Review



limk1 inhibitor limki330 32  (Tocris)


Bioz Verified Symbol Tocris is a verified supplier
Bioz Manufacturer Symbol Tocris manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 93
      Buy from Supplier

    Structured Review

    Tocris limk1 inhibitor limki330 32
    FIGURE 3 Arhgef6 regulates signaling to Cofilin via PAK2 and <t>LIMK1.</t> (A) Western blots of total PAK2 and phospho-PAK2 (pPAK2) in wild-type (WT) and Arhgef6−/−(KO) CD4+ T cells with quantification (right). Total PAK2: Arhgef6−/−T cells normalized to WT, pPAK2: ratio of pPAK2/PAK2 for Arhgef6−/−T cells normalized to WT ratio. (B, C) Cells as in A, but for phospho-LIMK1 (pLIMK1) (B) and phospho-Cofilin (pCofilin) (C) (n = 3 experiments with one mouse of each genotype per experiment per Western blot). ns = not significant, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, by Student’s t-test. Values are mean ± SEM
    Limk1 Inhibitor Limki330 32, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 27 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/limk1 inhibitor limki330 32/product/Tocris
    Average 93 stars, based on 27 article reviews
    limk1 inhibitor limki330 32 - by Bioz Stars, 2026-02
    93/100 stars

    Images

    1) Product Images from "Arhgef6 (alpha‐PIX) cytoskeletal regulator signals to GTPases and Cofilin to couple T cell migration speed and persistence"

    Article Title: Arhgef6 (alpha‐PIX) cytoskeletal regulator signals to GTPases and Cofilin to couple T cell migration speed and persistence

    Journal: Journal of Leukocyte Biology

    doi: 10.1002/jlb.1a1219-719r

    FIGURE 3 Arhgef6 regulates signaling to Cofilin via PAK2 and LIMK1. (A) Western blots of total PAK2 and phospho-PAK2 (pPAK2) in wild-type (WT) and Arhgef6−/−(KO) CD4+ T cells with quantification (right). Total PAK2: Arhgef6−/−T cells normalized to WT, pPAK2: ratio of pPAK2/PAK2 for Arhgef6−/−T cells normalized to WT ratio. (B, C) Cells as in A, but for phospho-LIMK1 (pLIMK1) (B) and phospho-Cofilin (pCofilin) (C) (n = 3 experiments with one mouse of each genotype per experiment per Western blot). ns = not significant, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, by Student’s t-test. Values are mean ± SEM
    Figure Legend Snippet: FIGURE 3 Arhgef6 regulates signaling to Cofilin via PAK2 and LIMK1. (A) Western blots of total PAK2 and phospho-PAK2 (pPAK2) in wild-type (WT) and Arhgef6−/−(KO) CD4+ T cells with quantification (right). Total PAK2: Arhgef6−/−T cells normalized to WT, pPAK2: ratio of pPAK2/PAK2 for Arhgef6−/−T cells normalized to WT ratio. (B, C) Cells as in A, but for phospho-LIMK1 (pLIMK1) (B) and phospho-Cofilin (pCofilin) (C) (n = 3 experiments with one mouse of each genotype per experiment per Western blot). ns = not significant, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, by Student’s t-test. Values are mean ± SEM

