Anti-53BP1 (phospho S25) antibody

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

53BP1 also known as p53-binding protein 1 is a protein that plays an important role in DNA damage response. The 53BP1 protein has a molecular weight of approximately 213 kDa. It is a nuclear protein and it mainly expresses in cells during the DNA damage repair processes. Researchers commonly utilize immunofluorescence and anti-53BP1 antibodies to detect its presence especially for studying DNA repair mechanisms. 53BP1 proves important for maintenance of genomic stability.

Biological function summary

As a DNA damage response mediator 53BP1 functions to recognize and bind to sites of double-strand breaks in DNA promoting non-homologous end joining (NHEJ). This protein is a component of a larger protein complex that recruits factors necessary for DNA repair. Its interaction with DNA lesions also involves chromatin remodeling aiming to facilitate successful repair of the DNA. 53BP1 works in concert with other proteins such as H2AX and MDC1.

Pathways

Researchers observe 53BP1 in processes such as the DNA damage checkpoint and repair pathways. This protein significantly contributes to the pathways involved in maintaining cell cycle checkpoints. It interacts with proteins like ATM and BRCA1 coordinating the cellular response to DNA damage and ensuring that genomic integrity checks occur properly before cell cycle progression continues. These interactions place 53BP1 at a pivotal position in decision-making between repair pathways.

Associated diseases and disorders

Researchers often focus on 53BP1's involvement in cancer development and therapy resistance due to its role in DNA repair. Alterations or deficiencies in 53BP1 levels can contribute to increased susceptibility to tumor development affecting processes like breast cancer and ovarian cancer through its relationship with BRCA1. The improper function of 53BP1 in DNA repair pathways may lead to an accumulation of genetic mutations driving tumorigenesis and impacting the efficacy of certain cancer treatments.