STK4 (serine/threonine kinase 4) is a kinase protein, which is ubiquitous in nature. It is homologous to yeast Ste20 and Drosophila Hippo protein. It has a molecular weight of 63kDa, and is a resident of the cytoplasm. It is also called MST1 (mammalian sterile 20-like protein), and has its active site at its N-terminal. It also contains an autoinhibitory domain, and a coiled-coil SARAH domain at its C-terminal. This domain is responsible for protein hetero- and homodimerization.
Synonyms: Anti-MST-1; Anti-Mammalian STE20-like protein kinase 1; Anti-STE20-like kinase MST1; Anti-Serine/threonine-protein kinase 4; Anti-Serine/threonine-protein kinase Krs-2
Storage: -20C
Application: Anti-STK4 antibody produced in rabbit, a Prestige Antibody, is developed and validated by the Human Protein Atlas (HPA) project (www.proteinatlas.org). Each antibody is tested by immunohistochemistry against hundreds of normal and disease tissues. These images can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. The antibodies are also tested using immunofluorescence and western blotting. To view these protocols and other useful information about Prestige Antibodies and the HPA, visit sigma.com/prestige.
Biochem Physiol Actions: STK4 (serine/threonine kinase 4) functions as both apoptotic and anti-apoptotic protein. It acts as an apoptotic protein upon its cleavage by caspases, which produces an N-terminal fragment of 36kDa. This fragment moves to the nucleus, where it phosphorylates histone proteins, resulting in apoptosis initiation. It also interacts with JNK (Jun N-terminal kinase) and RASSF1A (Ras association domain family member 1) to induce apoptosis. It phosphorylates FOXO1 (forkhead box O1) and FOXO3, which are transcription factors of FOXO family, in stress-response pathway. Thus, it maintains the viability of cell. Inactivation of this gene in lymphocytes and neutrophils leads to abnormal mitochondrial membrane potential. This results in increased chances of apoptotic death. Thus, loss of this gene, in humans is a cause of primary immunodeficiency syndrome. It is essential for the homing and maintenance of naïve T-cells, and deficiency in this gene leads to abnormal development and/or maintenance of regulatory T-cells.
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