HCSGD entry for TP53BP1
1. General information
| Official gene symbol | TP53BP1 |
|---|---|
| Entrez ID | 7158 |
| Gene full name | tumor protein p53 binding protein 1 |
| Other gene symbols | 53BP1 p202 |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0000724 | Double-strand break repair via homologous recombination | TAS | biological_process |
| GO:0000777 | Condensed chromosome kinetochore | IEA | cellular_component |
| GO:0000781 | Chromosome, telomeric region | IDA | cellular_component |
| GO:0001102 | RNA polymerase II activating transcription factor binding | IPI | molecular_function |
| GO:0001104 | RNA polymerase II transcription cofactor activity | IMP | molecular_function |
| GO:0002039 | P53 binding | IPI | molecular_function |
| GO:0003684 | Damaged DNA binding | IEA | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005634 | Nucleus | IDA | cellular_component |
| GO:0005654 | Nucleoplasm | TAS | cellular_component |
| GO:0005657 | Replication fork | IEA | cellular_component |
| GO:0005737 | Cytoplasm | IDA | cellular_component |
| GO:0006281 | DNA repair | TAS | biological_process |
| GO:0006302 | Double-strand break repair | TAS | biological_process |
| GO:0006366 | Transcription from RNA polymerase II promoter | IMP | biological_process |
| GO:0006974 | Cellular response to DNA damage stimulus | IDA | biological_process |
| GO:0035064 | Methylated histone residue binding | IDA | molecular_function |
| GO:0042162 | Telomeric DNA binding | IEA | molecular_function |
| GO:0045893 | Positive regulation of transcription, DNA-templated | NAS | biological_process |
| GO:0045944 | Positive regulation of transcription from RNA polymerase II promoter | IMP | biological_process |
| GO:0051091 | Positive regulation of sequence-specific DNA binding transcription factor activity | IC | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.0738013297 | 0.8236192356 | 0.5771018419 | 1.0000000000 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
| Data source | Up or down | Log fold change |
|---|---|---|
| GSE11954 | Up | 0.1335688120 |
| GSE13712_SHEAR | Down | -0.2116994539 |
| GSE13712_STATIC | Down | -0.1326174076 |
| GSE19018 | Up | 0.1668577840 |
| GSE19899_A1 | Down | -0.0835469343 |
| GSE19899_A2 | Down | -0.4453859918 |
| PubMed_21979375_A1 | Down | -0.1497173172 |
| PubMed_21979375_A2 | Up | 0.1858374300 |
| GSE35957 | Up | 0.1725619233 |
| GSE36640 | Up | 0.1999863138 |
| GSE54402 | Down | -0.0684083102 |
| GSE9593 | Down | -0.0602951270 |
| GSE43922 | Up | 0.0245539093 |
| GSE24585 | Up | 0.4345195583 |
| GSE37065 | Down | -0.0888938389 |
| GSE28863_A1 | Up | 1.0812899847 |
| GSE28863_A2 | Up | 1.0363856256 |
| GSE28863_A3 | Up | 0.0683864942 |
| GSE28863_A4 | Up | 0.1206697676 |
| GSE48662 | Up | 0.1413471591 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Not regulated by drugs
- MicroRNAs
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-505-3p | MIMAT0002876 | MIRT041027 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-361-5p | MIMAT0000703 | MIRT044109 | CLASH | Functional MTI (Weak) | 23622248 |
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- mirRecord
No target information from mirRecord
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 29 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 27349711 | Compared with the healthy group, hemodialyzed and transplanted patients exhibited a significant decrease in telomere length, an increase in p16(INK4A) mRNA expression and in lymphocytes with 53BP1 foci |
| 27160904 | We find that a reduced USP1 level causes aberrant aggregation of its target FANCD2 concomitant with replication stress, accumulation, and colocalization of gamma-H2Ax and p53-binding protein 1 (53BP1) in large and unusual sparse DNA damage foci and an increased number of polyploid cells and cells arrested in G2/M, as well as a sensitization of senescence-bypassing cells to DNA interstrand crosslinking-mediated cell death |
| 27041576 | Here, we show that oncogenic Ras expression in human primary cells results in the downregulation of BRCA1 and 53BP1, two key factors in DNA DSB repair by homologous recombination and non-homologous end joining, respectively |
