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| Sample Type | Average | Range |
|---|---|---|
| Cell lysate | 100% | 85%-110% |
| Sample | n | mean (ng/mL) | SD | CV% |
|---|---|---|---|---|
| 1 | 20 | 82.0 | 5.5 | 6.7 |
| 2 | 20 | 28.5 | 0.8 | 2.8 |
| 3 | 20 | 6.3 | 0.3 | 5.3 |
| Sample | n | mean (ng/mL) | SD | CV% |
|---|---|---|---|---|
| 1 | 24 | 86.0 | 6.3 | 7.3 |
| 2 | 24 | 28.0 | 2.0 | 7.2 |
| 3 | 24 | 5.5 | 0.5 | 8.9 |
JNK is also named as MAPK8 (Mitogen-activated protein kinase 8), PRKM8, SAPK1, SAPK1C and belongs to the MAP kinase subfamily. JNK is activated by dual phosphorylation at a Thr-Pro-Tyr motif during response to UV light. JNK functions to phosphorylate c-Jun at N-terminal serine regulatory sites of Ser-63 and Ser-73, mapping within the transactivation domain. Phosphorylation of these sites in response to UV results in transcriptional activation of c-Jun. JNK activity is abnormally elevated in obesity. Furthermore, an absence of JNK results in decreased adiposity, significantly improved insulin sensitivity, and enhanced insulin receptor signaling capacity in 2 different models of mouse obesity, including ob/ob. JNK is a crucial mediator of obesity and insulin resistance and a potential target for therapeutics. The ELISA kit is suitable for testing cell lysates.
