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Tytuł pozycji:

53BP1 and p53 synergize to suppress genomic instability and lymphomagenesis.

Tytuł:
53BP1 and p53 synergize to suppress genomic instability and lymphomagenesis.
Autorzy:
Morales JC; Department of Biochemistry and Molecular Biology, University of Texas Health Sciences Center, Houston, 77030, USA.
Franco S
Murphy MM
Bassing CH
Mills KD
Adams MM
Walsh NC
Manis JP
Rassidakis GZ
Alt FW
Carpenter PB
Źródło:
Proceedings of the National Academy of Sciences of the United States of America [Proc Natl Acad Sci U S A] 2006 Feb 28; Vol. 103 (9), pp. 3310-5. Date of Electronic Publication: 2006 Feb 21.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Original Publication: Washington, DC : National Academy of Sciences
MeSH Terms:
Genomic Instability/*genetics
Intracellular Signaling Peptides and Proteins/*metabolism
Lymphoma/*genetics
Lymphoma/*pathology
Phosphoproteins/*metabolism
Thymus Neoplasms/*metabolism
Thymus Neoplasms/*pathology
Tumor Suppressor Protein p53/*metabolism
Animals ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Cell Transformation, Neoplastic/pathology ; Cells, Cultured ; Chromosomal Proteins, Non-Histone ; Chromosomes, Mammalian/genetics ; Cytosol/metabolism ; DNA-Binding Proteins ; Intracellular Signaling Peptides and Proteins/deficiency ; Intracellular Signaling Peptides and Proteins/genetics ; Lymphoma/metabolism ; Mice ; Mice, Knockout ; Mutation/genetics ; Phosphoproteins/deficiency ; Phosphoproteins/genetics ; Survival Rate ; Thymus Neoplasms/genetics ; Tumor Suppressor Protein p53/deficiency ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor p53-Binding Protein 1
References:
Mol Carcinog. 1995 Sep;14(1):16-22. (PMID: 7546219)
Cell Cycle. 2005 Dec;4(12):1854-61. (PMID: 16294047)
Mol Cell Biol. 1998 Jun;18(6):3495-501. (PMID: 9584189)
Mol Cell Biol. 2004 Dec;24(23):10448-55. (PMID: 15542852)
Nature. 2004 Nov 18;432(7015):406-11. (PMID: 15525939)
J Cell Sci. 2002 Jan 1;115(Pt 1):71-9. (PMID: 11801725)
Cell. 2002 Apr;109 Suppl:S45-55. (PMID: 11983152)
Science. 2002 May 3;296(5569):922-7. (PMID: 11934988)
Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8173-8. (PMID: 12034884)
Cancer Res. 2002 Nov 1;62(21):6194-204. (PMID: 12414647)
Mol Cell Biol. 2002 Dec;22(24):8635-47. (PMID: 12446782)
Nat Cell Biol. 2002 Dec;4(12):993-7. (PMID: 12447390)
Nature. 2003 Feb 27;421(6926):961-6. (PMID: 12607005)
Mol Cell Biol. 2003 Apr;23(7):2556-63. (PMID: 12640136)
J Biol Chem. 2003 Apr 25;278(17):14971-7. (PMID: 12578828)
J Biol Chem. 2003 May 30;278(22):19579-82. (PMID: 12697768)
Cell. 2003 Aug 8;114(3):359-70. (PMID: 12914700)
Cell. 2003 Aug 8;114(3):371-83. (PMID: 12914701)
J Biol Chem. 2003 Sep 19;278(38):36487-95. (PMID: 12824158)
Mol Cell. 2003 Dec;12(6):1511-23. (PMID: 14690604)
Cancer Res. 2003 Dec 15;63(24):8586-91. (PMID: 14695167)
Cell Cycle. 2004 Feb;3(2):149-53. (PMID: 14712078)
Genes Dev. 2004 Jan 1;18(1):1-11. (PMID: 14724175)
Proc Natl Acad Sci U S A. 2004 Feb 24;101(8):2410-5. (PMID: 14983023)
Nat Immunol. 2004 May;5(5):481-7. (PMID: 15077110)
J Cell Biol. 2004 May 24;165(4):459-64. (PMID: 15159415)
DNA Repair (Amst). 2004 Aug-Sep;3(8-9):945-52. (PMID: 15279780)
J Cell Biol. 2004 Sep 13;166(6):801-13. (PMID: 15364958)
Nature. 1992 Mar 19;356(6366):215-21. (PMID: 1552940)
Curr Biol. 1994 Jan 1;4(1):1-7. (PMID: 7922305)
Mol Cell Biol. 2005 Jan;25(2):661-70. (PMID: 15632067)
Cell. 2005 Feb 25;120(4):497-512. (PMID: 15734682)
Nature. 2005 Apr 14;434(7035):907-13. (PMID: 15829965)
J Cell Biol. 2005 Jul 18;170(2):201-11. (PMID: 16009723)
Mol Cell Biol. 2005 Nov;25(22):10079-86. (PMID: 16260621)
Nat Genet. 1996 Nov;14(3):312-5. (PMID: 8896561)
Grant Information:
P01 CA109901 United States CA NCI NIH HHS; GM65812 United States GM NIGMS NIH HHS; P01 CA092625 United States CA NCI NIH HHS; R56 GM065812 United States GM NIGMS NIH HHS; CA92625 United States CA NCI NIH HHS; R01 GM065812 United States GM NIGMS NIH HHS; CA109901 United States CA NCI NIH HHS
Substance Nomenclature:
0 (Chromosomal Proteins, Non-Histone)
0 (DNA-Binding Proteins)
0 (Intracellular Signaling Peptides and Proteins)
0 (Phosphoproteins)
0 (Trp53bp1 protein, mouse)
0 (Tumor Suppressor Protein p53)
0 (Tumor Suppressor p53-Binding Protein 1)
Entry Date(s):
Date Created: 20060224 Date Completed: 20060410 Latest Revision: 20181113
Update Code:
20240104
PubMed Central ID:
PMC1413919
DOI:
10.1073/pnas.0511259103
PMID:
16492765
Czasopismo naukowe
p53-binding protein 1 (53BP1) participates in the cellular response to DNA double-stranded breaks where it associates with various DNA repair/cell cycle factors including the H2AX histone variant. Mice deficient for 53BP1 (53BP1(-/-)) are sensitive to ionizing radiation and immunodeficient because of impaired Ig heavy chain class switch recombination. Here we show that, as compared with p53(-/-) mice, 53BP1(-/-)/p53(-/-) animals more rapidly develop tumors, including T cell lymphomas and, at lower frequency, B lineage lymphomas, sarcomas, and teratomas. In addition, T cells from animals deficient for both 53BP1 and p53 (53BP1(-/-)/p53(-/-)) display elevated levels of genomic instability relative to T cells deficient for either 53BP1 or p53 alone. In contrast to p53(-/-) T cell lymphomas, which routinely display aneuploidy but not translocations, 53BP1(-/-)/p53(-/-) thymic lymphomas fall into two distinct cytogenetic categories, with many harboring clonal translocations (40%) and the remainder showing aneuploidy (60%). We propose that 53BP1, in the context of p53 deficiency, suppresses T cell lymphomagenesis through its roles in both cell-cycle checkpoints and double-stranded break repair.

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