| 27041576 | As a consequence, Ras-induced senescent cells are hindered in their ability to recruit BRCA1 and 53BP1 to DNA damage sites |
| 27041576 | Whereas BRCA1 is downregulated at transcripts levels, 53BP1 loss is caused by activation of cathepsin L-mediated degradation of 53BP1 protein |
| 26871293 | These effects of As2O3 trigger an extensive DNA damage response at the telomere, which includes up-regulation of ATM, ATR, 53BP1, gamma-H2AX and Mer11, in parallel with telomere fusion and 3'-overhang degradation |
| 26864624 | The RCC1-induced inhibition of senescence required Ran and exportin 1 and involved the activation of importin beta-dependent nuclear import of 53BP1, a large NCT cargo |
| 26718258 | Previously, we showed that the sesquiterpene lactone, dehydroleucodine (DhL), promotes the accumulation of DNA damage markers, such as H2AX and 53BP1, in human tumor cells |
| 26414019 | Senescence-associated beta-galactosidase (SA-betaGal) activity, Ki67 (cycling cells), large 53BP1 foci (irreparable DNA strand breaks) and p16(INK) (4A) (late senescence) were used as markers of cellular senescence and were quantified using indirect immunofluorescence and the ImageJ program |
| 25238775 | X) in cells treated with 3,3',4,4'-THS was diminished, which coincided with suppression of the DNA damage response transducer, 53BP1 |
| 25171524 | Double strand break (DSB) repair is suppressed during mitosis because RNF8 and downstream DNA damage response (DDR) factors, including 53BP1, do not localize to mitotic chromatin |
| 24155329 | Accumulation of prelamin A in nuclei of cells from centenarians elicits loss of heterochromatin, as well as recruitment of the inactive form of 53BP1, associated with rapid response to oxidative stress |
| 24155329 | These effects, including the prelamin-A-mediated increase of nuclear 53BP1, can be reproduced by rapamycin treatment of cells from younger individuals |
| 24155329 | These data identify prelamin A and 53BP1 as new targets of rapamycin that are associated with human longevity |
| 23979016 | While mIno80 is required for efficient repair of DNA double strand breaks, its depletion did not impact upon the formation of gamma-H2AX and 53BP1 DNA damage foci, or the activation of the ATM-CHK2-dependent DNA damage response |
| 23691119 | Electron microscopy combined with immunogold-labeling showed multiple small 53BP1 clusters diffusely distributed throughout the highly compacted heterochromatin of aged HFSCs, but single large 53BP1 clusters in irradiated HFSCs |
| 23691119 | These remaining 53BP1 clusters did not colocalize with core components of non-homologous end-joining, but with heterochromatic histone modifications |
| 23341930 | We demonstrate for the first time that treatment of cancer cells with DhL, promotes the accumulation of DNA damage markers such as phosphorylation of ATM and focal organization of gammaH2AX and 53BP1 |
| 21641119 | Recently, accumulating evidences have showed that p53-binding protein 1 (53BP1) plays an important role in DNA double-strand breaks (DSBs) repair induced by radiation |
| 21641119 | In vivo studies also showed suppressive effect of 53BP1 on tumor initiation and progression |
| 21641119 | Therefore, we hypothesize that 53BP1 has a profound effect on suppressing breast cancer as a tumor suppressor and will be an important new biomarker for breast cancer prognosis |
| 21641119 | Furthermore, 53BP1 gene therapy will be a potential therapeutic strategy for breast cancer |
| 21408175 | Using combined immunofluorescence and telomere-fluorescence in-situ hybridization we show that gammaH2AX-foci co-localize consistently with other repair factors such as pATM, MDC1 and 53BP1, but not significantly with telomeres, strongly supporting the telomere-independent origin for the majority of foci |
| 26097382 | As an IRIF reporter, we have expressed an inducible green fluorescent protein (GFP) fusion to the IRIF-binding domain (IBD) of 53BP1 (GFP-IBD) in the breast cancer cell line MCF7 |
