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rac1 specific antibody  (Cytoskeleton Inc)


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    Cytoskeleton Inc rac1 specific antibody
    Fig. 1. Loss of NF1 reduces <t>RAC1-driven</t> melanoblast migration. A. Scratch-like migration assay representing the percentage of cell coverage after 6 h, 9 h and 12 h using either WT or NF1+/−melanoblasts (MB) in the presence of a RAC1 activator (CN04). B. RAC1 activity was measured by G-lisa in WT and NF1+/−melanoblasts (MB). C. Scratch-like migration assay after 3 h, 6 h, 9 h and 12 h in NF1+/−melanoblasts 48 h-post transfection with either a scramble siRNA (SCR) or with an NF1-specific siRNA (siNF1). D. Expression status of NF1 and expression of phosphorylated and non-phosphorylated ERK and AKT in NF1+/−melanoblasts by western blot. α-actinin was used as a loading control. GTP-RAC1 pulldown and total lysates were blotted with α-RAC1 antibody. E. Scratch-like migration assay representing the percentage of cell coverage after 9 h and 12 h in NF1+/−melanoblasts 48 h-post transfection with either a scramble siRNA (SCR) or with an NF1-specific siRNA (siNF1) and in the presence or absence of a RAC1 activator (CN04). *: SCR vs. siNF1, #: -CN04 vs. +CN04. F. GTP-RAC1 pulldown and total lysates were blotted with α-RAC1 antibody in the presence or absence of a RAC1 activator (CN04). **P < 0.01, *P < 0.05, ns: not significant (unpaired Student's t-test). All error bars represent the SEM of at least three independent experiments.
    Rac1 Specific Antibody, supplied by Cytoskeleton Inc, used in various techniques. Bioz Stars score: 95/100, based on 181 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/tissue+microarray+based+immunohistochemistry+analysis/Rac1+Pull-down+Activation+Assay+Biochem+Kit/pm32891903-48-12-15
    Average 95 stars, based on 181 article reviews
    rac1 specific antibody - by Bioz Stars, 2026-11
    95/100 stars

    Images

    1) Product Images from "NF1-RAC1 axis regulates migration of the melanocytic lineage."

    Article Title: NF1-RAC1 axis regulates migration of the melanocytic lineage.

    Journal: Translational oncology

    doi: 10.1016/j.tranon.2020.100858

    Fig. 1. Loss of NF1 reduces RAC1-driven melanoblast migration. A. Scratch-like migration assay representing the percentage of cell coverage after 6 h, 9 h and 12 h using either WT or NF1+/−melanoblasts (MB) in the presence of a RAC1 activator (CN04). B. RAC1 activity was measured by G-lisa in WT and NF1+/−melanoblasts (MB). C. Scratch-like migration assay after 3 h, 6 h, 9 h and 12 h in NF1+/−melanoblasts 48 h-post transfection with either a scramble siRNA (SCR) or with an NF1-specific siRNA (siNF1). D. Expression status of NF1 and expression of phosphorylated and non-phosphorylated ERK and AKT in NF1+/−melanoblasts by western blot. α-actinin was used as a loading control. GTP-RAC1 pulldown and total lysates were blotted with α-RAC1 antibody. E. Scratch-like migration assay representing the percentage of cell coverage after 9 h and 12 h in NF1+/−melanoblasts 48 h-post transfection with either a scramble siRNA (SCR) or with an NF1-specific siRNA (siNF1) and in the presence or absence of a RAC1 activator (CN04). *: SCR vs. siNF1, #: -CN04 vs. +CN04. F. GTP-RAC1 pulldown and total lysates were blotted with α-RAC1 antibody in the presence or absence of a RAC1 activator (CN04). **P < 0.01, *P < 0.05, ns: not significant (unpaired Student's t-test). All error bars represent the SEM of at least three independent experiments.
    Figure Legend Snippet: Fig. 1. Loss of NF1 reduces RAC1-driven melanoblast migration. A. Scratch-like migration assay representing the percentage of cell coverage after 6 h, 9 h and 12 h using either WT or NF1+/−melanoblasts (MB) in the presence of a RAC1 activator (CN04). B. RAC1 activity was measured by G-lisa in WT and NF1+/−melanoblasts (MB). C. Scratch-like migration assay after 3 h, 6 h, 9 h and 12 h in NF1+/−melanoblasts 48 h-post transfection with either a scramble siRNA (SCR) or with an NF1-specific siRNA (siNF1). D. Expression status of NF1 and expression of phosphorylated and non-phosphorylated ERK and AKT in NF1+/−melanoblasts by western blot. α-actinin was used as a loading control. GTP-RAC1 pulldown and total lysates were blotted with α-RAC1 antibody. E. Scratch-like migration assay representing the percentage of cell coverage after 9 h and 12 h in NF1+/−melanoblasts 48 h-post transfection with either a scramble siRNA (SCR) or with an NF1-specific siRNA (siNF1) and in the presence or absence of a RAC1 activator (CN04). *: SCR vs. siNF1, #: -CN04 vs. +CN04. F. GTP-RAC1 pulldown and total lysates were blotted with α-RAC1 antibody in the presence or absence of a RAC1 activator (CN04). **P < 0.01, *P < 0.05, ns: not significant (unpaired Student's t-test). All error bars represent the SEM of at least three independent experiments.

