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1. |
PTIP regulates 53BP1-dependent signaling pathway following DNA damage |
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2. |
Observational study of gene-disease association, gene-environment interaction, and pharmacogenomic / toxicogenomic. (HuGE Navigator) |
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3. |
PP5 plays an important role in the regulation of 53BP1 phosphorylation and activity in vivo |
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4. |
Observational study of gene-disease association. (HuGE Navigator) |
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5. |
the interaction between 53BP1 and MDC1 plays a role in the regulation of mitosis |
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6. |
analysis of the 53BP1 Tudor domain recognition of p53 dimethylated at lysine 382 in DNA damage signaling |
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7. |
Additional elements in 53BP1 that facilitate recognition of DNA double-strand breaks, were identified. |
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8. |
Observational study and meta-analysis of gene-disease association. (HuGE Navigator) |
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9. |
NFBD1, 53BP1 and BRCA1 have both unique and redundant functions in radiation-induced phosphorylation and localization events in the ATM-Chk2 pathway. |
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10. |
53BP1 (also known as TRP53BP1), a component of DNA damage foci, changes the dynamic behaviour of chromatin to promote DNA repair |
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11. |
ATM phosphorylates the S1219 residue of 53BP1 in vitro; this residue is phosphorylated in cells exposed to ionizing radiation |
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12. |
Nbs1 has a function in ATR signalling in a manner distinct to any role at stalled replication forks. Replication-independent ATR signalling also requires the mediator proteins, 53BP1 and MDC1, providing direct evidence for their role in ATR signalling. |
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13. |
The two major roles of 53BP1, the checkpoint signaling and repair for DNA damage, can be functionally separated. |
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14. |
RNF8 ubiquitylation pathways are essential for 53BP1 regulation in response to ionizing radiation, whereas RNF8-independent pathways contribute to 53BP1 targeting and phosphorylation in response to UV light and other forms of DNA replication stress |
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15. |
a number of nuclear p53-binding protein 1 foci in human skin tumorigenesis |
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16. |
the phosphorylation-mediated interactions between BLM, 53BP1 and RAD51 are required for their regulatory roles during homologous recombination |
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17. |
Observational study of gene-disease association and gene-environment interaction. (HuGE Navigator) |
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18. |
Observational study of gene-disease association and gene-gene interaction. (HuGE Navigator) |
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19. |
These studies highlight the role of 53BP1 copy loss in primary human DLBCLs and the value of integrative analyses in detecting this genetic lesion in human tumors |
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20. |
analysis of 53BP1 expression can be a useful tool to estimate the level of genomic instability and, simultaneously, the malignant potency of human thyroid tumors. |
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21. |
Contrary to carcinomas, almost no activation or loss of MDC1 or 53BP1 were found among testicular germ-cell tumours (TGCTs), a tumour type with unique biology and exceptionally low incidence of p53 mutations. |
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22. |
These data indicate the existence of a DNA double-strand break-repair protein that functions upstream of 53BP1 and contributes to the normal development of the human immune system. |
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23. |
Genetic variation increases had and neck cancer risk. |
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24. |
53BP1 oligomerization is not dependent on the presence of disulfide bridges |
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25. |
BLM helicase-dependent and -independent roles of TP53BP1 during replication stress-mediated homologous recombination were studied. |
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26. |
Results suggest that 53BP1 and Snm1 may cooperate in the cellular response to genotoxic damage. |
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27. |
53BP1 senses DNA double-stranded breaks indirectly through changes in higher-order chromatin structure that expose the 53BP1 binding site |
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28. |
Thus, optimal repair of damaged replication fork lesions likely requires both ATR and ATM. BLM recruits 53BP1 to these lesions independent of its helicase activity, and optimal activation of ATM requires both p53 and BLM helicase activities. |
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29. |
Pts with p53 gene mutations were 3-times more likely to have an early onset breast cancer. Pts with both missense & silent mutations were 7-times & Pts with mutations in exon 8 of the p53 gene 6 times more likely to have early onset breast cancer. |
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30. |
demonstrated that 53BP1 is a key transducer of the DNA damage checkpoint signal; required for p53 accumulation, G2-M checkpoint arrest, and the intra-S-phase checkpoint in response to ionizing radiation |
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31. |
Jun activation domain-binding protein 1 (Jab1) was identified as a 53BP1-binding protein, and the interaction between them was confirmed to occur in mammalian cells. |
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32. |
Purification, crystallization and preliminary X-ray analysis of the BRCT domains of human 53BP1 bound to the p53 tumour suppressor |
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33. |
53BP1 is an activator of ATM in response to DNA damage [review] |
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34. |
P202 inhibits E2F1-mediated apoptosis in prostate cancer cells |
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35. |
In cells with wild-type Nbs1, suppression of 53BP1 expression had no effect on ATM activation but was associated with increased recruitment of NFBD1/MDC1 and Nbs1 to sites of DNA breaks. |
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36. |
a glycine-arginine rich (GAR) stretch of 53BP1 lying upstream of the Tudor motifs is methylated by PRMT1 |
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37. |
GAR (Glycine Arginine rich) motif is a region required for 53BP1 DNA binding activity and as the site of methylation by PRMT1. |
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38. |
crystal structure of human 53BP1 BRCT domains bound to p53 tumour suppressor |
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39. |
LC8 binds to p53-binding protein 1 and mediates DNA damage-induced p53 nuclear accumulation |
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40. |
Structure of the human 53BP1 BRCT region bound to p53 and its comparison to the rat Brca1 BRCT structure is presented. |
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41. |
53BP1 functions as a DNA damage checkpoint protein |
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42. |
Using X-ray crystallography and NMR spectroscopy, we show that, despite low amino acid sequence conservation, both 53BP1 and Crb2 contain tandem tudor domains that interact with histone H4 specifically dimethylated at Lys20 (H4-K20me2). |
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43. |
analysis of nonconserved residues that enforced p53 core domain binding with BRCA1-BRCT in a way similar to p53-53BP1 binding |
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44. |
53BP1 has the potential to participate directly in the repair of DNA double-strand breaks |
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45. |
the BRCA1 promoter is positively regulated by 53BP1 |
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46. |
Snm1 and 53BP1 are components of a mitotic stress checkpoint that negatively targets the APC prior to chromosome condensation |
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47. |
53BP1 only has limited checkpoint functions but rather acts as an adaptor in the repair of DNA double strand breaks |
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48. |
This protein interacts with HDAC4 protein to mediate DNA damage response. |
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49. |
53BP1 is involved in a pathway with NFBD1, H2AX, and Chk2 in recruitment of repair and signaling proteins to sites of DNA damage |
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50. |
RNA has a role in the binding of 53BP1 to chromatin damaged by ionizing radiation |