Product Name: GCK (167-173) pS170
Product Number: PE-04AMQ99
Size: 200 µg      Price:42.00
1 mg      $US84.00
5 mg      185.00
Peptide Name: GCK (167-173) pS170

Product Use: Services as a blocking peptide for use with the GCK-pS170 rabbit polyclonal antibody (Cat. No.: AB-PK646) that is also available from Kinexus. This phosphopeptide may also be useful as a substrate for screening the phosphatase activity of protein phosphatases. The peptide sequence is located in the protein kinase catalytic domain activation T loop region between subdomains VII and VIII. S170 phosphorylation stimulates phosphotransferase activity.

Peptide Production Method: Solid-phase peptide synthesis

Peptide Origin: Homo sapiens

Peptide Sequence: KRR-pS-FIG

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: βAla-Cys
Peptide Modifications Other: Phosphorylated

Peptide Molecular Mass Calculated: 1116.2 Da

Peptide Purity Percent after Synthesis and Purification: >95

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Related Product 1: GCK - pS170 phosphosite-specific antibody (Cat. No.: AB-PK646)

Scientific Background: GCK (MAP4K2) is a protein-serine/threonine kinase of the STE group and STE20 family. It participates in the regulation of the MAPK signalling pathway. It acts as a MAPK kinase kinase kinase (MAP4K) and is an upstream activator of the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signalling pathway and to a lesser extend of the p38 MAPKs signalling pathway. It is required for the efficient activation of JNKs by TRAF6-dependent stimuli, including pathogen-associated molecular patterns (PAMPs) such as polyinosine-polycytidine (poly(IC)), lipopolysaccharides (LPS), lipid A, peptidoglycan (PGN), or bacterial flagellin. IL-1 and engagement of CD40 also stimulate to a lessor degree GCK-mediated JNKs activation. GCK is important for LPS stimulation of c-Jun phosphorylation and induction of IL-8. It enhances MAP3K1 oligomerization, which may relieve N-terminal mediated MAP3K1 autoinhibition and lead to activation following autophosphorylation. It mediates the JNK signalling pathway and the p38 MAPKs signalling pathway through activation of the MAP3Ks MAP3K10/MLK2 and MAP3K11/MLK3. It may play a role in the regulation of vesicle targeting or fusion. regulation of vesicle targeting or fusion. It has been linked to insulinomas, which are tumours of the pancreas arising from beta cells, and which will secrete insulin.