|Other Names||MARCKS-related protein, MARCKS-like protein 1, Macrophage myristoylated alanine-rich C kinase substrate, Mac-MARCKS, MacMARCKS, MARCKSL1, MLP, MRP|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP2522a was selected from the N-term region of human MLP . A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Controls cell movement by regulating actin cytoskeleton homeostasis and filopodium and lamellipodium formation. When unphosphorylated, induces cell migration. When phosphorylated by MAPK8, induces actin bundles formation and stabilization, thereby reducing actin plasticity, hence restricting cell movement, including neuronal migration. May also affect cancer cell migration. May be involved in coupling the protein kinase C and calmodulin signal transduction systems (By similarity).|
|Cellular Location||Cytoplasm. Cell membrane. Membrane; Lipid-anchor Note=Associates with the membrane via the insertion of the N- terminal N-myristoyl chain and the partial insertion of the effector domain. Association of the effector domain with membranes may be regulated by Ca(2+)/calmodulin (By similarity). In prostate cancers, detected in the cytoplasm and associated with apical or basal membranes (By similarity).|
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Provided below are standard protocols that you may find useful for product applications.
Protein kinase C is a key enzyme of intracellular signal transduction. The myristoylated, alanine-rich protein MARCKS, is a widely expressed, prominent substrate for protein kinase C.The severe neural tube defects (NTD) including exencephaly, spina bifida, and tail flexion anomaly in approximately 60% of the homozygous mutants and in approximately 10% of heterozygous animals. The homozygous mutants without exencephaly survived despite brain abnormalities, which appear to occur secondarily to the NTD.It has been suggested that mutations in Mrp result in isolated NTD and therefore may provide an animal model for common human NTD.
Hsia, T.C., et al., Lung 180(3):173-179 (2002).Stumpo, D.J., et al., Genomics 49(2):253-264 (1998).Umekage, T., et al., FEBS Lett. 286 (1-2), 147-151 (1991).
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