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mouse polyclonal antibodies against rhoa  (Proteintech)


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    Proteintech mouse polyclonal antibodies against rhoa
    Mouse Polyclonal Antibodies Against Rhoa, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 201 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+polyclonal+antibodies+against+rhoa/RHOA+Antibody/pm33085791-86-2-32
    Average 96 stars, based on 201 article reviews
    mouse polyclonal antibodies against rhoa - by Bioz Stars, 2026-09
    96/100 stars

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    Related Articles

    Western Blot:

    Article Title: Regulation of hepatic stellate cell contraction and cirrhotic portal hypertension by Wnt/β-catenin signalling via interaction with Gli1.
    Article Snippet: Rabbit polyclonal antibodies against α-smooth muscle actin (α-SMA) (#19245, for IHC 1:200 dilution, and IF 1:200 dilution), β-actin (#4970, for WB 1:1,000 dilution), lamin B1 (#13435, for WB 1:1,000 dilution), myosin light chain 2 (MLC2) (#3672, for WB 1:1,000 dilution), phospho-MLC2Ser19 (#3671, for IHC 1:200 dilution, WB 1:1,000 dilution, and IF 1:50 dilution), and TCF4 (#2569, for Co-IP 1:50 dilution, and ChIP 1:50 dilution) and mouse polyclonal antibodies against Gli1 (#2643, for Co-IP 1:50 dilution) and β-catenin (#2698, for Co-IP 1:50 dilution) were purchased from Cell Signaling Technology (Danvers, MA, USA). .. Rabbit or mouse polyclonal antibodies against RhoA (10749-1-AP, for WB 1:1,000 dilution), LARG (22441-1-AP, for WB 1:1,000 dilution), and β-catenin (17565-1-AP, for IHC 1:200 dilution, and IF 1:200 dilution) were purchased from Proteintech Group (Chicago, IL, USA). .. Background and Purpose: Portal hypertension is a lethal complication of cirrhosis.. Its mechanism and therapeutic targets remain largely unknown.. Hepatic stellate cell (HSC) contraction increases intrahepatic vascular resistance contributing to portal hypertension.

    Article Title: Regulation of hepatic stellate cell contraction and cirrhotic portal hypertension by Wnt/β-catenin signalling via interaction with Gli1.
    Article Snippet: The readings were continuously monitored by the PowerLab System (AD Instruments, Colorado Springs, CO, USA) for 20 min. 2248 ZHANG ET AL. 14765381, 2021, 11, D ow nloaded from https://bpspubs.onlinelibrary.w iley.com /doi/10.1111/bph.15289 by IN A SP - N E PA L , W iley O nline L ibrary on [08/01/2025]. .. Background and Purpose: Portal hypertension is a lethal complication of cirrhosis.. Its mechanism and therapeutic targets remain largely unknown.. Hepatic stellate cell (HSC) contraction increases intrahepatic vascular resistance contributing to portal hypertension. .. Background and Purpose: Portal hypertension is a lethal complication of cirrhosis.. Its mechanism and therapeutic targets remain largely unknown.. Hepatic stellate cell (HSC) contraction increases intrahepatic vascular resistance contributing to portal hypertension.

    Immunohistochemistry:

    Article Title: Regulation of hepatic stellate cell contraction and cirrhotic portal hypertension by Wnt/β-catenin signalling via interaction with Gli1.
    Article Snippet: Rabbit polyclonal antibodies against α-smooth muscle actin (α-SMA) (#19245, for IHC 1:200 dilution, and IF 1:200 dilution), β-actin (#4970, for WB 1:1,000 dilution), lamin B1 (#13435, for WB 1:1,000 dilution), myosin light chain 2 (MLC2) (#3672, for WB 1:1,000 dilution), phospho-MLC2Ser19 (#3671, for IHC 1:200 dilution, WB 1:1,000 dilution, and IF 1:50 dilution), and TCF4 (#2569, for Co-IP 1:50 dilution, and ChIP 1:50 dilution) and mouse polyclonal antibodies against Gli1 (#2643, for Co-IP 1:50 dilution) and β-catenin (#2698, for Co-IP 1:50 dilution) were purchased from Cell Signaling Technology (Danvers, MA, USA). .. Rabbit or mouse polyclonal antibodies against RhoA (10749-1-AP, for WB 1:1,000 dilution), LARG (22441-1-AP, for WB 1:1,000 dilution), and β-catenin (17565-1-AP, for IHC 1:200 dilution, and IF 1:200 dilution) were purchased from Proteintech Group (Chicago, IL, USA). .. Background and Purpose: Portal hypertension is a lethal complication of cirrhosis.. Its mechanism and therapeutic targets remain largely unknown.. Hepatic stellate cell (HSC) contraction increases intrahepatic vascular resistance contributing to portal hypertension.