    Techniques Used: Migration, Activity Assay, Transfection, Expressing, Western Blot, Control

    Fig. 2. Loss of NF1 increases melanoma migration and is associated with increased PREX1 expression. A. NF1 mRNA expression under NF1 silencing with two siRNAs (NF1.6 and NF1.11) in SK-mel-23, Mel501, and SK-mel-103 melanoma cell lines. B. PREX1 mRNA expression under NF1 silencing with two siRNAs in SK-mel-23, Mel501, and SK- mel-103 cell lines. C. Scratch-like migration assay representing the percentage of cell coverage after 6 h, 12 h and 24 h under NF1 silencing in SK-mel-23, Mel501, and SK-mel- 103 cell lines. D. Scratch-like migration assay as in C, after additional transfection with siRNA control (scramble) or with PREX1 siRNA (siPREX1). E. Scratch-like migration assay as in C. in the absence (control) or presence (RAC1 inhibitor) of a RAC1 inhibitor. ***P < 0.001, **P < 0.01, *P < 0.05 (unpaired Student's t-test). All error bars rep- resent the SEM of at least three independent experiments.
    Figure Legend Snippet: Fig. 2. Loss of NF1 increases melanoma migration and is associated with increased PREX1 expression. A. NF1 mRNA expression under NF1 silencing with two siRNAs (NF1.6 and NF1.11) in SK-mel-23, Mel501, and SK-mel-103 melanoma cell lines. B. PREX1 mRNA expression under NF1 silencing with two siRNAs in SK-mel-23, Mel501, and SK- mel-103 cell lines. C. Scratch-like migration assay representing the percentage of cell coverage after 6 h, 12 h and 24 h under NF1 silencing in SK-mel-23, Mel501, and SK-mel- 103 cell lines. D. Scratch-like migration assay as in C, after additional transfection with siRNA control (scramble) or with PREX1 siRNA (siPREX1). E. Scratch-like migration assay as in C. in the absence (control) or presence (RAC1 inhibitor) of a RAC1 inhibitor. ***P < 0.001, **P < 0.01, *P < 0.05 (unpaired Student's t-test). All error bars rep- resent the SEM of at least three independent experiments.

    Techniques Used: Migration, Expressing, Transfection, Control

    Fig. 4. PREX is upregulated in low NF1 expressing melanoma metastases. A. Representative microphotographs of Tissue Microarray (TMA) containing primary and metastatic melanoma samples analysed by immunohistochemistry using a specific antibody against NF1, RAC1 and PREX1. Bar, 100 μm. B. Scoring of the immunohistochemistry staining was performed according to our previously described protocol [24]. Duplicates of valid punch samples are represented for each condition. Significance was tested using two-tailed t-test with *P < 0.05 and ns: not significant.
    Figure Legend Snippet: Fig. 4. PREX is upregulated in low NF1 expressing melanoma metastases. A. Representative microphotographs of Tissue Microarray (TMA) containing primary and metastatic melanoma samples analysed by immunohistochemistry using a specific antibody against NF1, RAC1 and PREX1. Bar, 100 μm. B. Scoring of the immunohistochemistry staining was performed according to our previously described protocol [24]. Duplicates of valid punch samples are represented for each condition. Significance was tested using two-tailed t-test with *P < 0.05 and ns: not significant.

