Product Name: KinSub1RTKSP
Product Number: PE-01AJP95
Size: | 200 µg | | Price: | 99.00 |
| | | $US | |
Peptide Name: KinSub1RTKSP
Product Use: For assaying the phosphotransferase activity of calcium/calmodulin-dependent protein-serine kinase 2 delta (CaMK2d, UniProt ID Q13557). The KinSub1RTKSP peptide demonstrated moderate phosphotransferase activity with TXK, and exhibited low 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: KinSub1RTKSP 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: HGRGRTKSPYVSTGY
Peptide Modifications N Terminus: Free amino
Peptide Modifications C Terminus: Amide
Peptide Molecular Mass Calculated: 1664.8 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: CaMK2d is one of several protein kinases that can phosphorylate KinSub1RTKSP. Human CaMK2d is a protein-serine/threonine kinase of 499 amino acid length, with a predicted molecular mass of 56,369 Da. It is a member of the CAMK group of protein kinases in the CAMK2 family. This kinase is moderate to highly expressed in most tested human tissues except apparently in the brain and spinal cord. CAMK2d is abundantly present in human cardiac and skeletal muscle and its levels are increased in the heart of patients suffering from cardiomyopathy (1). Orthologues of CaMK2d are highly conserved in animals and plants. CAMK2 is composed of up to four different chains: alpha, beta, gamma, and delta. The different isoforms assemble into homo- or heteromultimeric holoenzymes composed of 8 to 12 subunits. CaMK2d is activated by Ca2+/calmodulin to autophosphorylate at T287, which then stimulates its phosphotransferase activity in a Ca2+-independent manner. In cardiomyocytes, stimulation of beta-1-adrenergic receptor leads to induction of apoptosis, an effect that is mediated by activation of CAMK2d in a PKA-independent manner. Expression studies have revealed the downregulation of CAMK2D in human tumour cells.
References[1] Hoch B, Meyer R, Hetzer R, Krause EG, Karczewski P. Identification and expression of delta-isoforms of the multifunctional Ca2+/calmodulin-dependent protein kinase in failing and nonfailing human myocardium. Circ Res. 1999 Apr 2;84(6):713-21. PMID: 10189359.[2] Zhu WZ, Wang SQ, Chakir K, Yang D, Zhang T, Brown JH, Devic E, Kobilka BK, Cheng H, Xiao RP. Linkage of beta1-adrenergic stimulation to apoptotic heart cell death through protein kinase A-independent activation of Ca2+/calmodulin kinase II. J Clin Invest. 2003 Mar;111(5):617-25. PMID: 12618516.