Review



rac1 inhibitor w56  (MedChemExpress)


Bioz Verified Symbol MedChemExpress is a verified supplier
Bioz Manufacturer Symbol MedChemExpress manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 92
      Buy from Supplier

    Structured Review

    MedChemExpress rac1 inhibitor w56
    SIRT7 induces cytoskeletal remodeling via <t>RAC1.</t> ( A ) RAC1activation in H37Rv-infected Sirt7 −/− and Sirt7 +/+ BMDMs assayed at 0 min and 30 min post-infection. “Input” represents RAC1 protein levels in whole-cell lysates, while “IP: PAK1-PBD” indicates active RAC1 levels. ( B ) Immunoblot and immunoprecipitation assays illustrating the interaction of SIRT7 and RAC1 in THP1-derived macrophages transfected with si- RAC1 or normal control (si-NC) siRNA. ( C and G ) Flow cytometry analysis quantifying the phagocytosis of GFP-H37Ra by Sirt7 −/− and Sirt7 +/+ BMDMs under the conditions of RAC1 inhibitor or activator treatment. GFP + BMDMs represent cells that phagocytosed GFP-H37Ra. ( D ) Intracellular CFU counts of H37Rv at 4 hours post-infection in Sirt7 −/− and Sirt7 +/+ BMDMs. ( E and H ) Following a 4-hour infection period with H37Rv, macrophages were washed with phosphate-buffered saline (PBS) to eliminate unphagocytosed bacteria. Subsequently, a fresh complete medium was introduced, either containing an RAC1 inhibitor or activator. CFU counts were determined 68 hours later. ( F and I ) The survival ratio of H37Rv was evaluated in Sirt7 −/− BMDMs compared to WT BMDMs, following treatment with either RAC1 inhibitor or activator. ( J and K ) Immunoblot analysis was performed to assess the expression of LC3II in Sirt7 −/− and Sirt7 +/+ BMDMs treated with an RAC1 inhibitor or Baf-A1. The expression levels of LC3II were quantified and are shown relative to GAPDH, as indicated below the corresponding bands. Data are presented as means ± SEM, * P < 0.05, ** P < 0.01, and *** P < 0.001, as determined by one-way ANOVA with Tukey’s multiple comparisons test. Each experiment was independently replicated two to three times.
    Rac1 Inhibitor W56, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-p1382a/Rac1+Inhibitor+W56/pmc11481912-197-5-8
    Average 92 stars, based on 1 article reviews
    rac1 inhibitor w56 - by Bioz Stars, 2026-10
    92/100 stars

    Images

    1) Product Images from "SIRT7 remodels the cytoskeleton via RAC1 to enhance host resistance to Mycobacterium tuberculosis"

    Article Title: SIRT7 remodels the cytoskeleton via RAC1 to enhance host resistance to Mycobacterium tuberculosis

    Journal: mBio

    doi: 10.1128/mbio.00756-24

    SIRT7 induces cytoskeletal remodeling via RAC1. ( A ) RAC1activation in H37Rv-infected Sirt7 −/− and Sirt7 +/+ BMDMs assayed at 0 min and 30 min post-infection. “Input” represents RAC1 protein levels in whole-cell lysates, while “IP: PAK1-PBD” indicates active RAC1 levels. ( B ) Immunoblot and immunoprecipitation assays illustrating the interaction of SIRT7 and RAC1 in THP1-derived macrophages transfected with si- RAC1 or normal control (si-NC) siRNA. ( C and G ) Flow cytometry analysis quantifying the phagocytosis of GFP-H37Ra by Sirt7 −/− and Sirt7 +/+ BMDMs under the conditions of RAC1 inhibitor or activator treatment. GFP + BMDMs represent cells that phagocytosed GFP-H37Ra. ( D ) Intracellular CFU counts of H37Rv at 4 hours post-infection in Sirt7 −/− and Sirt7 +/+ BMDMs. ( E and H ) Following a 4-hour infection period with H37Rv, macrophages were washed with phosphate-buffered saline (PBS) to eliminate unphagocytosed bacteria. Subsequently, a fresh complete medium was introduced, either containing an RAC1 inhibitor or activator. CFU counts were determined 68 hours later. ( F and I ) The survival ratio of H37Rv was evaluated in Sirt7 −/− BMDMs compared to WT BMDMs, following treatment with either RAC1 inhibitor or activator. ( J and K ) Immunoblot analysis was performed to assess the expression of LC3II in Sirt7 −/− and Sirt7 +/+ BMDMs treated with an RAC1 inhibitor or Baf-A1. The expression levels of LC3II were quantified and are shown relative to GAPDH, as indicated below the corresponding bands. Data are presented as means ± SEM, * P < 0.05, ** P < 0.01, and *** P < 0.001, as determined by one-way ANOVA with Tukey’s multiple comparisons test. Each experiment was independently replicated two to three times.
    Figure Legend Snippet: SIRT7 induces cytoskeletal remodeling via RAC1. ( A ) RAC1activation in H37Rv-infected Sirt7 −/− and Sirt7 +/+ BMDMs assayed at 0 min and 30 min post-infection. “Input” represents RAC1 protein levels in whole-cell lysates, while “IP: PAK1-PBD” indicates active RAC1 levels. ( B ) Immunoblot and immunoprecipitation assays illustrating the interaction of SIRT7 and RAC1 in THP1-derived macrophages transfected with si- RAC1 or normal control (si-NC) siRNA. ( C and G ) Flow cytometry analysis quantifying the phagocytosis of GFP-H37Ra by Sirt7 −/− and Sirt7 +/+ BMDMs under the conditions of RAC1 inhibitor or activator treatment. GFP + BMDMs represent cells that phagocytosed GFP-H37Ra. ( D ) Intracellular CFU counts of H37Rv at 4 hours post-infection in Sirt7 −/− and Sirt7 +/+ BMDMs. ( E and H ) Following a 4-hour infection period with H37Rv, macrophages were washed with phosphate-buffered saline (PBS) to eliminate unphagocytosed bacteria. Subsequently, a fresh complete medium was introduced, either containing an RAC1 inhibitor or activator. CFU counts were determined 68 hours later. ( F and I ) The survival ratio of H37Rv was evaluated in Sirt7 −/− BMDMs compared to WT BMDMs, following treatment with either RAC1 inhibitor or activator. ( J and K ) Immunoblot analysis was performed to assess the expression of LC3II in Sirt7 −/− and Sirt7 +/+ BMDMs treated with an RAC1 inhibitor or Baf-A1. The expression levels of LC3II were quantified and are shown relative to GAPDH, as indicated below the corresponding bands. Data are presented as means ± SEM, * P < 0.05, ** P < 0.01, and *** P < 0.001, as determined by one-way ANOVA with Tukey’s multiple comparisons test. Each experiment was independently replicated two to three times.