    Techniques Used: Expressing, Microarray, Immunohistochemistry, Staining, Two Tailed Test

    Related Articles

    Activation Assay:

    Article Title: WNT11 suppresses tumor initiation and invasion by inactivating RAC1
    Article Snippet: .. RAC1 activation assays were performed using a pull-down assay kit to detect GTP-bound RAC1, following the manufacturer’s protocol from Cytoskeleton, Inc. (BK035; Denver, CO). ..

    Article Title: TLR4-paxillin-Rac1 signaling mediates LPS-induced dysregulation of keratinocyte function
    Article Snippet: .. Rac1 Activation Assay Kit , Cytoskeleton , CatBK035. .. BCA Protein Assay Kit , Thermo Fisher Scientific (Pierce) , Cat#23225.

    Article Title: Activated Rac1 promotes chondrocyte apoptosis through the NF-κB pathway in lumbar facet joint osteoarthritis.
    Article Snippet: Lumbar facet joint osteoarthritis (FJOA) is a spinal degenerative disease characterized by the degeneration of the articular cartilage of the lumbar facet joints, and it is one of the important causes of low back pain.. Similar to limb joints, the facet joint is a typical synovial joint, its main components include subchondral bone, articular cartilage, synovium and joint capsule (Kalichman and Hunter 2007).. FJOA is a pathological process involving the dysfunction of a facet joint, including the loss of articular cartilage and destruction of the extracellular matrix (ECM) balance (Gellhorn et al. 2013).

    Pull Down Assay:

    Article Title: WNT11 suppresses tumor initiation and invasion by inactivating RAC1
    Article Snippet: .. RAC1 activation assays were performed using a pull-down assay kit to detect GTP-bound RAC1, following the manufacturer’s protocol from Cytoskeleton, Inc. (BK035; Denver, CO). ..

    Article Title: Activated Rac1 promotes chondrocyte apoptosis through the NF-κB pathway in lumbar facet joint osteoarthritis.
    Article Snippet: Lumbar facet joint osteoarthritis (FJOA) is a spinal degenerative disease characterized by the degeneration of the articular cartilage of the lumbar facet joints, and it is one of the important causes of low back pain.. Similar to limb joints, the facet joint is a typical synovial joint, its main components include subchondral bone, articular cartilage, synovium and joint capsule (Kalichman and Hunter 2007).. FJOA is a pathological process involving the dysfunction of a facet joint, including the loss of articular cartilage and destruction of the extracellular matrix (ECM) balance (Gellhorn et al. 2013).

    other:

    Article Title: Protocol to identify covalent inhibitors targeting RhoA Cys16
    Article Snippet: Rac1 Pull-Down Activation Assay Biochem Kit , Cytoskeleton , Cat# BK035.

    Activity Assay:

    Article Title: Activated Rac1 promotes chondrocyte apoptosis through the NF-κB pathway in lumbar facet joint osteoarthritis.
    Article Snippet: Lumbar facet joint osteoarthritis (FJOA) is a spinal degenerative disease characterized by the degeneration of the articular cartilage of the lumbar facet joints, and it is one of the important causes of low back pain.. Similar to limb joints, the facet joint is a typical synovial joint, its main components include subchondral bone, articular cartilage, synovium and joint capsule (Kalichman and Hunter 2007).. FJOA is a pathological process involving the dysfunction of a facet joint, including the loss of articular cartilage and destruction of the extracellular matrix (ECM) balance (Gellhorn et al. 2013).



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    Cell type specific genes demonstrated at mRNA level. (A) Heat map of genes with cell type specific expression. (B) Heat map of selected genes with endothelial or epithelial cell type specific expression. (C) Immunohistochemistry staining of protein C1orf116 across human tissues showing its epithelial cell type specific expression. The panel shows a magnified view (20×) from tissue microarrays.

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