| Identification | Back Directory | [Name]
CREBtide | [CAS]
149155-45-3 | [Synonyms]
L-Arginine, L-lysyl-L-arginyl-L-arginyl-L-α-glutamyl-L-isoleucyl-L-leucyl-L-seryl-L-arginyl-L-arginyl-L-prolyl-L-seryl-L-tyrosyl- | [Molecular Formula]
C73H129N29O19 | [MOL File]
149155-45-3.mol | [Molecular Weight]
1716.99 |
| Hazard Information | Back Directory | [Uses]
CREBtide is a CREB (cAMP response element binding protein)-like peptide. CREBtide, a synthetic 13 amino acid peptide, has been reported as a PKA and PKC substrate. | [Biological Activity]
CREBtide is a synthetic 13 amino acid peptide that acts as a PKA substrate. | [in vitro]
delta-CREB is a spliced variant of cAMP response element binding protein (CREB). CREBtide (KRREILSRRPSYR), a synthetic peptide based on the phosphorylation sequence in delta-CREB. delta-CREB and CREBtide are tested as substrates of cAMP-dependent protein kinase (cAK). The apparent K m of CREBtide phosphorylation by cAK is 3.9 μM, which is 10-fold lower than that of Kemptide (K m =39 μM), the synthetic peptide substrate most often employed for cAK measurement. The V max values are 12.4 mumol/(min.mg) for CREBtide and 9.8 mumol/(min.mg) for Kemptide. The apparent K m of CREBtide phosphorylation by cGMP-dependent protein kinase (cGK) is 2.9 μM and the V max value is 3.2 mumol/(min.mg). Both delta -CREB and CREBtide are phosphorylated at a much slower rate by cGK as compared with cAK, implying that the high cAK/cGK specificity exhibits by delta-CREB is retained by the peptide. | [target]
| [References]
[1] Wu J, et al. A microPLC-based approach for determining kinase-substrate specificity. Assay Drug Dev Technol. 2007 Aug;5(4):559-66. DOI:10.1089/adt.2007.072
[2] Colbran JL, et al. cAMP-dependent protein kinase, but not the cGMP-dependent enzyme, rapidly phosphorylates delta-CREB, and a synthetic delta-CREB peptide. Biochem Cell Biol. 1992 Oct-Nov;70(10-11):1277-82. DOI:10.1139/o92-174
[3] Harum KH, et al. Cognitive impairment in Coffin-Lowry syndrome correlates with reduced RSK2 activation. Neurology. 2001 Jan 23;56(2):207-14. DOI:10.1212/wnl.56.2.207
[4] Peng J, et al. Protein kinase C-α signals P115RhoGEF phosphorylation and RhoA activation in TNF-α-induced mouse brain microvascular endothelial cell barrier dysfunction. J Neuroinflammation. 2011 Apr 8;8:28. DOI:10.1186/1742-2094-8-28 |
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Ontores Biotech
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0571-88760729 18072970094 |
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www.ontoresinc.cn |
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