Oncoproteins are proteins that play a significant role in the development and progression of cancer. They are typically derived from normal cellular proteins that have been altered or mutated, leading to abnormal pro-tumorigenic functions. These proteins thereby contribute to the uncontrolled growth and survival of cancer cells by disrupting normal cellular processes. The major classes of oncoproteins are: 1) the proto-oncogenes, normal genes that regulate cell growth, division, and differentiation. When mutated or activated, they can become oncogenes, leading to uncontrolled cell growth. Examples of proto-oncogenes include the HER2 gene and the RAS gene; 2) Growth factors and growth factor receptors. Oncoproteins also include growth factors, such as epidermal growth factor (EGF), and their receptors, such as the epidermal growth factor receptor (EGFR). Mutations or amplification of these genes can result in overactive signalling, leading to uncontrolled cell growth; 3) Transcription factors (TFs). These can also act as oncoproteins when overexpressed or activated by other mechanisms. Oncoproteins in this category include proteins like MYC and MYB, which control the expression of genes involved in cell cycle progression cell growth and altered metabolism. Abnormal expression or amplification of these transcription factors can drive uncontrolled cell division; 4) Cell cycle regulators. Oncoproteins like cyclins and cyclin-dependent kinases (CDKs) regulate cell cycle progression. Mutations or overexpression of these proteins can disrupt the balance of the cell cycle, leading to uncontrolled proliferation; 5) Anti-apoptotic proteins. Apoptosis eliminates cells with DNA damage or other abnormalities. Oncoproteins such as Bcl-2 and Bcl-xL can inhibit apoptosis, allowing cancer cells to survive and continue growing; 6) Oncogenic protein kinases. Mutational activation, overexpression or translocation/fusion can activate cytoplasmic enzymes involved in growth and proliferation signalling. Examples include a) BCR-ABL1 formed as a result of the Philadelphia chromosome translocation, commonly found in chronic myeloid leukaemia (CML) which exhibits constitutive tyrosine kinase activity, leading to uncontrolled proliferation of myeloid cells; b) BRAF. Mutant BRAF proteins activate the MAPK signalling pathway, promoting cell proliferation and survival with mutations found in melanoma and other cancers, including colorectal and lung cancer; c) ALK (Anaplastic Lymphoma Kinase). ALK gene rearrangements occur in certain types of lung cancer, such as non-small cell lung cancer (NSCLC). ALK fusion proteins lead to constitutive kinase activity and abnormal cell growth; d) c-MET: Overexpression or gene amplification of c-MET is associated with various cancers, including lung, liver, and gastric cancer. Activation of c-MET promotes cell migration, invasion, and angiogenesis; 7) Oncogenic lipid kinase, PI3K. PI3K mutations can occur in different components of the pathway, including the PI3K catalytic subunit (p110α, p110β, p110δ) and the regulatory subunit (p85). These mutations result in increased PI3K activity even in the absence of external signals. This sustained activation promotes uncontrolled cell proliferation and survival, as well as resistance to apoptosis (programmed cell death). Additionally, the dysregulated PI3K pathway can enhance tumour angiogenesis and promote metastasis. PI3K mutations are particularly common in breast, colorectal, ovarian and glioblastoma cancers. We offer a comprehensive product range of research tools for studying oncoproteins, including EGFR antibodies, Bcl-2 antibodies, c-Jun antibodies, EGFR ELISA Kits, and c-Jun ELISA Kits. Explore our full oncoproteins product range below and discover more, for less. Alternatively, you can explore our Growth Factor Receptors, Cell Survival & Death, and Growth Factors product ranges.