Product Name: LIMK1 (505-511) pT508
Product Number: PE-04ANI99
Size: 200 µg      Price:42.00
1 mg      $US84.00
5 mg      185.00
Peptide Name: LIMK1 (505-511) pT508

Product Use: Services as a blocking peptide for use with the LIMK1-pT508 rabbit polyclonal antibody (Cat. No.: AB-PK681) that is also available from Kinexus. This phosphopeptide may also be useful as a substrate for screening the phosphatase activity of protein phosphatases. The peptide sequence is located in the protein kinase catalytic domain. T508 phosphorylation stimulates phosphotransferase activity and protein interaction.

Peptide Production Method: Solid-phase peptide synthesis

Peptide Origin: Homo sapiens

Peptide Sequence: KRY-pT-VVG

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: βAla-Cys

Peptide Modifications Other: Phosphorylated

Peptide Molecular Mass Calculated: 1075.16 Da

Peptide Purity Percent after Synthesis and Purification: >95

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Related Product 1: LIMK1 - pT508 phosphosite-specific antibody (Cat. No.: AB-PK681)

Scientific Background: LIMK1 is a protein-serine/threonine kinase of the TKL group and LISK family. It can modulate actin filament actions. Upstream kinases from LIMK1 include ROCK1, PAK1 and PAK4 and LIMK1 is activated via phosphorylation of an active-site threonine. Phosphorylation at S323 and T508 increases phosphotransferase activity.Activation of LIMK1 by ROCK1 can be fully inhibited with a T508A mutation. LIMK1 will directly act on CFL1 (cofilin-1), CFL2 (cofilin-2), and DSTN (destrin), preventing the ability of these cytoskeletal proteins to polymerize. It also catalyzes an inactivating phosphorylation on TPPP to inhibit depolymerization and destablilization of actin and tubulin. It is involved in cell motility, cell morphology, cytokinesis and cell cycle progression. Overexpression leads to developing invasive phenotype and metastasis of cancers. Cell cycle progression, motility, and differentiation are all affected by this inhibited actin polymerization. In LIMK1, the mutations C84S, G177E + L178A, and T508EE can enhance aggregation of actin whereas D460N, and R503G + K504A + K505A will fully inhibit actin aggregation and T508V/E will partially inhibit actin aggregation.