TPL-2, a MEK kinase is essential for TLR4 activation of the ERK mitogen-activated protein kinase cascade in lipopolysaccharide (LPS)-stimulated macrophages. Interaction with p105 is required to maintain TPL-2 metabolic stability and also negatively regulates TPL-2 MEK kinase activity (1). The NF-kappaB1 gene encodes a larger precursor protein, p105, from which p50 is produced constitutively by proteasome-mediated removal of the p105 carboxy terminus. TPL-2 , which is homologous to MAP-kinase-kinase kinases in its catalytic domain, forms a complex with the carboxy terminus of p105. TPL-2 was originally identified, in a carboxy-terminal-deleted form, as an oncoprotein in rats and is more than 90% identical to the human oncoprotein COT. Expression of TPL-2 results in phosphorylation and increased degradation of p105 while maintaining p50 production. This releases associated Rel subunits or p50-Rel heterodimers to generate active nuclear NF-kappaB. Furthermore, kinase-inactive TPL-2 blocks the degradation of p105 induced by tumor-necrosis factor-alpha. TPL-2 is therefore a component of a new signaling pathway that controls proteolysis of NF-kappaB1 p105 (2).
Applications:
Suitable for use in Western Blot. Other applications not tested.
Recommended Dilution:
Western Blot: 1:500
Optimal dilutions to be determined by the researcher.
Storage and Stability:
May be stored at 4 degrees C for short-term only. For long-term storage, aliquot and store at -20 degrees C. Aliquots are stable for at least 12 months at -20 degrees C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Further dilutions can be made in assay buffer.
Manufactured incorporating RabMAb(R) technology under Epitomics US patents, No 5,675,063 and 7,429,487, owned by Abcam.
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