    Techniques Used: Western Blot

    FIGURE 7 LIMK1 inhibition increases wild-type (WT) T cell migration speed. (A) Total internal reflection fluorescence (TIRF) images from Supporting Information Videos S5 to S8 (t = 10 s each) of WT and Arhgef6−/−CD4+ T cells treated with control ethanol vehicle or LIMK1 inhibitor, LIMKi3 (10 𝜇M for 4 h), stained with CellBrite live cell membrane dye and migrating on ICAM-1 display increased lamellipodia size for WT cells. Scale bar, 5 𝜇m. (B) LIMK1 inhibition in WT T cells causes increased lamellipodial width and area but has no effect on Arhgef6−/−T cells. Quantifi- cation of lamellipodial length (left), width (center), and area (right) for WT and Arhgef6−/−T cells either untreated vehicle control (ctrl) or treated with LIMKi3 as shown in (A). Bars = mean ± SEM, (n = 3 experiments with 30 cells each). ns = not significant, ****P < 0.0001, by 2-way ANOVA followed by Bonferroni’s post hoc test. (C) Representative track plots for WT and Arhgef6−/−T cells migrating on ICAM-1 either untreated (ctrl) or treated with LIMKi3. (D) Quantification of velocity, displacement and straightness for the samples shown in (c). Mean ± SD. *P < 0.05, ***P < 0.001, ****P < 0.0001, by Student’s t-test
    Figure Legend Snippet: FIGURE 7 LIMK1 inhibition increases wild-type (WT) T cell migration speed. (A) Total internal reflection fluorescence (TIRF) images from Supporting Information Videos S5 to S8 (t = 10 s each) of WT and Arhgef6−/−CD4+ T cells treated with control ethanol vehicle or LIMK1 inhibitor, LIMKi3 (10 𝜇M for 4 h), stained with CellBrite live cell membrane dye and migrating on ICAM-1 display increased lamellipodia size for WT cells. Scale bar, 5 𝜇m. (B) LIMK1 inhibition in WT T cells causes increased lamellipodial width and area but has no effect on Arhgef6−/−T cells. Quantifi- cation of lamellipodial length (left), width (center), and area (right) for WT and Arhgef6−/−T cells either untreated vehicle control (ctrl) or treated with LIMKi3 as shown in (A). Bars = mean ± SEM, (n = 3 experiments with 30 cells each). ns = not significant, ****P < 0.0001, by 2-way ANOVA followed by Bonferroni’s post hoc test. (C) Representative track plots for WT and Arhgef6−/−T cells migrating on ICAM-1 either untreated (ctrl) or treated with LIMKi3. (D) Quantification of velocity, displacement and straightness for the samples shown in (c). Mean ± SD. *P < 0.05, ***P < 0.001, ****P < 0.0001, by Student’s t-test

    Techniques Used: Inhibition, Migration, Fluorescence, Control, Staining, Membrane

    FIGURE 8 Schematic representation of Arhgef6-controlled signaling pathways. In wild-type (WT) cells, Arhgef6 and Arhgef7, RhoGEFs for Rac1 and Cdc42, repress signaling to actin reorganization and restrict lamellipodial formation to limit cell speed and maintain rela- tive straightness. In T cells lacking Arhgef6, cells migrate faster and turn more. Cdc42 is mislo- calized to the ICAM1-coated migration surface and Rac1 is overactivated. Moreover, PAK2, LIMK1, and Cofilin are all hypophosphorylated meaning that Cofilin, which promotes actin severing and polymerization, is overactivated. The mechanisms for Rac1 activation of lamel- lipodial extension are not characterized here but may include hyperativation of WAVE and Arp2/3, both required for lamellipodia exten- sion. Arhgef7 expression is increased, likely due to its taking the place of Arhgef6 in the PIX-GIT complex, but it cannot compensate fully for the absence of Arhgef6 as the immune cell-specific Arhgef6 may be required for targeting the complex to T cell specific receptors
    Figure Legend Snippet: FIGURE 8 Schematic representation of Arhgef6-controlled signaling pathways. In wild-type (WT) cells, Arhgef6 and Arhgef7, RhoGEFs for Rac1 and Cdc42, repress signaling to actin reorganization and restrict lamellipodial formation to limit cell speed and maintain rela- tive straightness. In T cells lacking Arhgef6, cells migrate faster and turn more. Cdc42 is mislo- calized to the ICAM1-coated migration surface and Rac1 is overactivated. Moreover, PAK2, LIMK1, and Cofilin are all hypophosphorylated meaning that Cofilin, which promotes actin severing and polymerization, is overactivated. The mechanisms for Rac1 activation of lamel- lipodial extension are not characterized here but may include hyperativation of WAVE and Arp2/3, both required for lamellipodia exten- sion. Arhgef7 expression is increased, likely due to its taking the place of Arhgef6 in the PIX-GIT complex, but it cannot compensate fully for the absence of Arhgef6 as the immune cell-specific Arhgef6 may be required for targeting the complex to T cell specific receptors

    Techniques Used: Protein-Protein interactions, Migration, Activation Assay, Expressing



