Product Name: KinSub1RHGTP
Product Number: PE-01AHP95
Size: 200 µg      Price:99.00
      $US
Peptide Name: KinSub1RHGTP

Product Use: For assaying the phosphotransferase activity of MAPK/ERK kinase kinase 3; Mitogen-activated protein kinase kinase kinase 3 (MEKK3, UniProt ID Q99759). The KinSub1RHGTP peptide demonstrated high phosphotransferase activity with TXK, and exhibited medium specificity when assayed with over 200 other protein kinases. A listing of other kinases that show appreciable phosphotransferase activity towards this peptide are listed in Table 1.

Peptide Production Method: Solid-phase peptide synthesis

Peptide Origin: KinSub1RHGTP was originally identified using a microarray with peptides that were predicted as optimal substrates for 500 human protein kinases with a proprietary algorithm developed at Kinexus with our academic partners.

Peptide Sequence: GCDGRHGTPYKKGGW

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: Amide

Peptide Molecular Mass Calculated: 1617.8 Da

Peptide Purity Percent after Synthesis and Purification: >95

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Peptide Recommended Enzyme: TXK

Scientific Background: MEKK3 is one of several protein kinases that can phosphorylate KinSub1RHGTP. Human MEKK3 is a protein-serine/threonine kinase of 626 amino acid length, with a predicted molecular mass of 70,898 Da. It is a member of the STE group of protein kinases in the STE11 family. This kinase is highly expressed and widely distributed in most tested human tissues. Orthologues of MEKK3 are highly conserved in vertebrates, including amphibians. MEKK3 is activated by phosphorylation at T530. It is part of a complex with MAP2K3, Rac1 and CCM, and also interacts with MAP2K5 and SPAG9. MEKK3 directly regulates the JNK and ERK1/2 pathways, but apparently not the p38 MAPK pathway. MEKK3 modulates JNK and ERK activity by activating the upstream targets MKK4 and MEK1/2, respectively (1). Ksr2 can regulate the activity of MEKK3 and can reduce MEKK3-mediated ERK activation. Knockout of the MEKK3 gene in mice leads to disruption of blood vessel development and the structural integrity of the yolk sac (2). The blockage of angiogenesis in these mice is not a result of decreased VEGF1 expression but rather due to an intrinsic defect in MEKK3 -/- endothelial cells. MEKK3 is necessary for blood vessel development and may be a possible target for drugs that control angiogenesis.