    Article Title: Regulation of hepatic stellate cell contraction and cirrhotic portal hypertension by Wnt/β-catenin signalling via interaction with Gli1.
    Article Snippet: The readings were continuously monitored by the PowerLab System (AD Instruments, Colorado Springs, CO, USA) for 20 min. 2248 ZHANG ET AL. 14765381, 2021, 11, D ow nloaded from https://bpspubs.onlinelibrary.w iley.com /doi/10.1111/bph.15289 by IN A SP - N E PA L , W iley O nline L ibrary on [08/01/2025]. .. Background and Purpose: Portal hypertension is a lethal complication of cirrhosis.. Its mechanism and therapeutic targets remain largely unknown.. Hepatic stellate cell (HSC) contraction increases intrahepatic vascular resistance contributing to portal hypertension. .. Background and Purpose: Portal hypertension is a lethal complication of cirrhosis.. Its mechanism and therapeutic targets remain largely unknown.. Hepatic stellate cell (HSC) contraction increases intrahepatic vascular resistance contributing to portal hypertension.



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    mouse/rabbit polyclonal antibodies against rhoa ser188, akt thr180tyr182 and nfκb p50  (Cell Signaling Technology Inc)
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    Cell Signaling Technology Inc mouse/rabbit polyclonal antibodies against rhoa ser188, akt thr180tyr182 and nfκb p50
    The effect of chromogranin A (CHGA) and ubiquitin carboxyl‐terminal hydrolase isozyme L1 (UCHL1) silencing on <t>Rho‐GTPase/AKT/NFκB</t> pathway activation and the expression of EMT markers in CRC. After transfection with lentiviral shRNA targeting CHGA and UCHL1 (shCHGA and shUCHL1) or non‐targeting control (shControl), whole‐cell lysate proteins of HCT‐116 cells were subjected to western blotting, with antibodies against phosphorylation of Rho‐GTPase, AKT and <t>NFκB</t> <t>p50</t> (A) as well as β‐catenin, cyclin E, twist 1/2 and vimentin (B) β‐Actin served as the loading control. The protein levels were quantified through densitometric analysis with the ratio of the untreated control (Control) set as onefold. The quantitative data are presented as the mean of three repeats from three independent experiments. * p < 0.05, compared with the control group.
    Mouse/Rabbit Polyclonal Antibodies Against Rhoa Ser188, Akt Thr180tyr182 And Nfκb P50, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    mouse/rabbit polyclonal antibodies against rhoa ser188, akt thr180tyr182 and nfκb p50 - by Bioz Stars, 2026-09
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    mouse polyclonal antibodies against rhoa  (Proteintech)
    96
    Proteintech mouse polyclonal antibodies against rhoa
    The effect of chromogranin A (CHGA) and ubiquitin carboxyl‐terminal hydrolase isozyme L1 (UCHL1) silencing on <t>Rho‐GTPase/AKT/NFκB</t> pathway activation and the expression of EMT markers in CRC. After transfection with lentiviral shRNA targeting CHGA and UCHL1 (shCHGA and shUCHL1) or non‐targeting control (shControl), whole‐cell lysate proteins of HCT‐116 cells were subjected to western blotting, with antibodies against phosphorylation of Rho‐GTPase, AKT and <t>NFκB</t> <t>p50</t> (A) as well as β‐catenin, cyclin E, twist 1/2 and vimentin (B) β‐Actin served as the loading control. The protein levels were quantified through densitometric analysis with the ratio of the untreated control (Control) set as onefold. The quantitative data are presented as the mean of three repeats from three independent experiments. * p < 0.05, compared with the control group.
    Mouse Polyclonal Antibodies Against Rhoa, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    mouse polyclonal antibody against rhoa  (Santa Cruz Biotechnology)
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    The effect of chromogranin A (CHGA) and ubiquitin carboxyl‐terminal hydrolase isozyme L1 (UCHL1) silencing on <t>Rho‐GTPase/AKT/NFκB</t> pathway activation and the expression of EMT markers in CRC. After transfection with lentiviral shRNA targeting CHGA and UCHL1 (shCHGA and shUCHL1) or non‐targeting control (shControl), whole‐cell lysate proteins of HCT‐116 cells were subjected to western blotting, with antibodies against phosphorylation of Rho‐GTPase, AKT and <t>NFκB</t> <t>p50</t> (A) as well as β‐catenin, cyclin E, twist 1/2 and vimentin (B) β‐Actin served as the loading control. The protein levels were quantified through densitometric analysis with the ratio of the untreated control (Control) set as onefold. The quantitative data are presented as the mean of three repeats from three independent experiments. * p < 0.05, compared with the control group.
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    Image Search Results


    The effect of chromogranin A (CHGA) and ubiquitin carboxyl‐terminal hydrolase isozyme L1 (UCHL1) silencing on Rho‐GTPase/AKT/NFκB pathway activation and the expression of EMT markers in CRC. After transfection with lentiviral shRNA targeting CHGA and UCHL1 (shCHGA and shUCHL1) or non‐targeting control (shControl), whole‐cell lysate proteins of HCT‐116 cells were subjected to western blotting, with antibodies against phosphorylation of Rho‐GTPase, AKT and NFκB p50 (A) as well as β‐catenin, cyclin E, twist 1/2 and vimentin (B) β‐Actin served as the loading control. The protein levels were quantified through densitometric analysis with the ratio of the untreated control (Control) set as onefold. The quantitative data are presented as the mean of three repeats from three independent experiments. * p < 0.05, compared with the control group.