    Similar Products

    limk1 inhibitor limki330 32  (Tocris)
    93
    Tocris limk1 inhibitor limki330 32
    FIGURE 3 Arhgef6 regulates signaling to Cofilin via PAK2 and <t>LIMK1.</t> (A) Western blots of total PAK2 and phospho-PAK2 (pPAK2) in wild-type (WT) and Arhgef6−/−(KO) CD4+ T cells with quantification (right). Total PAK2: Arhgef6−/−T cells normalized to WT, pPAK2: ratio of pPAK2/PAK2 for Arhgef6−/−T cells normalized to WT ratio. (B, C) Cells as in A, but for phospho-LIMK1 (pLIMK1) (B) and phospho-Cofilin (pCofilin) (C) (n = 3 experiments with one mouse of each genotype per experiment per Western blot). ns = not significant, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, by Student’s t-test. Values are mean ± SEM
    Limk1 Inhibitor Limki330 32, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/limk1 inhibitor limki330 32/product/Tocris
    Average 93 stars, based on 1 article reviews
    limk1 inhibitor limki330 32 - by Bioz Stars, 2026-02
    93/100 stars
    		  Buy from Supplier

    Image Search Results


    FIGURE 3 Arhgef6 regulates signaling to Cofilin via PAK2 and LIMK1. (A) Western blots of total PAK2 and phospho-PAK2 (pPAK2) in wild-type (WT) and Arhgef6−/−(KO) CD4+ T cells with quantification (right). Total PAK2: Arhgef6−/−T cells normalized to WT, pPAK2: ratio of pPAK2/PAK2 for Arhgef6−/−T cells normalized to WT ratio. (B, C) Cells as in A, but for phospho-LIMK1 (pLIMK1) (B) and phospho-Cofilin (pCofilin) (C) (n = 3 experiments with one mouse of each genotype per experiment per Western blot). ns = not significant, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, by Student’s t-test. Values are mean ± SEM

    Journal: Journal of Leukocyte Biology

    Article Title: Arhgef6 (alpha‐PIX) cytoskeletal regulator signals to GTPases and Cofilin to couple T cell migration speed and persistence

    doi: 10.1002/jlb.1a1219-719r

    Figure Lengend Snippet: FIGURE 3 Arhgef6 regulates signaling to Cofilin via PAK2 and LIMK1. (A) Western blots of total PAK2 and phospho-PAK2 (pPAK2) in wild-type (WT) and Arhgef6−/−(KO) CD4+ T cells with quantification (right). Total PAK2: Arhgef6−/−T cells normalized to WT, pPAK2: ratio of pPAK2/PAK2 for Arhgef6−/−T cells normalized to WT ratio. (B, C) Cells as in A, but for phospho-LIMK1 (pLIMK1) (B) and phospho-Cofilin (pCofilin) (C) (n = 3 experiments with one mouse of each genotype per experiment per Western blot). ns = not significant, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, by Student’s t-test. Values are mean ± SEM

    Article Snippet: In some experiments the cells were additionally treated by adding LIMK1 inhibitor LIMKi330–32 (10 μM) (4745, Tocris,Wiesbaden, Germany) for 4 h before harvesting or with ethanol alone as a vehicle control at 0.05%.

    Techniques: Western Blot

    FIGURE 7 LIMK1 inhibition increases wild-type (WT) T cell migration speed. (A) Total internal reflection fluorescence (TIRF) images from Supporting Information Videos S5 to S8 (t = 10 s each) of WT and Arhgef6−/−CD4+ T cells treated with control ethanol vehicle or LIMK1 inhibitor, LIMKi3 (10 𝜇M for 4 h), stained with CellBrite live cell membrane dye and migrating on ICAM-1 display increased lamellipodia size for WT cells. Scale bar, 5 𝜇m. (B) LIMK1 inhibition in WT T cells causes increased lamellipodial width and area but has no effect on Arhgef6−/−T cells. Quantifi- cation of lamellipodial length (left), width (center), and area (right) for WT and Arhgef6−/−T cells either untreated vehicle control (ctrl) or treated with LIMKi3 as shown in (A). Bars = mean ± SEM, (n = 3 experiments with 30 cells each). ns = not significant, ****P < 0.0001, by 2-way ANOVA followed by Bonferroni’s post hoc test. (C) Representative track plots for WT and Arhgef6−/−T cells migrating on ICAM-1 either untreated (ctrl) or treated with LIMKi3. (D) Quantification of velocity, displacement and straightness for the samples shown in (c). Mean ± SD. *P < 0.05, ***P < 0.001, ****P < 0.0001, by Student’s t-test

