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selective inhibitor of limk activity  (Bristol Myers)

 
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    Structured Review

    Bristol Myers selective inhibitor of limk activity
    <t>LIMK</t> <t>activity</t> promotes VSMC migration. The activation of RhoA/ROCK by stimuli such as PDFG-BB leads to the phosphorylation of LIMK and inactivation of cofilin, thereby promoting actin polymerization. Concurrently, ROCK phosphorylates MLCP and inhibits its activity, resulting in increased phosphorylation of MLC and subsequent VSMC contraction. Activation of inflammatory cytokines such as CCR8, CKLF1, and CXCL12 also modulates cell migration via lamellipodia formation. These inflammatory processes likely promote VSMC migration in a LIMK-dependent manner. Whether inflammatory cytokines activate LIMK via Rac2 activation remains unknown. (PDFG-BB: Platelet derived growth factor BB; Arp 2/3: Actin related protein 2/3; CCR8: chemokine receptor-8; CKLF1: Chemokine-like factor 1; CXCL12: C-X-C motif chemokine 12; MLCP: Myosin light chain phosphatase).
    Selective Inhibitor Of Limk Activity, supplied by Bristol Myers, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/selective+inhibitor+of+limk+activity/selective+inhibitor+of+limk+activity/pmc11688343-310-12-15
    Average 90 stars, based on 1 article reviews
    selective inhibitor of limk activity - by Bioz Stars, 2026-08
    90/100 stars

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    1) Product Images from "LIM kinases in cardiovascular health and disease"

    Article Title: LIM kinases in cardiovascular health and disease

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2024.1506356

    LIMK activity promotes VSMC migration. The activation of RhoA/ROCK by stimuli such as PDFG-BB leads to the phosphorylation of LIMK and inactivation of cofilin, thereby promoting actin polymerization. Concurrently, ROCK phosphorylates MLCP and inhibits its activity, resulting in increased phosphorylation of MLC and subsequent VSMC contraction. Activation of inflammatory cytokines such as CCR8, CKLF1, and CXCL12 also modulates cell migration via lamellipodia formation. These inflammatory processes likely promote VSMC migration in a LIMK-dependent manner. Whether inflammatory cytokines activate LIMK via Rac2 activation remains unknown. (PDFG-BB: Platelet derived growth factor BB; Arp 2/3: Actin related protein 2/3; CCR8: chemokine receptor-8; CKLF1: Chemokine-like factor 1; CXCL12: C-X-C motif chemokine 12; MLCP: Myosin light chain phosphatase).
    Figure Legend Snippet: LIMK activity promotes VSMC migration. The activation of RhoA/ROCK by stimuli such as PDFG-BB leads to the phosphorylation of LIMK and inactivation of cofilin, thereby promoting actin polymerization. Concurrently, ROCK phosphorylates MLCP and inhibits its activity, resulting in increased phosphorylation of MLC and subsequent VSMC contraction. Activation of inflammatory cytokines such as CCR8, CKLF1, and CXCL12 also modulates cell migration via lamellipodia formation. These inflammatory processes likely promote VSMC migration in a LIMK-dependent manner. Whether inflammatory cytokines activate LIMK via Rac2 activation remains unknown. (PDFG-BB: Platelet derived growth factor BB; Arp 2/3: Actin related protein 2/3; CCR8: chemokine receptor-8; CKLF1: Chemokine-like factor 1; CXCL12: C-X-C motif chemokine 12; MLCP: Myosin light chain phosphatase).

    Techniques Used: Activity Assay, Migration, Activation Assay, Phospho-proteomics, Derivative Assay

    Representative studies on the role of LIMK in cardiovascular diseases.
    Figure Legend Snippet: Representative studies on the role of LIMK in cardiovascular diseases.

