The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Protein concentration is above or equal to 0.05 mg/ml.
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Preparation and Storage
Stability and Storage
Shipped on dry ice. Upon delivery aliquot and store at -80ºC. Avoid freeze / thaw cycles.
pH: 8.00 Constituents: 0.31% Glutathione, 0.79% Tris HCl
MADS box transcription factor 2 polypeptide D
Myocyte enhancer factor 2D
Myocyte specific enhancer factor 2, polypeptide D
Myocyte specific enhancer factor 2D
Myocyte-specific enhancer factor 2D
Transcriptional activator which binds specifically to the MEF2 element, 5'-YTA[AT](4)TAR-3', found in numerous muscle-specific, growth factor- and stress-induced genes. Mediates cellular functions not only in skeletal and cardiac muscle development, but also in neuronal differentiation and survival. Plays diverse roles in the control of cell growth, survival and apoptosis via p38 MAPK signaling in muscle-specific and/or growth factor-related transcription. Plays a critical role in the regulation of neuronal apoptosis.
Belongs to the MEF2 family. Contains 1 MADS-box domain. Contains 1 Mef2-type DNA-binding domain.
Present in myotubes and also in undifferentiated myoblasts.
The beta domain, missing in a number of isoforms, is required for enhancement of transcriptional activity.
Phosphorylated on Ser-444 by CDK5 is required for Lys-439 sumoylation and inhibits transcriptional activity. In neurons, enhanced CDK5 activity induced by neurotoxins promotes caspase 3-mediated cleavage leading to neuron apoptosis. Phsophorylation on Ser-180 can be enhanced by EGF. Acetylated on Lys-439 by CREBBP. Deacetylated by SIRT1. Sumoylated on Lys-439 by SUMO2 but not SUMO1; which inhibits transcriptional activity and myogenic activity. Desumoylated by SENP3. Proteolytically cleaved in cerebellar granule neurons on several sites by caspase 7 following neurotoxicity. Preferentially cleaves the CDK5-mediated hyperphosphorylated form which leads to neuron apoptosis and transcriptional inactivation.