    Techniques Used: Infection, Western Blot, Immunoprecipitation, Derivative Assay, Transfection, Control, Flow Cytometry, Saline, Bacteria, Expressing

    Overexpression of Sirt7 enhanced host anti-TB immunity. ( A and B ) Intracellular CFU counts of H37Rv at 4 hours and 72 hours post-infection in Sirt7 +/+ and Sirt7 TG BMDMs. ( C ) The survival ratio of H37Rv was evaluated in Sirt7 TG BMDMs compared to WT controls. ( D ) LC3II expression was elevated in Sirt7 TG BMDMs compared to WT controls. ( E ) RAC1 activation in H37Rv-infected Sirt7 +/+ and Sirt7 TG BMDMs assayed at 0 min and 30 min post-infection, with “Input” indicating total RAC1 and “IP: PAK1-PBD” indicates active RAC1. ( F and G ) Bacterial burden in the lungs and spleens of Sirt7 +/+ and Sirt7 TG mice was assessed in the tissue homogenates. ( H ) Histopathological analysis of lung sections from Sirt7 +/+ and Sirt7 TG mice infected with H37Rv. Sections were stained with hematoxylin and eosin, and images were captured using a NanoZoomer digital pathology system. Data are presented as means ± SEM, * P < 0.05, ** P < 0.01, and *** P < 0.001 by Student’s two-tailed unpaired t-test. Each experiment was independently replicated two to three times.
    Figure Legend Snippet: Overexpression of Sirt7 enhanced host anti-TB immunity. ( A and B ) Intracellular CFU counts of H37Rv at 4 hours and 72 hours post-infection in Sirt7 +/+ and Sirt7 TG BMDMs. ( C ) The survival ratio of H37Rv was evaluated in Sirt7 TG BMDMs compared to WT controls. ( D ) LC3II expression was elevated in Sirt7 TG BMDMs compared to WT controls. ( E ) RAC1 activation in H37Rv-infected Sirt7 +/+ and Sirt7 TG BMDMs assayed at 0 min and 30 min post-infection, with “Input” indicating total RAC1 and “IP: PAK1-PBD” indicates active RAC1. ( F and G ) Bacterial burden in the lungs and spleens of Sirt7 +/+ and Sirt7 TG mice was assessed in the tissue homogenates. ( H ) Histopathological analysis of lung sections from Sirt7 +/+ and Sirt7 TG mice infected with H37Rv. Sections were stained with hematoxylin and eosin, and images were captured using a NanoZoomer digital pathology system. Data are presented as means ± SEM, * P < 0.05, ** P < 0.01, and *** P < 0.001 by Student’s two-tailed unpaired t-test. Each experiment was independently replicated two to three times.

    Techniques Used: Over Expression, Infection, Expressing, Activation Assay, Staining, Two Tailed Test

    Related Articles

    Activity Assay:

    Article Title: MicroRNA-129-5p-mediated translational repression of microglial ROCK1 leads to enhanced phagocytosis.
    Article Snippet: .. Similar observation was noted when Rac1 activity was inhibited using Rac1 inhibitor, NSC 23766 trihydrochloride (Cat: HY-15723A, Medchem express) (Fig. 7H). ..

    Article Title: MicroRNA-129-5p-mediated translational repression of microglial ROCK1 leads to enhanced phagocytosis
    Article Snippet: .. Similar observation was noted when Rac1 activity was inhibited using Rac1 inhibitor, NSC 23766 trihydrochloride (Cat: HY-15723A, Medchem express) ( H ). ..

    Flow Cytometry:

    Article Title: SIRT7 remodels the cytoskeleton via RAC1 to enhance host resistance to Mycobacterium tuberculosis .
    Article Snippet: The following antibodies were used: Anti-SIRT7 (Santa Cruz Biotechnology, #sc-365344), anti-RAC1 (Abcam, #ab155938), anti-RAC1 (cytoskeleton, #ARC03), anti-LC3II (R&D, #MAB85581), anti-P62 (Abcam, #ab109012), Mouse mAb IgG1 Isotype (cell signal ing technology, # 5415), Rat anti-Mouse IgG1 Secondary (Invitrogen, #11–4015-82), PE/Cyanine7 anti-human CD3 (Biolegend, #300316), APC anti-human CD14 (Biole gend, #325608), APC/Cyanine7 anti-human CD19 (Biolegend, #302218), anti-GAPDH (Abcam, #ab9485), Acetylated-Lysine Antibody (CST, #9441), Zombie Aqua (Biolegend, #423102), PE/Cyanine7 anti-mouse CD3 (Biolegend, #100220), APC anti-mouse CD45 (Biolegend, #147708), PE anti-mouse Ly-6G (Biolegend, #127608), Brilliant Violet 605 anti-mouse Ly-6C (Biolegend, #128036), Alexa Fluor 488 anti-mouse CD170 (Biole gend, # 155524), PE/Cyanine5 anti-mouse/human CD11b (Biolegend, #101210), and APC/Cyanine7 anti-mouse CD19 (Biolegend, #115530). .. The following chemicals were used: RAC1 Inhibitor W56 (Medchemexpress, #HY-P1382), RAC/CDC42 Activator II (cytoskeleton, #CN02), pHrodo Red succinimidyl (NHS) ester (Invitrogen, #P36600), Mouse Intracellular (nuclear/transcription factor) Protein Flow Cytometry Workflow Kit (Invitrogen, # A53017), pHrodo Red succinimidyl ester (Invitrogen, #P36600), Active Rac1 Pull-Down and Detection Kit (Thermo Scientific, #16118), SPHEROTM Fluorescent Particles (Spherotech, #FL-6068), Bafilomycin A1 (MCE, #HY-100558), Chloroquine (MCE, # HY-17589A), fluorescein isothiocyanate (FITC) Annexin V Apoptosis Detection Kit with PI (BioLegend, #640914), MitoSOX Mitochondrial Superoxide Indicators (Invitrogen, # M36008), H2DCF-DA (Invitrogen, # D399), Mouse CXCL1 ELISA Kit (HUABIO, # EM0017), Mouse CXCL2 ELISA Kit (HUABIO, # EM0018). ..

