Oncoproteins are a diverse group of proteins associated with the development and progression of cancer. They can be derived from mutated or dysregulated normal cellular proteins (proto-oncogenes) but can also be present in some viruses associated with cancer development. Perhaps the best-known oncoproteins belong to the Ras family. Ras proteins (e.g., H-Ras, K-Ras, N-Ras) are critical regulators of cell proliferation and differentiation. Mutations in Ras genes frequently result in constitutively active Ras proteins, leading to uncontrolled cell proliferation, inhibition of apoptosis and metabolic reprogramming. Ras proteins activate multiple downstream signalling pathways involved in these processes, such as the MAPK and PI3K-Akt pathways. Downstream of Ras family proteins, BRAF is a protein kinase also involved in the mitogen-activated protein kinase (MAPK) signalling pathway. Mutations in the BRAF gene, particularly the V600E mutation, are frequently found in melanoma, colorectal cancer, and other malignancies. These mutations also result in constitutive activation of the MAPK pathway, driving uncontrolled cell growth and survival. HER2 (ErbB2) is another important oncoprotein and is a member of the EGFR family of receptor tyrosine kinases. Overexpression or amplification of the HER2 gene is observed in various cancers, such as breast and gastric cancers and leads to excessive activation of downstream signalling pathways. The EGF receptor itself is also a potential oncoprotein with mutations or amplification of the EGFR gene promoting cancer cell growth and survival. EGFR mutations are found in lung cancer (NSCLC), whilst EGFR amplification can occur in several cancer types. An additional mechanism to generate oncoproteins is exemplified by the BCR-ABL fusion protein. BCR-ABL exhibits constitutive tyrosine kinase activity and is generated by a chromosomal translocation that occurs in chronic myeloid leukemia (CML) and some cases of acute lymphoblastic leukemia (ALL). Targeted therapies using tyrosine kinase inhibitors (e.g. imatinib/Gleevec) specifically inhibit BCR-ABL activity. Finally, viral oncoproteins provide another example of oncoproteins. The E6 and E7 proteins are found in some human papillomavirus (HPV) strains responsible for the development of cervical and other HPV-associated cancers. E6 binds to and promotes the degradation of the p53 tumour suppressor protein, whilst E7 binds to and inactivates the retinoblastoma (Rb) protein, leading to uncontrolled cell proliferation and genomic instability. In contrast to oncoproteins, tumour suppressors genes (TSGs) inhibit the development and progression of cancer. TSGs are present in normal cells to restrict cell division and promote apoptosis if a cell is damaged. They prevent tumour development by distinct mechanisms. Firstly, some help regulate the cell cycle, the process by which cells divide and replicate, ensuring that cells only divide when necessary and that DNA is accurately replicated. Some are involved in DNA repair mechanisms sensing and alerting the DNA damage response to mutations or DNA strand breaks, thereby preventing the accumulation of genetic alterations to daughter cells that can contribute to cancer. Thirdly, some tumour suppressors inhibit cancer development by triggering apoptosis. If a cell sustains significant DNA damage or is otherwise unable to repair itself, tumour suppressors can initiate apoptosis to eliminate the damaged cell. This process helps prevent the survival and proliferation of cells with potentially harmful mutations. Finally, some tumour suppressors (eg E-cadherin) are involved in maintaining cell adhesion, which is crucial for the organization and structure of tissues. They maintain tissue integrity and prevent cells from becoming invasive. Loss of tumour suppressor function in these instances can lead to reduced cell adhesion and increased cell migration, facilitating tumour growth and metastasis. Inherited germ-line mutations in certain tumour suppressor genes, such as BRCA1/BRCA2 and p53, significantly raise the susceptibility of an individual to cancer, whilst acquired (somatic) mutations that occur during a person's lifetime also disrupt tumour suppressor function and promote cancer. We offer a wide product catalogue of research reagents for investigating oncoproteins and suppressors, including p53 antibodies, EGFR antibodies, Bcl-2 antibodies, p53 ELISA Kits, and EGFR ELISA Kits. Explore our full oncoproteins and suppressors product range below and discover more, for less. Alternatively, you can explore our Oncoproteins, Tumor Suppressors, and Viral Proteins product ranges.