Cat. # | Size | Qty. | Price |
---|---|---|---|
2075S | 100 µl |
|
REACTIVITY | H M R |
SENSITIVITY | Endogenous |
MW (kDa) | 80, 88, 140 |
SOURCE | Rabbit |
Product Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
For western blots, incubate membrane with diluted primary antibody in 5% w/v BSA, 1X TBS, 0.1% Tween® 20 at 4°C with gentle shaking, overnight.
NOTE: Please refer to primary antibody product webpage for recommended antibody dilution.
From sample preparation to detection, the reagents you need for your Western Blot are now in one convenient kit: #12957 Western Blotting Application Solutions Kit
NOTE: Prepare solutions with reverse osmosis deionized (RODI) or equivalent grade water.
Load 20 µl onto SDS-PAGE gel (10 cm x 10 cm).
NOTE: Loading of prestained molecular weight markers (#59329, 10 µl/lane) to verify electrotransfer and biotinylated protein ladder (#7727, 10 µl/lane) to determine molecular weights are recommended.
NOTE: Volumes are for 10 cm x 10 cm (100 cm2) of membrane; for different sized membranes, adjust volumes accordingly.
* Avoid repeated exposure to skin.
posted June 2005
revised June 2020
Protocol Id: 10
Human, Mouse, Rat
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide of human Mena. Antibodies are purified by protein A and peptide affinity chromatography.
Mena, EVL, and VASP are all members of the Ena/VASP family, which is involved in controlling cell shape and cell movement by shielding actin filaments from capping proteins (1). Ena/VASP proteins have three distinct domains: an amino-terminal EVH1 domain controlling protein localization; a central proline-rich domain mediating interactions with SH3 and WW domain containing proteins, including profilin; and a carboxy-terminal domain that promotes tetramerization and actin binding (2). Mena (known also as ENAH, or Protein enabled homolog), interacts with actin filaments at the growing ends and is thus localized to lamellipodia and the tips of neuronal growth cone filopodia. Axons projecting from interhemispheric cortico-cortical neurons were shown to be misrouted in newborn, homozygous Mena knockout mice (3). Mena may be phosphorylated at Ser236 by PKA, a posttranslational modification that is reported to promote filopodial formation and elongation of the growth cone (4). Three forms of the Mena protein, with apparent molecular weights of 80, 88 and 140 kDa, have been described. The 80 kDa isoform is broadly expressed, whereas the 140 kDa isoform is reportedly enriched in neural cell types; these isoforms are generated by alternative splicing. The 88 kDa isoform is expressed primarily in embryonic cells and is likely the result of posttranslational modification of the 80 kDa isoform. Expression of all three forms is completely eliminated after homozygous deletion of ENAH, the gene encoding the Mena protein (1,3).
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