    Journal: Journal of Leukocyte Biology

    Article Title: Arhgef6 (alpha‐PIX) cytoskeletal regulator signals to GTPases and Cofilin to couple T cell migration speed and persistence

    doi: 10.1002/jlb.1a1219-719r

    Figure Lengend Snippet: FIGURE 7 LIMK1 inhibition increases wild-type (WT) T cell migration speed. (A) Total internal reflection fluorescence (TIRF) images from Supporting Information Videos S5 to S8 (t = 10 s each) of WT and Arhgef6−/−CD4+ T cells treated with control ethanol vehicle or LIMK1 inhibitor, LIMKi3 (10 𝜇M for 4 h), stained with CellBrite live cell membrane dye and migrating on ICAM-1 display increased lamellipodia size for WT cells. Scale bar, 5 𝜇m. (B) LIMK1 inhibition in WT T cells causes increased lamellipodial width and area but has no effect on Arhgef6−/−T cells. Quantifi- cation of lamellipodial length (left), width (center), and area (right) for WT and Arhgef6−/−T cells either untreated vehicle control (ctrl) or treated with LIMKi3 as shown in (A). Bars = mean ± SEM, (n = 3 experiments with 30 cells each). ns = not significant, ****P < 0.0001, by 2-way ANOVA followed by Bonferroni’s post hoc test. (C) Representative track plots for WT and Arhgef6−/−T cells migrating on ICAM-1 either untreated (ctrl) or treated with LIMKi3. (D) Quantification of velocity, displacement and straightness for the samples shown in (c). Mean ± SD. *P < 0.05, ***P < 0.001, ****P < 0.0001, by Student’s t-test

    Article Snippet: In some experiments the cells were additionally treated by adding LIMK1 inhibitor LIMKi330–32 (10 μM) (4745, Tocris,Wiesbaden, Germany) for 4 h before harvesting or with ethanol alone as a vehicle control at 0.05%.

    Techniques: Inhibition, Migration, Fluorescence, Control, Staining, Membrane

    FIGURE 8 Schematic representation of Arhgef6-controlled signaling pathways. In wild-type (WT) cells, Arhgef6 and Arhgef7, RhoGEFs for Rac1 and Cdc42, repress signaling to actin reorganization and restrict lamellipodial formation to limit cell speed and maintain rela- tive straightness. In T cells lacking Arhgef6, cells migrate faster and turn more. Cdc42 is mislo- calized to the ICAM1-coated migration surface and Rac1 is overactivated. Moreover, PAK2, LIMK1, and Cofilin are all hypophosphorylated meaning that Cofilin, which promotes actin severing and polymerization, is overactivated. The mechanisms for Rac1 activation of lamel- lipodial extension are not characterized here but may include hyperativation of WAVE and Arp2/3, both required for lamellipodia exten- sion. Arhgef7 expression is increased, likely due to its taking the place of Arhgef6 in the PIX-GIT complex, but it cannot compensate fully for the absence of Arhgef6 as the immune cell-specific Arhgef6 may be required for targeting the complex to T cell specific receptors

    Journal: Journal of Leukocyte Biology

    Article Title: Arhgef6 (alpha‐PIX) cytoskeletal regulator signals to GTPases and Cofilin to couple T cell migration speed and persistence

    doi: 10.1002/jlb.1a1219-719r

    Figure Lengend Snippet: FIGURE 8 Schematic representation of Arhgef6-controlled signaling pathways. In wild-type (WT) cells, Arhgef6 and Arhgef7, RhoGEFs for Rac1 and Cdc42, repress signaling to actin reorganization and restrict lamellipodial formation to limit cell speed and maintain rela- tive straightness. In T cells lacking Arhgef6, cells migrate faster and turn more. Cdc42 is mislo- calized to the ICAM1-coated migration surface and Rac1 is overactivated. Moreover, PAK2, LIMK1, and Cofilin are all hypophosphorylated meaning that Cofilin, which promotes actin severing and polymerization, is overactivated. The mechanisms for Rac1 activation of lamel- lipodial extension are not characterized here but may include hyperativation of WAVE and Arp2/3, both required for lamellipodia exten- sion. Arhgef7 expression is increased, likely due to its taking the place of Arhgef6 in the PIX-GIT complex, but it cannot compensate fully for the absence of Arhgef6 as the immune cell-specific Arhgef6 may be required for targeting the complex to T cell specific receptors

    Article Snippet: In some experiments the cells were additionally treated by adding LIMK1 inhibitor LIMKi330–32 (10 μM) (4745, Tocris,Wiesbaden, Germany) for 4 h before harvesting or with ethanol alone as a vehicle control at 0.05%.

    Techniques: Protein-Protein interactions, Migration, Activation Assay, Expressing