Protein kinases and phosphatases are enzymes that play crucial roles in normal development and cell function and can be deregulated in diseases such as cancer. Protein kinases add phosphate moieties to specific amino acid residues thereby altering protein function or localization. They play a vital role in various cellular processes, and their dysregulation can contribute to the development of several diseases. For example, in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease, abnormal activation or inhibition of protein kinases can contribute to neuronal dysfunction and cell death with activation of kinases such as glycogen synthase kinase 3-beta (GSK-3β) and cyclin-dependent kinase 5 (CDK5) implicated in Alzheimer's disease pathogenesis. Protein kinase signalling pathways are also involved in the regulation of the immune response, and dysregulation of kinases can contribute to autoimmune disorders. For example, in rheumatoid arthritis, Janus kinase (JAK) inhibitors are used to target aberrant JAK-STAT signalling, which plays a role in immune-mediated inflammation, whilst in cardiovascular diseases abnormal activation or inhibition of protein kinases can contribute to cardiovascular conditions such as hypertension, heart failure, and arrhythmias with both protein kinase C (PKC) and mitogen-activated protein kinases (MAPKs) implicated in cardiac hypertrophy and remodelling. Protein kinases of the cyclin-dependent kinase (CDK) family are crucial for the regulation of the normal 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 new blood vessel formation (angiogenesis). 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, PKCα and PKCβ, 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 control of cell signalling pathways. For example, the lipid phosphatase PTEN is frequently mutated or inactivated in various cancers, leading to reduced apoptosis. Some phosphatases are also involved in normal 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 large product catalogue of research tools for studying kinases and phosphatases, including PTEN antibodies, JAK2 antibodies, Alkaline Phosphatase antibodies, Cdk5 ELISA Kits, and JAK2 ELISA Kits. Explore our full kinases and phosphatases product range below and discover more, for less. Alternatively, you can explore our Phosphatases, CDKs, and CDK Regulators product ranges.