Protein kinases and phosphatases are enzymes that play crucial roles in the development and progression of cancer. Protein kinases add phosphate groups to specific amino acids thereby altering their function. They are involved in various signal transduction pathways and dysregulation of these pathways can contribute to cancer development. Protein kinases can be activated by mutations, gene amplification, or chromosomal translocation, or by mutational activation of upstream oncogenes. Oncogenic kinases include BRAF, BCR-ABL (active in chronic myeloid leukemia, CML) and EGFR in certain NSCL (lung) cancers. Protein kinases of the cyclin-dependent kinase (CDK) family are crucial for the regulation of the cell cycle, ensuring proper progression through the different phases. Dysregulation of CDKs can lead to uncontrolled cell division and genomic instability, contributing to cancer development. A variety of protein kinases regulate processes involved in angiogenesis in the tumour microenvironment. Some key protein kinases in this process include: 1) Vascular Endothelial Growth Factor Receptors (VEGFRs), receptor tyrosine kinases that are activated by Vascular Endothelial Growth Factors (VEGFs). VEGFRs promote angiogenesis by stimulating endothelial cell proliferation, migration, and vessel permeability; 2) Platelet-Derived Growth Factor Receptors (PDGFR), receptor tyrosine kinases that binds to Platelet-Derived Growth Factors (PDGFs). PDGF signalling contributes to angiogenesis by promoting the recruitment and proliferation of pericytes and smooth muscle cells, which provide structural support to blood vessels; 3) Fibroblast Growth Factor Receptors (FGFR), receptor tyrosine kinases that bind to Fibroblast Growth Factors (FGFs). Activation of FGFR signalling promotes angiogenesis by stimulating endothelial cell proliferation, migration, and tube formation; 4) Protein Kinase C (PKC): PKC is a family of serine/threonine kinases involved in various cellular processes, including angiogenesis. PKC isoforms, PKC alpha and PKC beta, regulate endothelial cell proliferation, migration, and tube formation in response to pro-angiogenic signals; 5) Mitogen-Activated Protein Kinase (MAPK): MAPKs, including extracellular signal-regulated kinases (ERKs), p38 MAPK, and c-Jun N-terminal kinases (JNKs), are serine/threonine kinases that participate in angiogenesis. They are activated by growth factors and cytokines, and their signalling pathways regulate endothelial cell functions crucial for angiogenesis; 6) Akt (Protein Kinase B): Akt is a serine/threonine kinase that is activated downstream of multiple receptor tyrosine kinases. Akt signalling promotes angiogenesis by enhancing endothelial cell survival, proliferation, and migration. Counteracting protein kinase activity are phosphatases which remove phosphate groups. Dysregulation of phosphatases can contribute to abnormal cell growth and cancer progression. For example, the lipid phosphatase PTEN is frequently mutated or inactivated in various cancers, leading to reduced apoptosis. Some phosphatases are also involved in DNA repair mechanisms, helping to maintain genomic stability. Examples include: 1) PP1 a serine/threonine phosphatase which dephosphorylates the DNA damage checkpoint kinase Chk1; protein phosphatase 2A (PP2A) a serine/threonine phosphatase that dephosphorylates and regulates DNA-dependent protein kinase (DNA-PK); and 3) Protein phosphatase Mg2+/Mn2+-dependent 1D (PPM1D, also known as WIP1) which dephosphorylates and inactivates p53, ATM (ataxia-telangiectasia mutated), and Chk2, thus attenuating the DNA damage signalling and repair processes. We offer a wide product catalogue of research reagents for studying kinases and phosphatases, including Chk1 antibodies, PTEN antibodies, Chk2 antibodies, JAK2 ELISA Kits, and Chk1 ELISA Kits. Explore our full kinases and phosphatases product range below and discover more, for less. Alternatively, you can explore our Phosphatases, CDKs, and Aurora product ranges.