Cell Signaling Technology

Product Pathways - Neuroscience

Mena Antibody #2075

Applications Reactivity Sensitivity MW (kDa) Source
W H M R Endogenous 80, 88, 140 Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse  R=Rat
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

Mena Antibody detects endogenous levels of total Mena protein.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide of human Mena. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from C6 and A431 cells using Mena Antibody.

Background

Mena (mammalian enabled), EVL, and VASP are 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 specific domains: an amino-terminal EVH1 domain controlling protein localization; a central proline-rich domain mediating interactions with both SH3 and WW domain containing proteins, including profilin; and a carboxy-terminal domain causing tetramerization and binding to actin (2). Mena interacts with actin filaments at the growing ends localizing to lamellipodia and to tips of growth cone filopodia in neurons. Axons projecting from interhemispheric cortico-cortical neurons are misrouted in newborn, homozygous Mena knock-out mice (3). Mena is phosphorylated at Ser236 by PKA, thereby promoting filopodial formation and elongation in the growth cone (4).Three forms of Mena corresponding to 80, 88 and 140 kD are known. The 80 kD protein is broadly expressed in contrast to the 140 kD protein which is enriched in neural cell types. Alternative splicing produces these forms. The 88 kD protein is mainly found in embryonic cell types and is likely the result of post-translational modification. Expression of all three forms is completely eliminated in Mena homozygous mutant animals (1, 3).

  1. Gertler, F.B. et al. (1996) Cell 87, 227-39.
  2. Small, J.V. (2008) Nat Cell Biol 10, 118-20.
  3. Lanier, L.M. et al. (1999) Neuron 22, 313-25.
  4. Lebrand, C. et al. (2004) Neuron 42, 37-49.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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