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Proteintech bcar3

<t>BCAR3</t> was identified as a substrate of PTPN14. A) The results of IP‐MS, following CompPASS analysis, yielded high‐confidence candidate PTPN14‐interacting proteins. B) Exogenous IP‐Western Blot analysis validated the interaction of PTPN14 and BCAR3. Three independent experiments were performed. C) Endogenous IP‐Western Blot analysis validated the interaction of PTPN14 and BCAR3. D) BCAR3 was knockdown in control or PTPN14‐KO MDA‐MB‐231 cells and cell viability under ULA conditions was assessed every 24 h for 5 days using the CCK8 assay (left); validation of protein expression levels in each cell group through Western Blotting (right). Three independent experiments were performed. E) After the knockdown of BCAR3 in PTPN14‐KO MDA‐MB‐231 cells, the phosphorylation levels of AKT and ERK were assessed. Three independent experiments were performed. F) Tyrosine phosphorylated protein IP‐Western Blot analysis was conducted in both control MDA‐MB‐231 cells and PTPN14‐KO MDA‐MB‐231 cells. Three independent experiments were performed. G) Tyrosine phosphorylated protein IP‐Western Blot analysis was conducted in both PTPN14‐HA MDA‐MB‐231 cells and PTPN14‐D1079A‐HA MDA‐MB‐231 cells.

Bcar3, supplied by Proteintech, used in various techniques. Bioz Stars score: 92/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/bcar3/BCAR3+Antibody/pmc11348215-273-44-53
Average 92 stars, based on 3 article reviews

bcar3 - by Bioz Stars, 2026-09

92/100 stars

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1) Product Images from "mRNA‐Lipid Nanoparticle‐Mediated Restoration of PTPN14 Exhibits Antitumor Effects by Overcoming Anoikis Resistance in Triple‐Negative Breast Cancer"

Article Title: mRNA‐Lipid Nanoparticle‐Mediated Restoration of PTPN14 Exhibits Antitumor Effects by Overcoming Anoikis Resistance in Triple‐Negative Breast Cancer

Journal: Advanced Science

doi: 10.1002/advs.202309988

BCAR3 was identified as a substrate of PTPN14. A) The results of IP‐MS, following CompPASS analysis, yielded high‐confidence candidate PTPN14‐interacting proteins. B) Exogenous IP‐Western Blot analysis validated the interaction of PTPN14 and BCAR3. Three independent experiments were performed. C) Endogenous IP‐Western Blot analysis validated the interaction of PTPN14 and BCAR3. D) BCAR3 was knockdown in control or PTPN14‐KO MDA‐MB‐231 cells and cell viability under ULA conditions was assessed every 24 h for 5 days using the CCK8 assay (left); validation of protein expression levels in each cell group through Western Blotting (right). Three independent experiments were performed. E) After the knockdown of BCAR3 in PTPN14‐KO MDA‐MB‐231 cells, the phosphorylation levels of AKT and ERK were assessed. Three independent experiments were performed. F) Tyrosine phosphorylated protein IP‐Western Blot analysis was conducted in both control MDA‐MB‐231 cells and PTPN14‐KO MDA‐MB‐231 cells. Three independent experiments were performed. G) Tyrosine phosphorylated protein IP‐Western Blot analysis was conducted in both PTPN14‐HA MDA‐MB‐231 cells and PTPN14‐D1079A‐HA MDA‐MB‐231 cells.

Figure Legend Snippet: BCAR3 was identified as a substrate of PTPN14. A) The results of IP‐MS, following CompPASS analysis, yielded high‐confidence candidate PTPN14‐interacting proteins. B) Exogenous IP‐Western Blot analysis validated the interaction of PTPN14 and BCAR3. Three independent experiments were performed. C) Endogenous IP‐Western Blot analysis validated the interaction of PTPN14 and BCAR3. D) BCAR3 was knockdown in control or PTPN14‐KO MDA‐MB‐231 cells and cell viability under ULA conditions was assessed every 24 h for 5 days using the CCK8 assay (left); validation of protein expression levels in each cell group through Western Blotting (right). Three independent experiments were performed. E) After the knockdown of BCAR3 in PTPN14‐KO MDA‐MB‐231 cells, the phosphorylation levels of AKT and ERK were assessed. Three independent experiments were performed. F) Tyrosine phosphorylated protein IP‐Western Blot analysis was conducted in both control MDA‐MB‐231 cells and PTPN14‐KO MDA‐MB‐231 cells. Three independent experiments were performed. G) Tyrosine phosphorylated protein IP‐Western Blot analysis was conducted in both PTPN14‐HA MDA‐MB‐231 cells and PTPN14‐D1079A‐HA MDA‐MB‐231 cells.

