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SKU: FC0103
LIM domain kinase 1

WB of LIMK-1 Antibody 1:500 dilution with THP-1 cells. Apparent MW 78 kDa


Host Species: 
Synthetic peptide from the N-Terminal region within amino acids 115-170 of the human LIMK-1.  The peptide is conserved in several other species.  The selected peptide was post-synthetically modified for coupling to carrier protein.
Reactive Species: 
Highly conserved suggesting multiple species
This antibody can be conjugated to fluorophores and other detection molecules as an additional service.
Buffer & Formulation: 
0.5 mg/ml in antibody stabilization buffer.
Aliquot and freeze at -20° C. Avoid freeze-thaw cycles.


Western Blotting: 
Not tested
Not tested
Flow Cytometry: 
Not tested

LIM Kinase family comprise of two members:  LIM Kinase 1 (LIMK1) and LIM Kinase 2 (LIMK2).  LIMK1 regulates actin dynamics by phosphorylating cofilin on serine 3, rendering it inactive, as phosphorylated cofilin is unable to bind actin and mediate actin depolymerization (1). In turn, LIMK1 is activated after phosphorylation by two protein kinases, p21-activated kinases (PAKs) and Rho-associated kinase (ROCK), effectors of the small GTPases Rac, Cdc42, and Rho(1).  In addition to its kinase domain, LIMK1 contains two LIM domains and one PDZ domain.

LIM kinase 1 (LIMK1) is a member of a novel class of serine‐threonine protein kinases, which plays an important role in malignant transformation(2). High expression of LIM kinase 1 (LIMK1) has been detected in various invasive cancers(2).  Over expression of LIMK1 was also associated with high TNM stage and lymph node metastasis in patients. Moreover, RNAi-mediated suppression of LIMK1 expression markedly inhibited migration and invasion of 801D lung cancer cells(2). Furthermore, silencing of LIMK1 sensitized 801D cells to chemotherapeutic drugs of cisplatin and gemcitabine. These results indicate that the overexpression of LIMK1 is tightly associated with an aggressive phenotype of lung cancer cells, knockdown of LIMK1 suppressed cell migration and invasion, enhanced chemosensitivity, suggesting a potential therapeutic target for lung cancer(2).

It has also been determined that LIMK1 plays a pro-inflammatory role in mouse lungs via disruption of endothelial barrier function and promotion of leukocyte diapedesis through regulation of cytoskeleton dynamics (unpublished data)(3). The important role of LIMK1 during inflammatory response and its possible cross-talk with TGF-β have led us to hypothesize that LIMK1 may be involved in inflammation through TGF-β signaling, and that down regulation of LIMK1 might be an effective strategy to suppress ocular inflammation and fibrosis(3). The in vitro and in vivo results underscore the potential of a novel therapy for preventing the inflammatory response and fibrosis or scarring in ocular diseases and after glaucoma filtration surgery. This approach may also have applications for other surface tissues, including the skin(3). More information at UniProtKB#P53667


1.   Victoria C. Foletta, et al. Direct signaling by the BMP type II receptor via the cytoskeletal regulator LIMK1. J Cell Biology September 15, 2003; Vol. 162(6): 1089–1098.

2.   Chen, Qingyong; Jiao, Demin; Hu, Huizhen; Song, Jia; Yan, Jie; Wu, Lijun; Xu, Li-Qun. Downregulation of LIMK1 Level Inhibits Migration of Lung Cancer Cells and Enhances Sensitivity to Chemotherapy Drugs.  Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics Volume 20, Number 11, 2012, pp. 491-498(8).

3.   Matvey Gorovoy, Takahisa Koga, [...], and Tatyana Voyno-Yasenetskaya. Downregulation of LIM kinase 1 suppresses ocular inflammation and fibrosis. Mol. Visi. 2008, 14: 1951-1959.

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