STK3 (MST2) Kinase Assay Kit
The STK3 (MST2) Kinase Assay Kit is designed to measure STK3 (serine/threonine-protein kinase 3) kinase activity for screening and profiling applications using Kinase-Glo® MAX as a detection reagent. The assay kit comes in a convenient 96-well format, with enough purified recombinant STK3 (MST2) kinase, kinase substrate, ATP, and kinase assay buffer for 100 enzyme reactions.
- Kinase-Glo® MAX (Promega #V6071)
- DTT (Dithiothreitol), 1 M, optional
- Microplate reader capable of reading luminescence
- Adjustable micropipettor and sterile tips
- 30°C incubator
| Catalog # | Name | Amount | Storage |
| 40013 | STK3 (MST2), GST-Tag* | 1 µg | -80°C |
| 79334 | 5x Kinase Assay Buffer 1 | 1.5 ml | -20°C |
| 79686 | 500 µM ATP | 100 µl | -20°C |
| 78514 | Myelin Basic Protein (MBP) (5 mg/ml) |
100 µl | -20°C |
| 79696 | White 96-well plate | 1 | Room Temp |
*The concentration of the protein is lot-specific and will be indicated on the tube.
STK3, also known as serine/threonine-protein kinase 3 or MST2, is involved in the Hippo signaling pathway, a pathway crucial for cell development, proliferation and apoptosis and stress responses. STK3 is activated by autophosphorylation, which can be triggered by cellular stress signals. Once activated it can phosphorylate LATS1/LATS2 (large tumor suppressor kinase), which in turn inhibits YAP1 (yes-associated protein 1). It was found that kinases such as MAP4K (mitogen-activated protein kinase kinase kinase kinase) and TAOK (thousand and one kinase) function in parallel with STK3/4, depending on the cell type and stress inducer. Inhibited YAP1 cannot translocate to the cell nucleus and activate transcription, being targeted for degradation by the SCF (Skp, cullin, F-box containing) complex. Activated MST2 also phosphorylates FOXO (forkhead box O) factors and transcription of apoptotic genes. Interestingly, STK3 is inhibited by the proto-oncogene c-Raf, and this association is found in many cancers. STK3 can inhibit cancer progression, and it was found at low levels in gastric cancer and hepatocellular carcinoma. Conversely, high levels have also been found in breast cancer and oral squamous cell carcinoma. The development of inhibitors able to disrupt the interaction between c-Raf and STK3 may prove beneficial against some cancer types, but a better understanding of the opposite roles of STK3 in different cancers is still necessary.
Yue L., et al., 2023 International Journal of General Medicine, 16:3115-3124.
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