    Article Title: SIRT7 remodels the cytoskeleton via RAC1 to enhance host resistance to Mycobacterium tuberculosis
    Article Snippet: The following antibodies were used: Anti-SIRT7 (Santa Cruz Biotechnology, #sc-365344), anti-RAC1 (Abcam, #ab155938), anti-RAC1 (cytoskeleton, #ARC03), anti-LC3II (R&D, #MAB85581), anti-P62 (Abcam, #ab109012), Mouse mAb IgG1 Isotype (cell signaling technology, # 5415), Rat anti-Mouse IgG1 Secondary (Invitrogen, #11–4015-82), PE/Cyanine7 anti-human CD3 (Biolegend, #300316), APC anti-human CD14 (Biolegend, #325608), APC/Cyanine7 anti-human CD19 (Biolegend, #302218), anti-GAPDH (Abcam, #ab9485), Acetylated-Lysine Antibody (CST, #9441), Zombie Aqua (Biolegend, #423102), PE/Cyanine7 anti-mouse CD3 (Biolegend, #100220), APC anti-mouse CD45 (Biolegend, #147708), PE anti-mouse Ly-6G (Biolegend, #127608), Brilliant Violet 605 anti-mouse Ly-6C (Biolegend, #128036), Alexa Fluor 488 anti-mouse CD170 (Biolegend, # 155524), PE/Cyanine5 anti-mouse/human CD11b (Biolegend, #101210), and APC/Cyanine7 anti-mouse CD19 (Biolegend, #115530). .. The following chemicals were used: RAC1 Inhibitor W56 (Medchemexpress, #HY-P1382), RAC/CDC42 Activator II (cytoskeleton, #CN02), pHrodo Red succinimidyl (NHS) ester (Invitrogen, #P36600), Mouse Intracellular (nuclear/transcription factor) Protein Flow Cytometry Workflow Kit (Invitrogen, # A53017), pHrodo Red succinimidyl ester (Invitrogen, #P36600), Active Rac1 Pull-Down and Detection Kit (Thermo Scientific, #16118), SPHEROTM Fluorescent Particles (Spherotech, #FL-6068), Bafilomycin A1 (MCE, #HY-100558), Chloroquine (MCE, # HY-17589A), fluorescein isothiocyanate (FITC) Annexin V Apoptosis Detection Kit with PI (BioLegend, #640914), MitoSOX Mitochondrial Superoxide Indicators (Invitrogen, # M36008), H2DCF-DA (Invitrogen, # D399), Mouse CXCL1 ELISA Kit (HUABIO, # EM0017), Mouse CXCL2 ELISA Kit (HUABIO, # EM0018). ..

    Enzyme-linked Immunosorbent Assay:

    Article Title: SIRT7 remodels the cytoskeleton via RAC1 to enhance host resistance to Mycobacterium tuberculosis .
    Article Snippet: The following antibodies were used: Anti-SIRT7 (Santa Cruz Biotechnology, #sc-365344), anti-RAC1 (Abcam, #ab155938), anti-RAC1 (cytoskeleton, #ARC03), anti-LC3II (R&D, #MAB85581), anti-P62 (Abcam, #ab109012), Mouse mAb IgG1 Isotype (cell signal ing technology, # 5415), Rat anti-Mouse IgG1 Secondary (Invitrogen, #11–4015-82), PE/Cyanine7 anti-human CD3 (Biolegend, #300316), APC anti-human CD14 (Biole gend, #325608), APC/Cyanine7 anti-human CD19 (Biolegend, #302218), anti-GAPDH (Abcam, #ab9485), Acetylated-Lysine Antibody (CST, #9441), Zombie Aqua (Biolegend, #423102), PE/Cyanine7 anti-mouse CD3 (Biolegend, #100220), APC anti-mouse CD45 (Biolegend, #147708), PE anti-mouse Ly-6G (Biolegend, #127608), Brilliant Violet 605 anti-mouse Ly-6C (Biolegend, #128036), Alexa Fluor 488 anti-mouse CD170 (Biole gend, # 155524), PE/Cyanine5 anti-mouse/human CD11b (Biolegend, #101210), and APC/Cyanine7 anti-mouse CD19 (Biolegend, #115530). .. The following chemicals were used: RAC1 Inhibitor W56 (Medchemexpress, #HY-P1382), RAC/CDC42 Activator II (cytoskeleton, #CN02), pHrodo Red succinimidyl (NHS) ester (Invitrogen, #P36600), Mouse Intracellular (nuclear/transcription factor) Protein Flow Cytometry Workflow Kit (Invitrogen, # A53017), pHrodo Red succinimidyl ester (Invitrogen, #P36600), Active Rac1 Pull-Down and Detection Kit (Thermo Scientific, #16118), SPHEROTM Fluorescent Particles (Spherotech, #FL-6068), Bafilomycin A1 (MCE, #HY-100558), Chloroquine (MCE, # HY-17589A), fluorescein isothiocyanate (FITC) Annexin V Apoptosis Detection Kit with PI (BioLegend, #640914), MitoSOX Mitochondrial Superoxide Indicators (Invitrogen, # M36008), H2DCF-DA (Invitrogen, # D399), Mouse CXCL1 ELISA Kit (HUABIO, # EM0017), Mouse CXCL2 ELISA Kit (HUABIO, # EM0018). ..