Techniques Used: Western Blot, Knockdown, Control, CCK-8 Assay, Expressing

Western Blot:

Article Title: mRNA‐Lipid Nanoparticle‐Mediated Restoration of PTPN14 Exhibits Antitumor Effects by Overcoming Anoikis Resistance in Triple‐Negative Breast Cancer
Article Snippet: .. The following antibodies were used for Western Blot analysis: Cell Signaling Technology: PTPN14 (13808S, 1:1000 dilution), Cleaved PARP (5625S, 1:1000 dilution), Cleaved Caspase‐3 (9661S, 1:1000 dilution), p‐AKT (Ser473) (4060S, 1:2000 dilution), AKT (pan) (4691S, 1:1000 dilution), p‐ERK1/2 (4370S, 1:2000 dilution), ERK1/2 (4695S, 1:1000 dilution), BCAR3 (24032S, 1:1000 dilution), and HA‐Tag (3724S, 1:1000 dilution); Proteintech: GAPDH (60004‐1‐Ig, 1:50000 dilution), β‐actin (66009‐1‐Ig, 1:20000 dilution) and GFP tag (50430‐2‐AP, 1:1000 dilution); ABclonal: active + pro Caspase‐3 (A19654, 1:1000 dilution). ..

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(a) Representative sum-intensity z-projections of immunofluorescence imaging provide additional evidence of persistent mechanical conditioning for the tumor suppressor gene BCAR3 . (b) Representative sum-intensity z-projections of the metastasis marker RAC3 are shown to further support protein conversion from RNA-based analyses. (c) Quantification of sum-intensity z-projection fluorescence is shown for the tumor suppressor gene BCAR3 . Raw fluorescence intensity was normalized to cell area. Significance was calculated using the mean, standard deviation, and number of replicates with a Student’s t -test. (d) Quantification of sum-intensity z-projection fluorescence is shown for the metastasis-related gene, RAC3 . Raw fluorescence intensity was normalized to the cell area, and means and standard deviations are shown. Significance was calculated using a Student’s t -test. ( p -values are denoted as * < 0.05, ** < 0.01, *** < 0.001, **** < 0.0001).

Journal: ACS Biomaterials Science & Engineering

Article Title: Survival-Associated Cellular Response Maintained in Pancreatic Ductal Adenocarcinoma (PDAC) Switched Between Soft and Stiff 3D Microgel Culture

doi: 10.1021/acsbiomaterials.3c01079

Figure Lengend Snippet: (a) Representative sum-intensity z-projections of immunofluorescence imaging provide additional evidence of persistent mechanical conditioning for the tumor suppressor gene BCAR3 . (b) Representative sum-intensity z-projections of the metastasis marker RAC3 are shown to further support protein conversion from RNA-based analyses. (c) Quantification of sum-intensity z-projection fluorescence is shown for the tumor suppressor gene BCAR3 . Raw fluorescence intensity was normalized to cell area. Significance was calculated using the mean, standard deviation, and number of replicates with a Student’s t -test. (d) Quantification of sum-intensity z-projection fluorescence is shown for the metastasis-related gene, RAC3 . Raw fluorescence intensity was normalized to the cell area, and means and standard deviations are shown. Significance was calculated using a Student’s t -test. ( p -values are denoted as * < 0.05, ** < 0.01, *** < 0.001, **** < 0.0001).

Article Snippet: Primary antibodies used were acetyl-alpha Tubulin (Lys40) (Thermo Fisher, cat. no. 32-2700), BCAR3 (ThermoFisher, cat. no. PA5-101074), and RAC3 (Thermo Fisher, Cat. no. 16117-1-AP).

Techniques: Immunofluorescence, Imaging, Marker, Fluorescence, Standard Deviation

Journal: Advanced Science

Article Title: mRNA‐Lipid Nanoparticle‐Mediated Restoration of PTPN14 Exhibits Antitumor Effects by Overcoming Anoikis Resistance in Triple‐Negative Breast Cancer

