LIMK1 (C-terminus) polyclonal, anti-human, mouse, rat

Background:
LIM kinases (LIMK1 and LIMK2) are serine/threonine kinases that have two zinc finger motifs, known as LIM motifs, in their amino-terminal regulatory domains. LIM kinases are involved in actin cytoskeletal regulation downstream of Rho-family GTPases, PAKs, and ROCK. PAK1 and ROCK phosphorylate LIMK1 or LIMK2 at the conserved Thr-508 or Thr-505 residues in the activation loop, increasing LIMK activity. In addition, VEGF-induced stress fiber formation has been linked to p38-mediated activation of LIMK through MK-2 phosphorylation of Ser-323. Activated LIM kinases inhibit the actin depolymerization activity of cofilin by phosphorylation at the amino-terminal Ser-3 residue of cofilin. In addition, LIMKs may have a function in the nucleus. It has been shown that the nuclear localization of LIMKs can mediate suppression of Rac/Cdc42-mediated cyclin D1 expression. This effect of LIMKs was independent of cofilin phosphorylation and the regulation of actin dynamics.

Immunogen: LIMK1 (C-terminus) synthetic peptide (coupled to carrier protein) corresponding to amino acids at the C-terminus of human LIMK1. This sequence is conserved in rat and mouse LIMK1, and is not found in LIMK2.

Specificity: This antibody was affinity purified using LIMK1 (C-terminus) peptide (without carrier). The antibody detects a 72 kDa* protein corresponding to the molecular mass of LIMK1 on SDS-PAGE immunoblots of mouse recombinant LIMK1.

Buffer/Storage:
Rabbit polyclonal, affinity-purified antibody is supplied in 100μl phosphate-buffered saline, 50% glycerol, 1 mg/ml BSA, and 0.05% sodium azide. Store at –20°C. Stable for 1 year.