    Article Title: SIRT7 remodels the cytoskeleton via RAC1 to enhance host resistance to Mycobacterium tuberculosis
    Article Snippet: The following antibodies were used: Anti-SIRT7 (Santa Cruz Biotechnology, #sc-365344), anti-RAC1 (Abcam, #ab155938), anti-RAC1 (cytoskeleton, #ARC03), anti-LC3II (R&D, #MAB85581), anti-P62 (Abcam, #ab109012), Mouse mAb IgG1 Isotype (cell signaling technology, # 5415), Rat anti-Mouse IgG1 Secondary (Invitrogen, #11–4015-82), PE/Cyanine7 anti-human CD3 (Biolegend, #300316), APC anti-human CD14 (Biolegend, #325608), APC/Cyanine7 anti-human CD19 (Biolegend, #302218), anti-GAPDH (Abcam, #ab9485), Acetylated-Lysine Antibody (CST, #9441), Zombie Aqua (Biolegend, #423102), PE/Cyanine7 anti-mouse CD3 (Biolegend, #100220), APC anti-mouse CD45 (Biolegend, #147708), PE anti-mouse Ly-6G (Biolegend, #127608), Brilliant Violet 605 anti-mouse Ly-6C (Biolegend, #128036), Alexa Fluor 488 anti-mouse CD170 (Biolegend, # 155524), PE/Cyanine5 anti-mouse/human CD11b (Biolegend, #101210), and APC/Cyanine7 anti-mouse CD19 (Biolegend, #115530). .. The following chemicals were used: RAC1 Inhibitor W56 (Medchemexpress, #HY-P1382), RAC/CDC42 Activator II (cytoskeleton, #CN02), pHrodo Red succinimidyl (NHS) ester (Invitrogen, #P36600), Mouse Intracellular (nuclear/transcription factor) Protein Flow Cytometry Workflow Kit (Invitrogen, # A53017), pHrodo Red succinimidyl ester (Invitrogen, #P36600), Active Rac1 Pull-Down and Detection Kit (Thermo Scientific, #16118), SPHEROTM Fluorescent Particles (Spherotech, #FL-6068), Bafilomycin A1 (MCE, #HY-100558), Chloroquine (MCE, # HY-17589A), fluorescein isothiocyanate (FITC) Annexin V Apoptosis Detection Kit with PI (BioLegend, #640914), MitoSOX Mitochondrial Superoxide Indicators (Invitrogen, # M36008), H2DCF-DA (Invitrogen, # D399), Mouse CXCL1 ELISA Kit (HUABIO, # EM0017), Mouse CXCL2 ELISA Kit (HUABIO, # EM0018). ..

    Activation Assay:

    Article Title: Targeting CCL2-CCR4 axis suppress cell migration of head and neck squamous cell carcinoma.
    Article Snippet: .. CCL2 enhances HNSCC cell motility via promoting Rac1phosphorylated MLC (p-MLC) activation Given that the Rac1-p-MLC signal had been reported to play an important role in cell motility by promoting the contractile motion of the myosin light chain, we used interruption approaches with a specific inhibitor to block Rac1 (100 μM, NSC 23766, MedChemExpress, Monmouth Junction, NJ), we found that the cell migration was suppressed in HNSCC cells treated with CCL2 (Fig. 3A, B). ..

    Blocking Assay:

    Article Title: Targeting CCL2-CCR4 axis suppress cell migration of head and neck squamous cell carcinoma.
    Article Snippet: .. CCL2 enhances HNSCC cell motility via promoting Rac1phosphorylated MLC (p-MLC) activation Given that the Rac1-p-MLC signal had been reported to play an important role in cell motility by promoting the contractile motion of the myosin light chain, we used interruption approaches with a specific inhibitor to block Rac1 (100 μM, NSC 23766, MedChemExpress, Monmouth Junction, NJ), we found that the cell migration was suppressed in HNSCC cells treated with CCL2 (Fig. 3A, B). ..

    Migration:

    Article Title: Targeting CCL2-CCR4 axis suppress cell migration of head and neck squamous cell carcinoma.
    Article Snippet: .. CCL2 enhances HNSCC cell motility via promoting Rac1phosphorylated MLC (p-MLC) activation Given that the Rac1-p-MLC signal had been reported to play an important role in cell motility by promoting the contractile motion of the myosin light chain, we used interruption approaches with a specific inhibitor to block Rac1 (100 μM, NSC 23766, MedChemExpress, Monmouth Junction, NJ), we found that the cell migration was suppressed in HNSCC cells treated with CCL2 (Fig. 3A, B). ..



