMID 8622660.
- Panagopoulos I, Höglund M, Mertens F, et al. (1996). "Fusion of the EWS and CHOP genes in myxoid liposarcoma.". Oncogene 12 (3): 489–94. PMID 8637704.
- Wang XZ, Ron D (1996). "Stress-induced phosphorylation and activation of the transcription factor CHOP (GADD153) by p38 MAP Kinase.". Science 272 (5266): 1347–9. PMID 8650547.
- Fawcett TW, Eastman HB, Martindale JL, Holbrook NJ (1996). "Physical and functional association between GADD153 and CCAAT/enhancer-binding protein beta during cellular stress.". J. Biol. Chem. 271 (24): 14285–9. PMID 8662954.
- Ubeda M, Vallejo M, Habener JF (1999). "CHOP enhancement of gene transcription by interactions with Jun/Fos AP-1 complex proteins.". Mol. Cell. Biol. 19 (11): 7589–99. PMID 10523647.
- Cui K, Coutts M, Stahl J, Sytkowski AJ (2000). "Novel interaction between the transcription factor CHOP (GADD153) and the ribosomal protein FTE/S3a modulates erythropoiesis.". J. Biol. Chem. 275 (11): 7591–6. PMID 10713066.
- Gotoh T, Oyadomari S, Mori K, Mori M (2002). "Nitric oxide-induced apoptosis in RAW 264.7 macrophages is mediated by endoplasmic reticulum stress pathway involving ATF6 and CHOP.". J. Biol. Chem. 277 (14): 12343–50. doi: . PMID 11805088.
- Satoh T, Toyoda M, Hoshino H, et al. (2002). "Activation of peroxisome proliferator-activated receptor-gamma stimulates the growth arrest and DNA-damage inducible 153 gene in non-small cell lung carcinoma cells.". Oncogene 21 (14): 2171–80. doi: . PMID 11948400.
- Qiao D, Im E, Qi W, Martinez JD (2002). "Activator protein-1 and CCAAT/enhancer-binding protein mediated GADD153 expression is involved in deoxycholic acid-induced apoptosis.". Biochim. Biophys. Acta 1583 (1): 108–16. PMID 12069855.
- Talukder AH, Wang RA, Kumar R (2002). "Expression and transactivating functions of the bZIP transcription factor GADD153 in mammary epithelial cells.". Oncogene 21 (27): 4289–300. doi: . PMID 12082616.
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This article incorporates text from the United States National Library of Medicine, which is in the public domain.
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