    Techniques Used: Migration



    Similar Products

    selective inhibitor of limk activity  (Bristol Myers)
    90
    Bristol Myers selective inhibitor of limk activity
    <t>LIMK</t> <t>activity</t> promotes VSMC migration. The activation of RhoA/ROCK by stimuli such as PDFG-BB leads to the phosphorylation of LIMK and inactivation of cofilin, thereby promoting actin polymerization. Concurrently, ROCK phosphorylates MLCP and inhibits its activity, resulting in increased phosphorylation of MLC and subsequent VSMC contraction. Activation of inflammatory cytokines such as CCR8, CKLF1, and CXCL12 also modulates cell migration via lamellipodia formation. These inflammatory processes likely promote VSMC migration in a LIMK-dependent manner. Whether inflammatory cytokines activate LIMK via Rac2 activation remains unknown. (PDFG-BB: Platelet derived growth factor BB; Arp 2/3: Actin related protein 2/3; CCR8: chemokine receptor-8; CKLF1: Chemokine-like factor 1; CXCL12: C-X-C motif chemokine 12; MLCP: Myosin light chain phosphatase).
    Selective Inhibitor Of Limk Activity, supplied by Bristol Myers, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/selective+inhibitor+of+limk+activity/selective+inhibitor+of+limk+activity/pmc11688343-310-12-15
    Average 90 stars, based on 1 article reviews
    selective inhibitor of limk activity - by Bioz Stars, 2026-08
    90/100 stars
    		  Buy from Supplier

    Image Search Results


    LIMK activity promotes VSMC migration. The activation of RhoA/ROCK by stimuli such as PDFG-BB leads to the phosphorylation of LIMK and inactivation of cofilin, thereby promoting actin polymerization. Concurrently, ROCK phosphorylates MLCP and inhibits its activity, resulting in increased phosphorylation of MLC and subsequent VSMC contraction. Activation of inflammatory cytokines such as CCR8, CKLF1, and CXCL12 also modulates cell migration via lamellipodia formation. These inflammatory processes likely promote VSMC migration in a LIMK-dependent manner. Whether inflammatory cytokines activate LIMK via Rac2 activation remains unknown. (PDFG-BB: Platelet derived growth factor BB; Arp 2/3: Actin related protein 2/3; CCR8: chemokine receptor-8; CKLF1: Chemokine-like factor 1; CXCL12: C-X-C motif chemokine 12; MLCP: Myosin light chain phosphatase).

    Journal: Frontiers in Physiology

    Article Title: LIM kinases in cardiovascular health and disease

    doi: 10.3389/fphys.2024.1506356

    Figure Lengend Snippet: LIMK activity promotes VSMC migration. The activation of RhoA/ROCK by stimuli such as PDFG-BB leads to the phosphorylation of LIMK and inactivation of cofilin, thereby promoting actin polymerization. Concurrently, ROCK phosphorylates MLCP and inhibits its activity, resulting in increased phosphorylation of MLC and subsequent VSMC contraction. Activation of inflammatory cytokines such as CCR8, CKLF1, and CXCL12 also modulates cell migration via lamellipodia formation. These inflammatory processes likely promote VSMC migration in a LIMK-dependent manner. Whether inflammatory cytokines activate LIMK via Rac2 activation remains unknown. (PDFG-BB: Platelet derived growth factor BB; Arp 2/3: Actin related protein 2/3; CCR8: chemokine receptor-8; CKLF1: Chemokine-like factor 1; CXCL12: C-X-C motif chemokine 12; MLCP: Myosin light chain phosphatase).

    Article Snippet: Since the first report on the development of a selective inhibitor of LIMK activity by Bristol-Myers-Squibb in 2006, only one such molecule has reached clinical trials for treating glaucoma ( ).

    Techniques: Activity Assay, Migration, Activation Assay, Phospho-proteomics, Derivative Assay

    Representative studies on the role of LIMK in cardiovascular diseases.

    Journal: Frontiers in Physiology

    Article Title: LIM kinases in cardiovascular health and disease

    doi: 10.3389/fphys.2024.1506356

    Figure Lengend Snippet: Representative studies on the role of LIMK in cardiovascular diseases.

    Article Snippet: Since the first report on the development of a selective inhibitor of LIMK activity by Bristol-Myers-Squibb in 2006, only one such molecule has reached clinical trials for treating glaucoma ( ).

    Techniques: Migration