    Similar Products

    rac1 inhibitor w56  (MedChemExpress)
    92
    MedChemExpress rac1 inhibitor w56
    SIRT7 induces cytoskeletal remodeling via <t>RAC1.</t> ( A ) RAC1activation in H37Rv-infected Sirt7 −/− and Sirt7 +/+ BMDMs assayed at 0 min and 30 min post-infection. “Input” represents RAC1 protein levels in whole-cell lysates, while “IP: PAK1-PBD” indicates active RAC1 levels. ( B ) Immunoblot and immunoprecipitation assays illustrating the interaction of SIRT7 and RAC1 in THP1-derived macrophages transfected with si- RAC1 or normal control (si-NC) siRNA. ( C and G ) Flow cytometry analysis quantifying the phagocytosis of GFP-H37Ra by Sirt7 −/− and Sirt7 +/+ BMDMs under the conditions of RAC1 inhibitor or activator treatment. GFP + BMDMs represent cells that phagocytosed GFP-H37Ra. ( D ) Intracellular CFU counts of H37Rv at 4 hours post-infection in Sirt7 −/− and Sirt7 +/+ BMDMs. ( E and H ) Following a 4-hour infection period with H37Rv, macrophages were washed with phosphate-buffered saline (PBS) to eliminate unphagocytosed bacteria. Subsequently, a fresh complete medium was introduced, either containing an RAC1 inhibitor or activator. CFU counts were determined 68 hours later. ( F and I ) The survival ratio of H37Rv was evaluated in Sirt7 −/− BMDMs compared to WT BMDMs, following treatment with either RAC1 inhibitor or activator. ( J and K ) Immunoblot analysis was performed to assess the expression of LC3II in Sirt7 −/− and Sirt7 +/+ BMDMs treated with an RAC1 inhibitor or Baf-A1. The expression levels of LC3II were quantified and are shown relative to GAPDH, as indicated below the corresponding bands. Data are presented as means ± SEM, * P < 0.05, ** P < 0.01, and *** P < 0.001, as determined by one-way ANOVA with Tukey’s multiple comparisons test. Each experiment was independently replicated two to three times.
    Rac1 Inhibitor W56, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-p1382a/Rac1+Inhibitor+W56/pmc11481912-197-5-8
    Average 92 stars, based on 1 article reviews
    rac1 inhibitor w56 - by Bioz Stars, 2026-10
    92/100 stars
    		  Buy from Supplier
    rac1 inhibitor assay  (MedChemExpress)
    92
    MedChemExpress rac1 inhibitor assay
    SIRT7 induces cytoskeletal remodeling via <t>RAC1.</t> ( A ) RAC1activation in H37Rv-infected Sirt7 −/− and Sirt7 +/+ BMDMs assayed at 0 min and 30 min post-infection. “Input” represents RAC1 protein levels in whole-cell lysates, while “IP: PAK1-PBD” indicates active RAC1 levels. ( B ) Immunoblot and immunoprecipitation assays illustrating the interaction of SIRT7 and RAC1 in THP1-derived macrophages transfected with si- RAC1 or normal control (si-NC) siRNA. ( C and G ) Flow cytometry analysis quantifying the phagocytosis of GFP-H37Ra by Sirt7 −/− and Sirt7 +/+ BMDMs under the conditions of RAC1 inhibitor or activator treatment. GFP + BMDMs represent cells that phagocytosed GFP-H37Ra. ( D ) Intracellular CFU counts of H37Rv at 4 hours post-infection in Sirt7 −/− and Sirt7 +/+ BMDMs. ( E and H ) Following a 4-hour infection period with H37Rv, macrophages were washed with phosphate-buffered saline (PBS) to eliminate unphagocytosed bacteria. Subsequently, a fresh complete medium was introduced, either containing an RAC1 inhibitor or activator. CFU counts were determined 68 hours later. ( F and I ) The survival ratio of H37Rv was evaluated in Sirt7 −/− BMDMs compared to WT BMDMs, following treatment with either RAC1 inhibitor or activator. ( J and K ) Immunoblot analysis was performed to assess the expression of LC3II in Sirt7 −/− and Sirt7 +/+ BMDMs treated with an RAC1 inhibitor or Baf-A1. The expression levels of LC3II were quantified and are shown relative to GAPDH, as indicated below the corresponding bands. Data are presented as means ± SEM, * P < 0.05, ** P < 0.01, and *** P < 0.001, as determined by one-way ANOVA with Tukey’s multiple comparisons test. Each experiment was independently replicated two to three times.
    Rac1 Inhibitor Assay, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-p1382a/Rac1+Inhibitor+W56/pm41274251-68-0-15
    Average 92 stars, based on 1 article reviews
    rac1 inhibitor assay - by Bioz Stars, 2026-10
    92/100 stars
    		  Buy from Supplier
    rac1 inhibitor  (MedChemExpress)
    92
    MedChemExpress rac1 inhibitor
    Effect of inhibition of ROCK1, miR-129-5p and <t>Rac1</t> on microglial phagocytosis. BV2 microglia were treated in vitro with various combination of arsenic, anti-miR and ROCK1 siRNA and cultured for 72 h. A , cells were harvested and the levels of miR-129-5p were checked in control and different treatment groups. B , the levels of ROCK1 mRNA were also checked using qRT-PCR. C , Levels of ROCK1 were checked using Western blot analysis in various experimental groups. D , phagocytic potential was also checked in control and treated BV2 cells. At 69th h of incubation CM-Dil dye-tagged neuronal debri were added to different treatment groups of BV2 cells and incubated further for 3 h and assessed for phagocytosis. E , level of Rac1 mRNA and ( F ) Rac1 protein were found to be unaffected by arsenic exposure. G , involvement of Rac1 in phagocytosis was determined by using siRNA. Rac1 siRNA was observed to reverse the arsenic-induced enhanced phagocytosis. H , phagocytosis assay was performed in exposure to various combinations of arsenic, anti-miR-129-5p, Rac1 inhibitor and ROCK1 siRNA to to confirm the signaling axis. Effect of arsenic and anti-miR-129-5p on the level of active Rac1 was also detected in BV2 cells, ( I ) the image of the Western blot represents the level of active Rac1 in the pull-down sample (equal volume of the pull down sample loaded in each lane). J , the image of Western blot represents the level of total Rac1 in the whole cell lysate. The band intensity of the blots were quantitated and represented as scatter bar graph. n = 3 to 5 independent in vitro experiments. All the quantitative data were represented as hybrid scatter-bar graph. Bar graphs represent mean ± SD. For comparing control and arsenic-exposed group Mann-whitney test was performed and “One-way ANOVA” was used for comparing more than two groups followed by post hoc analysis by “Tukey’s test”. “ p ” denotes the level of significance in comparison to control; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, non-significant.
    Rac1 Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-p1382a/Rac1+Inhibitor+W56/pmc12221357-288-0-9
    Average 92 stars, based on 1 article reviews
    rac1 inhibitor - by Bioz Stars, 2026-10
    92/100 stars
    		  Buy from Supplier
    inhibitor  (MedChemExpress)
    92
    MedChemExpress inhibitor
    Effect of inhibition of ROCK1, miR-129-5p and <t>Rac1</t> on microglial phagocytosis. BV2 microglia were treated in vitro with various combination of arsenic, anti-miR and ROCK1 siRNA and cultured for 72 h. A , cells were harvested and the levels of miR-129-5p were checked in control and different treatment groups. B , the levels of ROCK1 mRNA were also checked using qRT-PCR. C , Levels of ROCK1 were checked using Western blot analysis in various experimental groups. D , phagocytic potential was also checked in control and treated BV2 cells. At 69th h of incubation CM-Dil dye-tagged neuronal debri were added to different treatment groups of BV2 cells and incubated further for 3 h and assessed for phagocytosis. E , level of Rac1 mRNA and ( F ) Rac1 protein were found to be unaffected by arsenic exposure. G , involvement of Rac1 in phagocytosis was determined by using siRNA. Rac1 siRNA was observed to reverse the arsenic-induced enhanced phagocytosis. H , phagocytosis assay was performed in exposure to various combinations of arsenic, anti-miR-129-5p, Rac1 inhibitor and ROCK1 siRNA to to confirm the signaling axis. Effect of arsenic and anti-miR-129-5p on the level of active Rac1 was also detected in BV2 cells, ( I ) the image of the Western blot represents the level of active Rac1 in the pull-down sample (equal volume of the pull down sample loaded in each lane). J , the image of Western blot represents the level of total Rac1 in the whole cell lysate. The band intensity of the blots were quantitated and represented as scatter bar graph. n = 3 to 5 independent in vitro experiments. All the quantitative data were represented as hybrid scatter-bar graph. Bar graphs represent mean ± SD. For comparing control and arsenic-exposed group Mann-whitney test was performed and “One-way ANOVA” was used for comparing more than two groups followed by post hoc analysis by “Tukey’s test”. “ p ” denotes the level of significance in comparison to control; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, non-significant.
    Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-p1382a/Rac1+Inhibitor+W56/pm35177591-61-44-52
    Average 92 stars, based on 1 article reviews
    inhibitor - by Bioz Stars, 2026-10
    92/100 stars
    		  Buy from Supplier
    rac1  (MedChemExpress)
    92
    MedChemExpress rac1
    Effect of inhibition of ROCK1, miR-129-5p and <t>Rac1</t> on microglial phagocytosis. BV2 microglia were treated in vitro with various combination of arsenic, anti-miR and ROCK1 siRNA and cultured for 72 h. A , cells were harvested and the levels of miR-129-5p were checked in control and different treatment groups. B , the levels of ROCK1 mRNA were also checked using qRT-PCR. C , Levels of ROCK1 were checked using Western blot analysis in various experimental groups. D , phagocytic potential was also checked in control and treated BV2 cells. At 69th h of incubation CM-Dil dye-tagged neuronal debri were added to different treatment groups of BV2 cells and incubated further for 3 h and assessed for phagocytosis. E , level of Rac1 mRNA and ( F ) Rac1 protein were found to be unaffected by arsenic exposure. G , involvement of Rac1 in phagocytosis was determined by using siRNA. Rac1 siRNA was observed to reverse the arsenic-induced enhanced phagocytosis. H , phagocytosis assay was performed in exposure to various combinations of arsenic, anti-miR-129-5p, Rac1 inhibitor and ROCK1 siRNA to to confirm the signaling axis. Effect of arsenic and anti-miR-129-5p on the level of active Rac1 was also detected in BV2 cells, ( I ) the image of the Western blot represents the level of active Rac1 in the pull-down sample (equal volume of the pull down sample loaded in each lane). J , the image of Western blot represents the level of total Rac1 in the whole cell lysate. The band intensity of the blots were quantitated and represented as scatter bar graph. n = 3 to 5 independent in vitro experiments. All the quantitative data were represented as hybrid scatter-bar graph. Bar graphs represent mean ± SD. For comparing control and arsenic-exposed group Mann-whitney test was performed and “One-way ANOVA” was used for comparing more than two groups followed by post hoc analysis by “Tukey’s test”. “ p ” denotes the level of significance in comparison to control; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, non-significant.
    Rac1, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-p1382a/Rac1+Inhibitor+W56/pmc08278229__NIHMS1722138___supplement___2-426-1-17
    Average 92 stars, based on 1 article reviews
    rac1 - by Bioz Stars, 2026-10
    92/100 stars
    		  Buy from Supplier

