TP53-binding protein 1 Antibodies

TP53-binding protein 1 (TP53BP1)

Double-strand break (DSB) repair protein involved in response to DNA damage, telomere dynamics and class-switch recombination (CSR) through antibody genesis (PubMed:12364621, PubMed:22553214, PubMed:23333306, PubMed:17190600, PubMed:21144835, PubMed:28241136). Plays a vital role in the repair of double-strand DNA breaks (DSBs) in response to DNA damage by promoting non-homologous end joining (NHEJ)-mediated repair of DSBs and specifically counteracting the function of the homologous recombination (HR) repair protein BRCA1 (PubMed:22553214, PubMed:23727112, PubMed:23333306).

In response to DSBs, phosphorylation by ATM promotes interaction with RIF1 and dissociation from NUDT16L1/TIRR, leading to recruitment to DSBs websites (PubMed:28241136). Recruited to DSBs websites by recognizing and binding histone H2A monoubiquitinated at'Lys-15' (H2AK15Ub) and histone H4 dimethylated at'Lys-20' (H4K20me2), two histone marks that are found at DSBs websites (PubMed:23760478, PubMed:28241136, PubMed:17190600).

Gene Information

Human
Gene Name:	TP53BP1
Uniprot:	Q12888
Entrez:	7158

Family

Belongs to:
No superfamily

Alternative Names

53BP1; FLJ41424; MGC138366; p202; p53-binding protein 1; p53bp1; TP53BP1; tumor protein 53-binding protein, 1; tumor protein p53 binding protein 1; tumor protein p53-binding protein, 1; tumor suppressor p53-binding protein 1

Molecular Weight

Mass (kDA):
213.574 kDA

Genomic Context

Human
Location:	15q15.3
Sequence:	15; NC_000015.10 (43403061..43510640, complement)

Subcellular Localizations

Nucleus. Chromosome. Chromosome, centromere, kinetochore. Localizes to the nucleus in absence of DNA damage (PubMed:28241136). Following DNA damage, recruited to sites of DNA damage, such as double stand breaks (DSBs): recognizes and binds histone H2A monoubiquitinated at 'Lys-15' (H2AK15Ub) and histone H4 dimethylated at 'Lys-20' (H4K20me2), two histone marks that are present at DSBs sites (PubMed:23333306, PubMed:23760478, PubMed:24703952, PubMed:28241136, PubMed:17190600). Associated with kinetochores during mitosis (By similarity).

Diseases

• Malignant Neoplasms
• Neoplasms
• Ataxia Telangiectasia
• Ataxia
• Telangiectasis
• Mammary Neoplasms
• Malignant Neoplasm Of Breast
• Genomic Instability
• Cell Transformation, Neoplastic
• Carcinoma
• Cytogenetic Abnormality
• Retinoblastoma
• Exposure To Ionizing Radiation

• Malignant Paraganglionic Neoplasm
• Malignant Neoplasm Of Lung
• Growth Arrest
• Osteosarcoma
• Prostatic Neoplasms
• Malignant Squamous Cell Neoplasm
• Immunologic Deficiency Syndromes

Interacting Proteins

• ATM
• BRCA1
• H2AFX
• HIST1H3A
• HIST1H4A

• MEOX2
• MYC
• NCOA6
• PAXIP1
• Paxip1

• PLK1
• SUMO1
• TP53
• VAC14
• VRK1

• ZNHIT1

Pathways

• Dna Repair
• Cell Cycle
• Dna Damage Checkpoint
• Cell Growth
• Dna Replication
• Localization
• Cell Proliferation
• Cell Cycle Checkpoint
• Double-strand Break Repair
• Mitosis
• Senescence
• Methylation
• Cell Death

• Response To Ionizing Radiation
• S Phase
• Hypersensitivity
• Cell Cycle Arrest
• Aging
• Interphase
• Chromatin Remodeling

PTMs

• Phosphorylation
• Methylation
• Ubiquitination
• Deamination

• Dephosphorylation
• Sumoylation
• Demethylation
• Cleavage

• Acetylation

Research Areas

• Breast Cancer
• Cancer
• Checkpoint signaling
• DNA Double Strand Break Repair
• DNA Repair

• Epigenetics
• Tumor Suppressors

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/TP53BP1

Best Uses Of The TP53BP1 Marker

There are several reasons why you should use the TP53BP1 Marker, including its isoform specificity and application range. This article will discuss these and other factors that affect the choice. For example, you might want to use it to identify the presence of certain TP53BP1 isoforms in cancer cells. If you need to test a large number of samples, you should consider using a multichannel pipette. The price of the TP53BP1 is very affordable, and the Boster company offers credit for sharing your results on their website.

TP53BP1 Marker

TP53BP1 is a unique gene that is essential for DNA repair and ribosome synthesis. Its gene product is responsible for the formation of 53BP1 nuclear bodies, a critical step in correct handling of stress-related damage. In addition, it also promotes the assembly of 53BP1 IRIFs, which form at double-strand breaks. However, the authors did not specify how many IRIF foci were observed in cells lacking the 53BP1 gene.

The TP53BP1 antibody from Boster Bio is part of their Picoband(tm) catalog. It reacts with Human. Each vial contains five micrograms of BSA, 0.9 milligrams of sodium chloride and 0.2 mg of Na2HPO4.