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Use of iTRAQ ‐based quantitative proteomic identification of CHGA and UCHL1 correlated with lymph node metastasis in colorectal carcinoma

    doi: 10.1111/jcmm.17793

    Figure Lengend Snippet: The effect of chromogranin A (CHGA) and ubiquitin carboxyl‐terminal hydrolase isozyme L1 (UCHL1) silencing on Rho‐GTPase/AKT/NFκB pathway activation and the expression of EMT markers in CRC. After transfection with lentiviral shRNA targeting CHGA and UCHL1 (shCHGA and shUCHL1) or non‐targeting control (shControl), whole‐cell lysate proteins of HCT‐116 cells were subjected to western blotting, with antibodies against phosphorylation of Rho‐GTPase, AKT and NFκB p50 (A) as well as β‐catenin, cyclin E, twist 1/2 and vimentin (B) β‐Actin served as the loading control. The protein levels were quantified through densitometric analysis with the ratio of the untreated control (Control) set as onefold. The quantitative data are presented as the mean of three repeats from three independent experiments. * p < 0.05, compared with the control group.

    Article Snippet: The antibodies were respectively obtained by Abcam Technology (Abcam) and Cell Signalling Technology, including mouse/rabbit polyclonal antibodies against RhoA Ser188, AKT Thr180Tyr182 and NFκB p50 bought from all culture materials were obtained from Gibco (Grand Island, NY, USA).

    Techniques: Ubiquitin Proteomics, Activation Assay, Expressing, Transfection, shRNA, Control, Western Blot, Phospho-proteomics

    Schematic presentation of the working model of CHGA and UCHL1 participate in promotion of the LNM‐associated CRC through endogenous Rho‐GTPase/AKT/NFκB signalling pathways‐mediated histone modification (H3K4me3) as reliable candidate LNM‐associated markers.

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Use of iTRAQ ‐based quantitative proteomic identification of CHGA and UCHL1 correlated with lymph node metastasis in colorectal carcinoma

    doi: 10.1111/jcmm.17793

    Figure Lengend Snippet: Schematic presentation of the working model of CHGA and UCHL1 participate in promotion of the LNM‐associated CRC through endogenous Rho‐GTPase/AKT/NFκB signalling pathways‐mediated histone modification (H3K4me3) as reliable candidate LNM‐associated markers.

    Article Snippet: The antibodies were respectively obtained by Abcam Technology (Abcam) and Cell Signalling Technology, including mouse/rabbit polyclonal antibodies against RhoA Ser188, AKT Thr180Tyr182 and NFκB p50 bought from all culture materials were obtained from Gibco (Grand Island, NY, USA).

    Techniques: Modification

    Alternation of histone modification of CHGA and UCHL1 promoters by the Rho‐GTPase/AKT/NFκB signalling pathways. After incubation with various concentrations of the specific inhibitors such as CCG‐1423, PDTC and wortmannin for 24 h, chromatin immunoprecipitation (ChIP) assays using antibodies against H3K4me3 was performed to pull down associated DNA in the HCT‐116 cells. Polymerase chain reaction amplified the precipitated DNA by using primer sets specific to the target sites (−1185 to −940 and −407 to −230) of CHGA and UCHL1 promoters. After normalized signal to the negative control ChIP asΔCT by subtracting the mean CT of the input from that of the individual region among the untreated control group, using the ΔΔCt method to calculate the effect of the specific inhibitors on specific genes. The data are presented as fold change of the untreated group (mean ± SD) of three independent experiments with * p < 0.01.

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Use of iTRAQ ‐based quantitative proteomic identification of CHGA and UCHL1 correlated with lymph node metastasis in colorectal carcinoma

    doi: 10.1111/jcmm.17793

    Figure Lengend Snippet: Alternation of histone modification of CHGA and UCHL1 promoters by the Rho‐GTPase/AKT/NFκB signalling pathways. After incubation with various concentrations of the specific inhibitors such as CCG‐1423, PDTC and wortmannin for 24 h, chromatin immunoprecipitation (ChIP) assays using antibodies against H3K4me3 was performed to pull down associated DNA in the HCT‐116 cells. Polymerase chain reaction amplified the precipitated DNA by using primer sets specific to the target sites (−1185 to −940 and −407 to −230) of CHGA and UCHL1 promoters. After normalized signal to the negative control ChIP asΔCT by subtracting the mean CT of the input from that of the individual region among the untreated control group, using the ΔΔCt method to calculate the effect of the specific inhibitors on specific genes. The data are presented as fold change of the untreated group (mean ± SD) of three independent experiments with * p < 0.01.

    Article Snippet: The antibodies were respectively obtained by Abcam Technology (Abcam) and Cell Signalling Technology, including mouse/rabbit polyclonal antibodies against RhoA Ser188, AKT Thr180Tyr182 and NFκB p50 bought from all culture materials were obtained from Gibco (Grand Island, NY, USA).

    Techniques: Modification, Incubation, Chromatin Immunoprecipitation, Polymerase Chain Reaction, Amplification, Negative Control, Control