Product Name: CAMK2b (449-467)
Product Number: PE-01BCH85
Size: | 1 mg | | Price: | 96.00 |
| 5 mg | | $US | 208.00 |
| 20 mg | | | 368.00 |
Peptide Name: CAMK2b (449-467)
Product Use: Services as a blocking peptide for use with the CaMK2b-PAD rabbit polyclonal antibody (Cat. No.: AB-NK018-3) that is also available from Kinexus. The peptide sequence is located before the CaMAD, repeated 3X.
Peptide Production Method: Solid-phase peptide synthesis
Peptide Origin: Homo sapiens
Peptide Sequence: RISDILNSVRRGSGTPEAEC
Peptide Modifications N Terminus: Free amino
Peptide Modifications C Terminus: Amide
Peptide Molecular Mass Calculated: 2159.4 Da
Peptide Purity Percent after Synthesis and Purification: >80
Scientific Background: CaMK2b is a protein-serine/threonine kinase of the CAMK group and CAMK2 family. It is a calcium/calmodulin-dependent protein kinase. Autophosphorylation at T287 increases phosphotransferase activity in a Ca(2+)-independent manner. It is an important kinase in the central nervous system and functions as components in long-term potentiation and neurotransmitter release. It is involved in dendritic spine and synapse formation, neuronal plasticity and regulation of sarcoplamic reticulum Ca2+ transport in skeletal muscle. In neurons, plays an essential structural role in the reorganization of the actin cytoskeleton during plasticity by binding and bundling actin filaments in a kinase-independent manner. This structural function is required for correct targeting of CaMK2 isoforms, which acts downstream of NMDAR to promote dendritic spine and synapse formation and maintain synaptic plasticity which enables long-term potentiation (LTP) and hippocampus-dependent learning. In developing hippocampal neurons, promotes arborization of the dendritic tree and in mature neurons, promotes dendritic remodeling. CaMK2b participates in the regulation of skeletal muscle function in response to exercise. In slow-twitch muscles, is involved in regulation of sarcoplamic reticulum (SR) Ca2+ transport and in fast-twitch muscle participates to the control of Ca2+ release from the SR through phosphorylation of triadin, a ryanodine receptor-coupling factor, and phospholamban (PLN/PLB), an endogenous inhibitor of SERCA2A/ATP2A2.