doi: 10.1002/advs.202309988

Figure Lengend Snippet: BCAR3 was identified as a substrate of PTPN14. A) The results of IP‐MS, following CompPASS analysis, yielded high‐confidence candidate PTPN14‐interacting proteins. B) Exogenous IP‐Western Blot analysis validated the interaction of PTPN14 and BCAR3. Three independent experiments were performed. C) Endogenous IP‐Western Blot analysis validated the interaction of PTPN14 and BCAR3. D) BCAR3 was knockdown in control or PTPN14‐KO MDA‐MB‐231 cells and cell viability under ULA conditions was assessed every 24 h for 5 days using the CCK8 assay (left); validation of protein expression levels in each cell group through Western Blotting (right). Three independent experiments were performed. E) After the knockdown of BCAR3 in PTPN14‐KO MDA‐MB‐231 cells, the phosphorylation levels of AKT and ERK were assessed. Three independent experiments were performed. F) Tyrosine phosphorylated protein IP‐Western Blot analysis was conducted in both control MDA‐MB‐231 cells and PTPN14‐KO MDA‐MB‐231 cells. Three independent experiments were performed. G) Tyrosine phosphorylated protein IP‐Western Blot analysis was conducted in both PTPN14‐HA MDA‐MB‐231 cells and PTPN14‐D1079A‐HA MDA‐MB‐231 cells.

Article Snippet: The following antibodies were used for Western Blot analysis: Cell Signaling Technology: PTPN14 (13808S, 1:1000 dilution), Cleaved PARP (5625S, 1:1000 dilution), Cleaved Caspase‐3 (9661S, 1:1000 dilution), p‐AKT (Ser473) (4060S, 1:2000 dilution), AKT (pan) (4691S, 1:1000 dilution), p‐ERK1/2 (4370S, 1:2000 dilution), ERK1/2 (4695S, 1:1000 dilution), BCAR3 (24032S, 1:1000 dilution), and HA‐Tag (3724S, 1:1000 dilution); Proteintech: GAPDH (60004‐1‐Ig, 1:50000 dilution), β‐actin (66009‐1‐Ig, 1:20000 dilution) and GFP tag (50430‐2‐AP, 1:1000 dilution); ABclonal: active + pro Caspase‐3 (A19654, 1:1000 dilution).

Techniques: Western Blot, Knockdown, Control, CCK-8 Assay, Expressing

Journal: Advanced Science

Article Title: mRNA‐Lipid Nanoparticle‐Mediated Restoration of PTPN14 Exhibits Antitumor Effects by Overcoming Anoikis Resistance in Triple‐Negative Breast Cancer

doi: 10.1002/advs.202309988

Article Snippet: The following antibodies were used for immunoprecipitation: BCAR3 (24032S, Cell Signaling Technology), antiphospho‐tyrosine (P‐Tyr‐100) (9411S, Cell Signaling Technology), and Rabbit IgG (A7016, Beyotime).

Techniques: Western Blot, Knockdown, Control, CCK-8 Assay, Expressing

Differential expression of Bcar3 in IPF patient samples and pulmonary fibrosis mouse model. ( A and B ) show heatmaps displaying co-overexpressed genes in IL-4- and TGF-β1-treated macrophage and fibroblast, respectively, with colors representing the fold enrichment. ( C and D ) present the RT-PCR data of Bcar3 in macrophage and fibroblast after IL-4 and TGF-β1 induction, respectively. ( E ) depicts the Western blot results of Bcar3 in the lung homogenates of IPF patients (n=5) and control subjects (n=5). ( F and G ) display representative coimmunostaining data of Bcar3 and CD68 or PDGFR-β in the lung tissues of IPF patients and healthy controls. The nuclei exhibited a blue with DAPI. Magnification ×400. ( H ) shows the Western blot results of fibronectin, Collagen 1, a-SMA, and Bcar3 in the lung tissues of mice (n=5) at different time points after BLM stimulation. ( I – K ) demonstrate RT-PCR assays of the correlations among Bcar3, Acta2, Col1a1 , and Fn1 upon TGF-β1 stimulation. ( L and M ) exhibit representative coimmunostaining data of Bcar3 and PDGFR-β or F4/80 in the lung tissues of mice exposed to BLM or PBS. The nuclei exhibited a blue staining with DAPI. Magnification ×400. Mean±SEM. *p<0.05; **p<0.01; ***p<0.001.

Journal: International Journal of Nanomedicine

Article Title: Localized Administration of Bcar3 siRNA via Nano-Self-Assembly to Treat Idiopathic Pulmonary Fibrosis by Disrupting Macrophage-Fibroblast Crosstalk