    Image Search Results


    SIRT7 induces cytoskeletal remodeling via RAC1. ( A ) RAC1activation in H37Rv-infected Sirt7 −/− and Sirt7 +/+ BMDMs assayed at 0 min and 30 min post-infection. “Input” represents RAC1 protein levels in whole-cell lysates, while “IP: PAK1-PBD” indicates active RAC1 levels. ( B ) Immunoblot and immunoprecipitation assays illustrating the interaction of SIRT7 and RAC1 in THP1-derived macrophages transfected with si- RAC1 or normal control (si-NC) siRNA. ( C and G ) Flow cytometry analysis quantifying the phagocytosis of GFP-H37Ra by Sirt7 −/− and Sirt7 +/+ BMDMs under the conditions of RAC1 inhibitor or activator treatment. GFP + BMDMs represent cells that phagocytosed GFP-H37Ra. ( D ) Intracellular CFU counts of H37Rv at 4 hours post-infection in Sirt7 −/− and Sirt7 +/+ BMDMs. ( E and H ) Following a 4-hour infection period with H37Rv, macrophages were washed with phosphate-buffered saline (PBS) to eliminate unphagocytosed bacteria. Subsequently, a fresh complete medium was introduced, either containing an RAC1 inhibitor or activator. CFU counts were determined 68 hours later. ( F and I ) The survival ratio of H37Rv was evaluated in Sirt7 −/− BMDMs compared to WT BMDMs, following treatment with either RAC1 inhibitor or activator. ( J and K ) Immunoblot analysis was performed to assess the expression of LC3II in Sirt7 −/− and Sirt7 +/+ BMDMs treated with an RAC1 inhibitor or Baf-A1. The expression levels of LC3II were quantified and are shown relative to GAPDH, as indicated below the corresponding bands. Data are presented as means ± SEM, * P < 0.05, ** P < 0.01, and *** P < 0.001, as determined by one-way ANOVA with Tukey’s multiple comparisons test. Each experiment was independently replicated two to three times.