| 21118958 | Importantly, depletion of the DNA-SCARS-stabilizing component histone H2AX did not deplete 53BP1 from DNA-SCARS but diminished the presence of MDC1 and activated CHK2 |
| 20610628 | As an IRIF reporter, we tracked the relocalization of green fluorescent protein fused to a chromatin binding domain of the checkpoint adapter protein 53BP1 after IR of breast cancer cells and tumors |
| 19946210 | Importantly, there was no accumulation of 53BP1 in gammaH2AX foci of senescent cells |
| 19806024 | DNA damage foci in mitosis are devoid of 53BP1 |
| 19806024 | 53BP1 is one central mediator of the DNA damage response and a component of active DNA damage foci |
| 19806024 | Using an AcGFP-53BP1c fluorescent fusion protein that quantitatively reports DNA damage, we show that the recruitment of 53BP1 into gammaH2A |
| 19716796 | A selective requirement for 53BP1 in the biological response to genomic instability induced by Brca1 deficiency |
| 19716796 | Using mouse embryonic fibroblasts with constitutively increased DNA damage due to the absence of the full-length form of the tumor suppressor Brca1 (Brca1(Delta 11/Delta 11)), we show that deletion of p53 binding protein 1 (53BP1) selectivity abrogates senescence and cell death stimulated by reduced Brca1 activity |
| 19716796 | Furthermore, the embryonic lethality induced by Brca1 mutation can be alleviated by 53BP1 deletion |
| 19716796 | Together, these in vitro and in vivo data suggest that 53BP1 is specifically required for the development of premature senescence and apoptosis induced by Brca1 deficiency |
| 19651821 | Hypothesizing that this effect, known as the radiation-induced bystander effect, may be a specific instance of communication between damaged and undamaged cells regardless of damage source, we demonstrated that exposure of target cells to non-IR induces bystander damage in non-targeted cells as measured by gamma-H2AX and 53BP1 focal formation |
| 19651821 | One of these, transforming growth factor beta (TGF-beta), and nitric oxide (NO) were found to elevate numbers of gamma-H2AX/53BP1 foci in normal cell cultures similar to levels found in bystander cells, and this elevation was abrogated by NO synthase inhibitors, TGF-beta blocking antibody and antioxidants |
| 19650831 | This characteristic phenotype included persistently activated DNA damage signalling (detected as 53BP1/gammaH2AX(+) foci), enhanced senescence-associated beta-galactosidase activity, expansion of promyelocytic leukaemia nuclear compartments and induced expression of several cytokines (especially interleukins IL-6, IL-8 and IL-24), overall features shared by cells undergoing replicative or premature cellular senescence |
| 19077045 | In agreement with the fact that telomere uncapping triggers lymphocyte senescence, we observed an increase in gamma-H2AX and 53BP1 foci as well as in the percentage of cells exhibiting DNA damage foci in telomeres |
| 18941635 | Indeed, we found a substantial increase in persistent 53BP1 and gammaH2AX DNA damage foci in Ku80-/- as compared to wild-type liver |
| 18440596 | The cellular DNA damage response (DDR) entails the activation of ATM, ATR and/or DNA PK protein kinases that causes modifications of proteins including Chk1, Chk2 and 53BP1, aggregation of DDR proteins into foci, and activation of p53 |
| 18001825 | We have shown that RNF8 facilitates the accumulation of checkpoint mediator proteins BRCA1 and 53BP1 to the damaged chromatin, on one hand through the phospho-dependent FHA domain-mediated binding of RNF8 to MDC1, on the other hand via its role in ubiquitylating H2AX and possibly other substrates at damage sites |
| 17981573 | The family includes structurally and functionally-related mouse (for example, p202, p203, and p204 proteins) and human (for example, MNDA, AIM2, and IFIX) proteins |
| 16287861 | Withdrawal of WRN or BLM produced accelerated cellular senescence phenotype and DNA damage response in normal fibroblasts, as evidenced by induction of gammaH2AX and 53BP1 nuclear foci |
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