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Gene Review

Trp53bp1  -  transformation related protein 53 binding...

Mus musculus

Synonyms: 53BP1, Tp53bp1, Tumor suppressor p53-binding protein 1, m53BP1, p53-binding protein 1, ...
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High impact information on Trp53bp1

  • Using a human cell line that faithfully recapitulated the Chk2-p53-PUMA pathway, we show that USP28 is required to stabilize Chk2 and 53BP1 in response to DNA damage [1].
  • Recruitment of p53 binding protein 1 (53BP1) and Rad51 to sites of DNA lesion is impaired in Zmpste24-/- MEFs and in HGPS fibroblasts, resulting in delayed checkpoint response and defective DNA repair [2].
  • The acceleration of NHEJ was unlikely to be due to increased presence of 53BP1 and Mre11 in TIFs, since knockdown of neither factor affected telomere fusions [3].
  • The current findings, in combination with the known 53BP1 functions and how it is activated, implicate the DNA damage response to DSBs in the joining phase of class-switch recombination [4].
  • We now examine potential functions for 53BP1 in the specific genomic alterations that occur in B lymphocytes [4].

Biological context of Trp53bp1


Anatomical context of Trp53bp1

  • GFP-M protein forms foci in mouse embryonic fibroblast cells lacking functional endogenous 53BP1 [7].
  • RT-PCR analysis revealed that p53BP1 was expressed specifically in fully grown oocytes, as was HDAC4 [8].

Associations of Trp53bp1 with chemical compounds

  • Aside from p53, we here identify 53BP1 as a critical mediator of nutlin-3-induced cytotoxicity [9].

Physical interactions of Trp53bp1


Enzymatic interactions of Trp53bp1


Other interactions of Trp53bp1

  • These data indicate that 53BP1 acts downstream of ATM and upstream of Chk2 in the DNA damage response pathway and is involved in tumor suppression [5].
  • Moreover, activated B cells deficient for ATM, 53BP1, or MDC1, which interact with H2AX during the DSB response, show similarly increased IgH locus breaks and translocations [11].
  • 53BP1 links DNA damage-response pathways to immunoglobulin heavy chain class-switch recombination [4].
  • Although 53BP1 was dispensable for V(D)J recombination and somatic hypermutation (SHM), the processes by which immunoglobulin (Ig) variable region exons are assembled and mutated, it was required for Igh class-switch recombination (CSR), the recombination and deletion process by which Igh constant region genes are exchanged [4].
  • One of the trapped genes was endoglin, an endothelial-specific transforming growth factor-beta type III receptor, and another was ASPP1, a p53-binding protein [12].

Analytical, diagnostic and therapeutic context of Trp53bp1

  • By generating mice defective in m53BP1 (m53BP1(tr/tr)), we have created an animal model to further explore its biochemical and genetic roles in vivo [10].


  1. A role for the deubiquitinating enzyme USP28 in control of the DNA-damage response. Zhang, D., Zaugg, K., Mak, T.W., Elledge, S.J. Cell (2006) [Pubmed]
  2. Genomic instability in laminopathy-based premature aging. Liu, B., Wang, J., Chan, K.M., Tjia, W.M., Deng, W., Guan, X., Huang, J.D., Li, K.M., Chau, P.Y., Chen, D.J., Pei, D., Pendas, A.M., Cadiñanos, J., López-Otín, C., Tse, H.F., Hutchison, C., Chen, J., Cao, Y., Cheah, K.S., Tryggvason, K., Zhou, Z. Nat. Med. (2005) [Pubmed]
  3. MDC1 accelerates nonhomologous end-joining of dysfunctional telomeres. Dimitrova, N., de Lange, T. Genes Dev. (2006) [Pubmed]
  4. 53BP1 links DNA damage-response pathways to immunoglobulin heavy chain class-switch recombination. Manis, J.P., Morales, J.C., Xia, Z., Kutok, J.L., Alt, F.W., Carpenter, P.B. Nat. Immunol. (2004) [Pubmed]
  5. p53 Binding protein 53BP1 is required for DNA damage responses and tumor suppression in mice. Ward, I.M., Minn, K., van Deursen, J., Chen, J. Mol. Cell. Biol. (2003) [Pubmed]
  6. 53BP1 and p53 synergize to suppress genomic instability and lymphomagenesis. Morales, J.C., Franco, S., Murphy, M.M., Bassing, C.H., Mills, K.D., Adams, M.M., Walsh, N.C., Manis, J.P., Rassidakis, G.Z., Alt, F.W., Carpenter, P.B. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  7. 53BP1 exchanges slowly at the sites of DNA damage and appears to require RNA for its association with chromatin. Pryde, F., Khalili, S., Robertson, K., Selfridge, J., Ritchie, A.M., Melton, D.W., Jullien, D., Adachi, Y. J. Cell. Sci. (2005) [Pubmed]
  8. Stage specific expression of histone deacetylase 4 (HDAC4) during oogenesis and early preimplantation development in mice. Kageyama, S., Liu, H., Nagata, M., Aoki, F. J. Reprod. Dev. (2006) [Pubmed]
  9. An shRNA barcode screen provides insight into cancer cell vulnerability to MDM2 inhibitors. Brummelkamp, T.R., Fabius, A.W., Mullenders, J., Madiredjo, M., Velds, A., Kerkhoven, R.M., Bernards, R., Beijersbergen, R.L. Nat. Chem. Biol. (2006) [Pubmed]
  10. Role for the BRCA1 C-terminal repeats (BRCT) protein 53BP1 in maintaining genomic stability. Morales, J.C., Xia, Z., Lu, T., Aldrich, M.B., Wang, B., Rosales, C., Kellems, R.E., Hittelman, W.N., Elledge, S.J., Carpenter, P.B. J. Biol. Chem. (2003) [Pubmed]
  11. H2AX prevents DNA breaks from progressing to chromosome breaks and translocations. Franco, S., Gostissa, M., Zha, S., Lombard, D.B., Murphy, M.M., Zarrin, A.A., Yan, C., Tepsuporn, S., Morales, J.C., Adams, M.M., Lou, Z., Bassing, C.H., Manis, J.P., Chen, J., Carpenter, P.B., Alt, F.W. Mol. Cell (2006) [Pubmed]
  12. Gene-trap expression screening to identify endothelial-specific genes. Hirashima, M., Bernstein, A., Stanford, W.L., Rossant, J. Blood (2004) [Pubmed]
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