    Journal: mBio

    Article Title: SIRT7 remodels the cytoskeleton via RAC1 to enhance host resistance to Mycobacterium tuberculosis

    doi: 10.1128/mbio.00756-24

    Figure Lengend Snippet: SIRT7 induces cytoskeletal remodeling via RAC1. ( A ) RAC1activation in H37Rv-infected Sirt7 −/− and Sirt7 +/+ BMDMs assayed at 0 min and 30 min post-infection. “Input” represents RAC1 protein levels in whole-cell lysates, while “IP: PAK1-PBD” indicates active RAC1 levels. ( B ) Immunoblot and immunoprecipitation assays illustrating the interaction of SIRT7 and RAC1 in THP1-derived macrophages transfected with si- RAC1 or normal control (si-NC) siRNA. ( C and G ) Flow cytometry analysis quantifying the phagocytosis of GFP-H37Ra by Sirt7 −/− and Sirt7 +/+ BMDMs under the conditions of RAC1 inhibitor or activator treatment. GFP + BMDMs represent cells that phagocytosed GFP-H37Ra. ( D ) Intracellular CFU counts of H37Rv at 4 hours post-infection in Sirt7 −/− and Sirt7 +/+ BMDMs. ( E and H ) Following a 4-hour infection period with H37Rv, macrophages were washed with phosphate-buffered saline (PBS) to eliminate unphagocytosed bacteria. Subsequently, a fresh complete medium was introduced, either containing an RAC1 inhibitor or activator. CFU counts were determined 68 hours later. ( F and I ) The survival ratio of H37Rv was evaluated in Sirt7 −/− BMDMs compared to WT BMDMs, following treatment with either RAC1 inhibitor or activator. ( J and K ) Immunoblot analysis was performed to assess the expression of LC3II in Sirt7 −/− and Sirt7 +/+ BMDMs treated with an RAC1 inhibitor or Baf-A1. The expression levels of LC3II were quantified and are shown relative to GAPDH, as indicated below the corresponding bands. Data are presented as means ± SEM, * P < 0.05, ** P < 0.01, and *** P < 0.001, as determined by one-way ANOVA with Tukey’s multiple comparisons test. Each experiment was independently replicated two to three times.

    Article Snippet: The following chemicals were used: RAC1 Inhibitor W56 (Medchemexpress, #HY-P1382), RAC/CDC42 Activator II (cytoskeleton, #CN02), pHrodo Red succinimidyl (NHS) ester (Invitrogen, #P36600), Mouse Intracellular (nuclear/transcription factor) Protein Flow Cytometry Workflow Kit (Invitrogen, # A53017), pHrodo Red succinimidyl ester (Invitrogen, #P36600), Active Rac1 Pull-Down and Detection Kit (Thermo Scientific, #16118), SPHEROTM Fluorescent Particles (Spherotech, #FL-6068), Bafilomycin A1 (MCE, #HY-100558), Chloroquine (MCE, # HY-17589A), fluorescein isothiocyanate (FITC) Annexin V Apoptosis Detection Kit with PI (BioLegend, #640914), MitoSOX Mitochondrial Superoxide Indicators (Invitrogen, # M36008), H2DCF-DA (Invitrogen, # D399), Mouse CXCL1 ELISA Kit (HUABIO, # EM0017), Mouse CXCL2 ELISA Kit (HUABIO, # EM0018).

    Techniques: Infection, Western Blot, Immunoprecipitation, Derivative Assay, Transfection, Control, Flow Cytometry, Saline, Bacteria, Expressing

    Overexpression of Sirt7 enhanced host anti-TB immunity. ( A and B ) Intracellular CFU counts of H37Rv at 4 hours and 72 hours post-infection in Sirt7 +/+ and Sirt7 TG BMDMs. ( C ) The survival ratio of H37Rv was evaluated in Sirt7 TG BMDMs compared to WT controls. ( D ) LC3II expression was elevated in Sirt7 TG BMDMs compared to WT controls. ( E ) RAC1 activation in H37Rv-infected Sirt7 +/+ and Sirt7 TG BMDMs assayed at 0 min and 30 min post-infection, with “Input” indicating total RAC1 and “IP: PAK1-PBD” indicates active RAC1. ( F and G ) Bacterial burden in the lungs and spleens of Sirt7 +/+ and Sirt7 TG mice was assessed in the tissue homogenates. ( H ) Histopathological analysis of lung sections from Sirt7 +/+ and Sirt7 TG mice infected with H37Rv. Sections were stained with hematoxylin and eosin, and images were captured using a NanoZoomer digital pathology system. Data are presented as means ± SEM, * P < 0.05, ** P < 0.01, and *** P < 0.001 by Student’s two-tailed unpaired t-test. Each experiment was independently replicated two to three times.

    Journal: mBio

    Article Title: SIRT7 remodels the cytoskeleton via RAC1 to enhance host resistance to Mycobacterium tuberculosis

    doi: 10.1128/mbio.00756-24

    Figure Lengend Snippet: Overexpression of Sirt7 enhanced host anti-TB immunity. ( A and B ) Intracellular CFU counts of H37Rv at 4 hours and 72 hours post-infection in Sirt7 +/+ and Sirt7 TG BMDMs. ( C ) The survival ratio of H37Rv was evaluated in Sirt7 TG BMDMs compared to WT controls. ( D ) LC3II expression was elevated in Sirt7 TG BMDMs compared to WT controls. ( E ) RAC1 activation in H37Rv-infected Sirt7 +/+ and Sirt7 TG BMDMs assayed at 0 min and 30 min post-infection, with “Input” indicating total RAC1 and “IP: PAK1-PBD” indicates active RAC1. ( F and G ) Bacterial burden in the lungs and spleens of Sirt7 +/+ and Sirt7 TG mice was assessed in the tissue homogenates. ( H ) Histopathological analysis of lung sections from Sirt7 +/+ and Sirt7 TG mice infected with H37Rv. Sections were stained with hematoxylin and eosin, and images were captured using a NanoZoomer digital pathology system. Data are presented as means ± SEM, * P < 0.05, ** P < 0.01, and *** P < 0.001 by Student’s two-tailed unpaired t-test. Each experiment was independently replicated two to three times.

