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PMID:9590286
| Citation |
Smith, L, Liu, SJ, Goodrich, L, Jacobson, D, Degnin, C, Bentley, N, Carr, A, Flaggs, G, Keegan, K, Hoekstra, M and Thayer, MJ (1998) Duplication of ATR inhibits MyoD, induces aneuploidy and eliminates radiation-induced G1 arrest. Nat. Genet. 19:39-46 |
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| Abstract |
Chromosome 3q alterations occur frequently in many types of tumours. In a genetic screen for loci present in rhabdomyosarcomas, we identified an isochromosome 3q [i(3q)], which inhibits muscle differentiation when transferred into myoblasts. The i(3q) inhibits MyoD function, resulting in a non-differentiating phenotype. Furthermore, the i(3q) induces a 'cut' phenotype, abnormal centrosome amplification, aneuploidy and loss of G1 arrest following gamma-irradiation. Testing candidate genes within this region reveals that forced expression of ataxia-telangiectasia and rad3-related (ATR) results in a phenocopy of the i(3q). Thus, genetic alteration of ATR leads to loss of differentiation as well as cell-cycle abnormalities. |
| Links |
PubMed Online version:10.1038/ng0598-39 |
| Keywords |
Aneuploidy; Cell Cycle Proteins/genetics; Cell Division; Chromosomes, Human, Pair 3; G1 Phase/radiation effects; Humans; Isochromosomes; Multigene Family; Muscles/cytology; MyoD Protein/antagonists & inhibitors; MyoD Protein/physiology; Protein-Serine-Threonine Kinases; Rhabdomyosarcoma/genetics; Rhabdomyosarcoma/pathology; Tumor Cells, Cultured |
| edit table |
Significance
Annotations
| Gene product | Qualifier | GO Term | Evidence Code | with/from | Aspect | Extension | Notes | Status |
|---|---|---|---|---|---|---|---|---|
|
involved_in |
GO:0007275: multicellular organism development |
ECO:0000304: author statement supported by traceable reference used in manual assertion |
P |
Seeded From UniProt |
complete | |||
See also
References
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