doi: 10.2147/IJN.S444470

Figure Lengend Snippet: Differential expression of Bcar3 in IPF patient samples and pulmonary fibrosis mouse model. ( A and B ) show heatmaps displaying co-overexpressed genes in IL-4- and TGF-β1-treated macrophage and fibroblast, respectively, with colors representing the fold enrichment. ( C and D ) present the RT-PCR data of Bcar3 in macrophage and fibroblast after IL-4 and TGF-β1 induction, respectively. ( E ) depicts the Western blot results of Bcar3 in the lung homogenates of IPF patients (n=5) and control subjects (n=5). ( F and G ) display representative coimmunostaining data of Bcar3 and CD68 or PDGFR-β in the lung tissues of IPF patients and healthy controls. The nuclei exhibited a blue with DAPI. Magnification ×400. ( H ) shows the Western blot results of fibronectin, Collagen 1, a-SMA, and Bcar3 in the lung tissues of mice (n=5) at different time points after BLM stimulation. ( I – K ) demonstrate RT-PCR assays of the correlations among Bcar3, Acta2, Col1a1 , and Fn1 upon TGF-β1 stimulation. ( L and M ) exhibit representative coimmunostaining data of Bcar3 and PDGFR-β or F4/80 in the lung tissues of mice exposed to BLM or PBS. The nuclei exhibited a blue staining with DAPI. Magnification ×400. Mean±SEM. *p<0.05; **p<0.01; ***p<0.001.

Article Snippet: Specific siRNAs targeting Bcar3 (5′-CAACTACATGATCCTTGAT-3′ in Bcar3 mRNA) were procured from RiboBio (Guangzhou, China), followed by transient transfection into fibroblasts with Lipofectamine3000 (Invitrogen, CA, USA).

Techniques: Quantitative Proteomics, Reverse Transcription Polymerase Chain Reaction, Western Blot, Control, Staining

The role of Bcar3 in promoting M2 macrophage polarization through enhanced p-Stat6 signaling. ( A and B ) show the Western blot results of Bcar3, Arg1, Ym1, and CD206 in BMDMs treated with various concentrations of IL-4 ( A ) and at various time points ( B ). ( C ) displays the Western blot results of Bcar3, Arg1, and Ym1 in BMDMs treated with AS1517499 after IL-4 induction. ( D ) demonstrates the attenuation of M2 macrophage polarization after Bcar3 knockdown, as shown by the Western blot results of Bcar3, Ym1, and Arg1. The corresponding mean data for each group are presented in the bar graph. ( E ) shows the RT-PCR data of Mrc1, Chil3, Arg1, and Retnla in BMDMs transfected with Bcar3 siRNA following IL-4 induction. ( F ) illustrates the Western blot results of Stat6 and p-Stat6 in BMDMs transfected with Bcar3 siRNA after 1 hour of IL-4 induction. ( G and H ) demonstrate the impact of Bcar3 overexpression on p-Stat6 and Arg1 in BMDMs treated with AS1517499 and induced with IL-4 for 1 hour and 24 hours, respectively. Mean±SEM. *p<0.05; **p<0.01; ***p<0.001.

Journal: International Journal of Nanomedicine

Article Title: Localized Administration of Bcar3 siRNA via Nano-Self-Assembly to Treat Idiopathic Pulmonary Fibrosis by Disrupting Macrophage-Fibroblast Crosstalk

doi: 10.2147/IJN.S444470

Figure Lengend Snippet: The role of Bcar3 in promoting M2 macrophage polarization through enhanced p-Stat6 signaling. ( A and B ) show the Western blot results of Bcar3, Arg1, Ym1, and CD206 in BMDMs treated with various concentrations of IL-4 ( A ) and at various time points ( B ). ( C ) displays the Western blot results of Bcar3, Arg1, and Ym1 in BMDMs treated with AS1517499 after IL-4 induction. ( D ) demonstrates the attenuation of M2 macrophage polarization after Bcar3 knockdown, as shown by the Western blot results of Bcar3, Ym1, and Arg1. The corresponding mean data for each group are presented in the bar graph. ( E ) shows the RT-PCR data of Mrc1, Chil3, Arg1, and Retnla in BMDMs transfected with Bcar3 siRNA following IL-4 induction. ( F ) illustrates the Western blot results of Stat6 and p-Stat6 in BMDMs transfected with Bcar3 siRNA after 1 hour of IL-4 induction. ( G and H ) demonstrate the impact of Bcar3 overexpression on p-Stat6 and Arg1 in BMDMs treated with AS1517499 and induced with IL-4 for 1 hour and 24 hours, respectively. Mean±SEM. *p<0.05; **p<0.01; ***p<0.001.