    Article Snippet: The following chemicals were used: RAC1 Inhibitor W56 (Medchemexpress, #HY-P1382), RAC/CDC42 Activator II (cytoskeleton, #CN02), pHrodo Red succinimidyl (NHS) ester (Invitrogen, #P36600), Mouse Intracellular (nuclear/transcription factor) Protein Flow Cytometry Workflow Kit (Invitrogen, # A53017), pHrodo Red succinimidyl ester (Invitrogen, #P36600), Active Rac1 Pull-Down and Detection Kit (Thermo Scientific, #16118), SPHEROTM Fluorescent Particles (Spherotech, #FL-6068), Bafilomycin A1 (MCE, #HY-100558), Chloroquine (MCE, # HY-17589A), fluorescein isothiocyanate (FITC) Annexin V Apoptosis Detection Kit with PI (BioLegend, #640914), MitoSOX Mitochondrial Superoxide Indicators (Invitrogen, # M36008), H2DCF-DA (Invitrogen, # D399), Mouse CXCL1 ELISA Kit (HUABIO, # EM0017), Mouse CXCL2 ELISA Kit (HUABIO, # EM0018).

    Techniques: Over Expression, Infection, Expressing, Activation Assay, Staining, Two Tailed Test

    Effect of inhibition of ROCK1, miR-129-5p and Rac1 on microglial phagocytosis. BV2 microglia were treated in vitro with various combination of arsenic, anti-miR and ROCK1 siRNA and cultured for 72 h. A , cells were harvested and the levels of miR-129-5p were checked in control and different treatment groups. B , the levels of ROCK1 mRNA were also checked using qRT-PCR. C , Levels of ROCK1 were checked using Western blot analysis in various experimental groups. D , phagocytic potential was also checked in control and treated BV2 cells. At 69th h of incubation CM-Dil dye-tagged neuronal debri were added to different treatment groups of BV2 cells and incubated further for 3 h and assessed for phagocytosis. E , level of Rac1 mRNA and ( F ) Rac1 protein were found to be unaffected by arsenic exposure. G , involvement of Rac1 in phagocytosis was determined by using siRNA. Rac1 siRNA was observed to reverse the arsenic-induced enhanced phagocytosis. H , phagocytosis assay was performed in exposure to various combinations of arsenic, anti-miR-129-5p, Rac1 inhibitor and ROCK1 siRNA to to confirm the signaling axis. Effect of arsenic and anti-miR-129-5p on the level of active Rac1 was also detected in BV2 cells, ( I ) the image of the Western blot represents the level of active Rac1 in the pull-down sample (equal volume of the pull down sample loaded in each lane). J , the image of Western blot represents the level of total Rac1 in the whole cell lysate. The band intensity of the blots were quantitated and represented as scatter bar graph. n = 3 to 5 independent in vitro experiments. All the quantitative data were represented as hybrid scatter-bar graph. Bar graphs represent mean ± SD. For comparing control and arsenic-exposed group Mann-whitney test was performed and “One-way ANOVA” was used for comparing more than two groups followed by post hoc analysis by “Tukey’s test”. “ p ” denotes the level of significance in comparison to control; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, non-significant.

    Journal: The Journal of Biological Chemistry

    Article Title: MicroRNA-129-5p-mediated translational repression of microglial ROCK1 leads to enhanced phagocytosis

    doi: 10.1016/j.jbc.2025.110293

    Figure Lengend Snippet: Effect of inhibition of ROCK1, miR-129-5p and Rac1 on microglial phagocytosis. BV2 microglia were treated in vitro with various combination of arsenic, anti-miR and ROCK1 siRNA and cultured for 72 h. A , cells were harvested and the levels of miR-129-5p were checked in control and different treatment groups. B , the levels of ROCK1 mRNA were also checked using qRT-PCR. C , Levels of ROCK1 were checked using Western blot analysis in various experimental groups. D , phagocytic potential was also checked in control and treated BV2 cells. At 69th h of incubation CM-Dil dye-tagged neuronal debri were added to different treatment groups of BV2 cells and incubated further for 3 h and assessed for phagocytosis. E , level of Rac1 mRNA and ( F ) Rac1 protein were found to be unaffected by arsenic exposure. G , involvement of Rac1 in phagocytosis was determined by using siRNA. Rac1 siRNA was observed to reverse the arsenic-induced enhanced phagocytosis. H , phagocytosis assay was performed in exposure to various combinations of arsenic, anti-miR-129-5p, Rac1 inhibitor and ROCK1 siRNA to to confirm the signaling axis. Effect of arsenic and anti-miR-129-5p on the level of active Rac1 was also detected in BV2 cells, ( I ) the image of the Western blot represents the level of active Rac1 in the pull-down sample (equal volume of the pull down sample loaded in each lane). J , the image of Western blot represents the level of total Rac1 in the whole cell lysate. The band intensity of the blots were quantitated and represented as scatter bar graph. n = 3 to 5 independent in vitro experiments. All the quantitative data were represented as hybrid scatter-bar graph. Bar graphs represent mean ± SD. For comparing control and arsenic-exposed group Mann-whitney test was performed and “One-way ANOVA” was used for comparing more than two groups followed by post hoc analysis by “Tukey’s test”. “ p ” denotes the level of significance in comparison to control; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, non-significant.

    Article Snippet: Rac1 inhibitor, NSC 23766 trihydrochloride (HY-15723A), was obtained from MedchemExpress.

    Techniques: Inhibition, In Vitro, Cell Culture, Control, Quantitative RT-PCR, Western Blot, Incubation, Phagocytosis Assay, MANN-WHITNEY, Comparison