Cancer susceptibility is influenced by a complex interplay of genetic, environmental, and lifestyle factors. Key nuclear proteins also play critical roles in genetic factors, either as oncogenes or tumour suppressors, by regulating DNA repair, cell cycle control, and apoptosis. TP53 is a nuclear protein involved in cancer susceptibility, serving as a tumour suppressor by regulating cellular responses to DNA damage and cellular stress. TP53's functions include: 1) The DNA Damage Response. TP53 plays an essential role in detecting DNA damage and initiating cell cycle arrest to allow for DNA repair. If the damage is irreparable, it can also induce apoptosis to eliminate potentially cancerous cells; 2) Cell Cycle Control. TP53 regulates the G1 checkpoint, preventing the progression of cells with damaged DNA into the S phase of the cell cycle. This prevents the propagation of potentially cancer-causing mutations; 3) Apoptosis. In cases of severe DNA damage or genomic instability, TP53 can activate apoptosis, eliminating cells at risk of becoming cancerous; 4) Senescence. TP53 also contributes to cellular senescence, the state of irreversible cell cycle arrest that prevents the proliferation of damaged cells. Mutations in TP53 are common in many cancer types and result in a loss of its tumour-suppressive functions, allowing for uncontrolled cell growth and increased cancer susceptibility. BRCA1 (Breast Cancer Gene 1) is a nuclear protein that plays an important role in DNA repair and maintenance of genomic stability. Mutations in BRCA1 are strongly associated with an increased risk of breast and ovarian cancers. BRCA1 functions include: 1) DNA Repair. BRCA1 is involved in homologous recombination, used in a high-fidelity form of repair of double strand DNA breaks, preventing the accumulation of genetic mutations; 2) Transcription Regulation: BRCA1 has also been shown to regulate the expression of genes involved in cell cycle control and DNA repair, thereby influencing responses to DNA damage; 3) Tumour Suppression. BRCA1 functions as a tumour suppressor by maintaining genomic integrity. Mutations in BRCA1 impair its DNA repair capabilities, leading to a higher probability of cancer development. The RB1 (Retinoblastoma Protein) plays a key role in regulating the cell cycle by inhibiting the progression from the G1 phase to the S phase. Its primary functions include: 1) Cell Cycle Control. RB1 acts as a tumour suppressor by preventing the uncontrolled proliferation of cells. It inhibits the activity of transcription factors like E2F, essential for entering the S phase of the cell cycle; 2) Apoptosis Regulation. RB1 modulates the expression of pro-apoptotic and anti-apoptotic genes, contributing to its tumour-suppressive functions; 3) Senescence. Like TP53, RB1 can induce cellular senescence to halt the growth of damaged or potentially cancerous cells. Mutations in RB1 are linked to the development of retinoblastoma and are associated with an elevated risk of developing osteosarcoma and small-cell lung cancer. Thus, key nuclear proteins such as TP53, BRCA1, and RB1 are critical regulators of cellular processes that maintain genomic stability and prevent cancer development. Mutations or dysregulation of these proteins can lead to an increased susceptibility to various cancers. We offer a comprehensive product catalogue of research tools for investigating cancer susceptibility, including p53 antibodies, Rb antibodies, PTEN antibodies, p53 ELISA Kits, and c-Fos ELISA Kits. Explore our full cancer susceptibility product range below and discover more, for less. Alternatively, you can explore our Tumor Suppressors and Protooncogenes product ranges.