In this study, the TP53BP1 NB (transcription factor 53BP) was found in cells lacking RIF1L. This protein is a crucial regulator of 53BP1-NBs in cells with low RIF1-L activity. In addition, 53BP1 NBs are also found around under-replicated DNA in Rif1-L-deficient cells. These cells are also prone to developing unrepaired DNA lesions.

Applications

The TP53BP1 marker was first used to study the effects of X-irradiation on male fertility. It was discovered that this marker, a component of sperm, did not increase following X-irradiation. Researchers also found that the marker could increase after ovulation. The next step in the application of the marker is cloning. The XL53BP1 gene has been described in EMBL and GenBank databases.

The TP53BP1 gene is a known sensor of DNA damage and is recruited to damaged cells through its methylated Lys 79 residue. The protein signals the occurrence of chromatin/DNA damage through the g-H2AX signal. The TP53BP1 gene is located in the nucleus. The gene is expressed on the nucleus of all human cells. Application of the TP53BP1 marker has benefited several fields.

Although the TP53BP1 gene is mutated in most cancers, its alterations in cell survival are due to the overexpression of ATM. In addition to inhibiting the TP53BP1 gene expression, it also inhibits the p53-Chk2 pathway. Moreover, the expression of 53BP1 may be important for the control of checkpoints or for signaling of damage to p53.

The expression of 53BP1 was correlated with the radiosensitivity of CRC cells. It was detected by western blot analysis in four CRC cell lines. Further, the expression levels of 53BP1 and the g-H2AX gene was related to clone formation and radiation dose. The gene's expression level is linearly proportional to the dose of radiation. This marker is used in biodosimetric settings.

Isoform-specificity

The TP53BP1 gene encodes a protein that promotes DNA damage repair and recruitment to sites of DNA damage. It also functions to promote effective repair of DNA DSBs, such as those caused by IR exposure. In addition, 53BP1 is known to have strong functional similarities to yeast orthologues and BRCA1 and MDC1 proteins. However, its function is not completely understood.

The 53BP1 gene was originally discovered in a yeast two-hybrid screen. It is a DNA-binding protein with two C-terminal BRCT motifs. BRCT domains are motifs containing 100-150 residues that are present in many proteins. They play a role in cellular responses to DNA damages. A novel function of the 53BP1 gene is its methylation, which has been associated with its possible DNA-binding activity.

Using a microbeam facility, we evaluated the foci of 53BP1 after radiation. We observed that the foci containing 53BP1 were not found in 15-9BI cells, despite the loss of this histone modification. We concluded that the lack of 53BP1 foci in these cells could be due to reduced or absent dimethylation of K-20 on histone H4. However, we cannot definitively rule out this possibility.

The binding specificity of 53BP1 has been established through interactions between the protein's dimer and modified nucleosomes. These interactions have been shown to disrupt 53BP1's interaction with the nucleosome, inhibit NHEJ, and promote HR. Interestingly, the binding specificity of 53BP1 is mediated by interactions between three different H2A PTMs, which include ubiquitin and USP51.

Cost

The cost of TP53BP1 markers vary widely, but it is generally much cheaper than other types of chromatin-based markers. Biolegend, for example, sells an anti-53BP1 antibody that is part of the W17184B clone. Cell Signaling Technology sells an anti-HA antibody, and Millipore/Sigma also offers an anti-53BP1 marker.

Researchers have shown that this gene plays a key role in protecting cells from genomic instability and DNA damage. The TP53BP1 marker helps in this process by regulating DSB repair. Another function of this gene is the maintenance of heterochromatin. TP53BP1 is also involved in regulating LLPS, which promotes genome stability. To find out whether this gene is present in your cells, you can order a genetic test that tests for this gene.

In this study, 53BP1 is needed for DSB repair, but it also has a role in puncta formation. The H4K20me and OD-4A regions overlap in 53BP1's domain, but the two are distinct functions. This study will determine if 53BP1 performs both functions independently. This is an interesting finding because it confirms the separation of function in this gene.

Safety

The safety of the TP53BP1 marker was evaluated by comparing the numbers of patients who were treated with gH2AX or a control group with no treatment. Untreated patients were not statistically different from those who were not treated. Pearson correlation coefficients were calculated for gH2AX foci and 53BP1 foci. These results were consistent across both groups. The TP53BP1 marker was associated with a significantly decreased risk of developing lung cancer.

In one trial, researchers found that the 53BP1 protein level increased in HR+ and TNBC patients. Although the signal was not correlated with genomic integrity, the TP53BP1 marker could detect features that were not due to DNA damage. The results of the study also indicated that patients with 53BP1 positivity experienced improved survival in the course of treatment. Additionally, patients with a positive 53BP1 test had improved survival through the final visit, which may provide a useful tool for monitoring dynamic changes in chemotherapeutic responsiveness.

In a separate study, Lottersberger and colleagues demonstrated that 53BP1 is required in cells to ensure genomic integrity. The protein needs dynamic microtubules connected to the nuclear envelope to ensure that DNA ends can roam and reconnect. The lack of mobility of DNA ends caused by Eribulin may explain the apparent increase in 53BP1 signals in CTCs from HR+ MBC patients. A second study has shown that Eribulin may affect DSB mobility.