|Positive WB detected in||mouse brain tissue|
|Western Blot (WB)||WB : 1:500-1:1000|
|Sample-dependent, check data in validation data gallery|
10002-2-AP targets Marcksl1 in WB, IHC, IF,ELISA applications and shows reactivity with human, mouse samples.
|Tested Reactivity||human, mouse|
|Cited Reactivity||human, mouse|
|Host / Isotype||Rabbit / IgG|
|Full Name||MARCKS-like 1|
|Calculated molecular weight||40 kDa|
|Observed molecular weight||60 kDa|
|GenBank accession number||BC006757|
|Gene ID (NCBI)||17357|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
MacMARCKS is a member of MARCKS family of PKC substrate. It is widely used in the signal transduction studies as an indictor of PKC activation. The protein has a calculated molecular weight of 20 kDa and an apparent molecular weight of 42-45 kDa in different species on SDS PAGE. MacMARCKS functions in many aspects of cell physiology including integrin activation, cell spreading and phagocytosis. Its functions are though to associate with its ability in binding and regulating actin and microtubule cytoskeleton. Current evidence indicated that this protein also involved controls membrane fluidity and molecular mobility of membrane proteins
Cell Stem Cell
Direct Reprogramming of Human Neurons Identifies MARCKSL1 as a Pathogenic Mediator of Valproic Acid-Induced Teratogenicity.
J Biol Chem
The long noncoding RNA lncZic2 drives the self-renewal of liver tumor-initiating cells via the protein kinase C substrates MARCKS and MARCKSL1.
Clin Exp Metastasis
Identification of estrogen-responsive genes involved in breast cancer metastases to the bone.
Exp Cell Res
The regulation of MacMARCKS expression by integrin beta3.
Colonic miRNA Expression/Secretion, Regulated by Intestinal Epithelial PepT1, Plays an Important Role in Cell-to-Cell Communication during Colitis.
Mol Cell Biol
c-Jun N-terminal kinase phosphorylation of MARCKSL1 determines actin stability and migration in neurons and in cancer cells.