Techniques: Western Blot, Knockdown, Reverse Transcription Polymerase Chain Reaction, Transfection, Over Expression

The involvement of Bcar3 in promoting fibroblast-to-myofibroblast differentiation through the TGF-β1/Smad3 pathway. ( A and B ) show the Western blot results of Bcar3, fibronectin, Collagen 1, and a-SMA in fibroblasts treated with different doses of TGF-β1 ( A ) and at various time points ( B ). ( C and D ) depict Western blot results of Bcar3, fibronectin, Collagen 1, and a-SMA in fibroblasts treated with SB431542 ( C ) or SIS3-HCl ( D ) after TGF-β1 induction for 24 hours. ( E ) shows the Western blot results of Bcar3, fibronectin, Collagen 1, TGF-β1, and a-SMA in fibroblasts transfected with Bcar3 siRNA after 24 hours of TGF-β1 stimulation. ( F ) presents the Western blot results of fibronectin, Collagen 1, and a-SMA in Bcar3-overexpressing fibroblasts. ( G and H ) display Western blot results of Bcar3, Smad2/3 and p-Smad2/3 in fibroblasts transfected with Bcar3 siRNA after 1 hour of TGF-β1 stimulation, and in Bcar3-overexpressing fibroblasts exposed to SIS3-HCl and induced with TGF-β1 for 1 hour, respectively. ( I ) presents the Western blot results of fibronectin, Collagen 1, and a-SMA in Bcar3-overexpressing fibroblasts treated with SIS3-HCl after TGF-β1 induction for 24 hours. Mean±SEM. *p<0.05; **p<0.01; ***p<0.001.

Journal: International Journal of Nanomedicine

Article Title: Localized Administration of Bcar3 siRNA via Nano-Self-Assembly to Treat Idiopathic Pulmonary Fibrosis by Disrupting Macrophage-Fibroblast Crosstalk

doi: 10.2147/IJN.S444470

Figure Lengend Snippet: The involvement of Bcar3 in promoting fibroblast-to-myofibroblast differentiation through the TGF-β1/Smad3 pathway. ( A and B ) show the Western blot results of Bcar3, fibronectin, Collagen 1, and a-SMA in fibroblasts treated with different doses of TGF-β1 ( A ) and at various time points ( B ). ( C and D ) depict Western blot results of Bcar3, fibronectin, Collagen 1, and a-SMA in fibroblasts treated with SB431542 ( C ) or SIS3-HCl ( D ) after TGF-β1 induction for 24 hours. ( E ) shows the Western blot results of Bcar3, fibronectin, Collagen 1, TGF-β1, and a-SMA in fibroblasts transfected with Bcar3 siRNA after 24 hours of TGF-β1 stimulation. ( F ) presents the Western blot results of fibronectin, Collagen 1, and a-SMA in Bcar3-overexpressing fibroblasts. ( G and H ) display Western blot results of Bcar3, Smad2/3 and p-Smad2/3 in fibroblasts transfected with Bcar3 siRNA after 1 hour of TGF-β1 stimulation, and in Bcar3-overexpressing fibroblasts exposed to SIS3-HCl and induced with TGF-β1 for 1 hour, respectively. ( I ) presents the Western blot results of fibronectin, Collagen 1, and a-SMA in Bcar3-overexpressing fibroblasts treated with SIS3-HCl after TGF-β1 induction for 24 hours. Mean±SEM. *p<0.05; **p<0.01; ***p<0.001.

Techniques: Western Blot, Transfection

The inhibitory effect of Bcar3 on reciprocal macrophage-fibroblast crosstalk. ( A ) presents a diagram illustrating the experimental setup of macrophage induction of fibroblast differentiation. ( B ) shows the Western blot results of fibronectin, Collagen 1, and a-SMA in fibroblasts treated with BMDM supernatant. Mean±SEM. *p<0.05; **p<0.01.

Journal: International Journal of Nanomedicine

Article Title: Localized Administration of Bcar3 siRNA via Nano-Self-Assembly to Treat Idiopathic Pulmonary Fibrosis by Disrupting Macrophage-Fibroblast Crosstalk

doi: 10.2147/IJN.S444470

Figure Lengend Snippet: The inhibitory effect of Bcar3 on reciprocal macrophage-fibroblast crosstalk. ( A ) presents a diagram illustrating the experimental setup of macrophage induction of fibroblast differentiation. ( B ) shows the Western blot results of fibronectin, Collagen 1, and a-SMA in fibroblasts treated with BMDM supernatant. Mean±SEM. *p<0.05; **p<0.01.

Techniques: Western Blot

The distribution pattern of Bcar3 siRNA liposomes following intratracheal administration. ( A ) shows the preparation of liposomes loaded with Bcar3 siRNA. ( B ) presents the zeta potential, PDI, hydrodynamic diameter, and entrapment efficiency of liposomes (Bcar3 siRNA-loaded or empty). ( C ) displays a representative TEM image of liposomes loaded with Bcar3 siRNA. ( D ) shows the hydrodynamic diameter distribution of liposomes loaded with Bcar3 siRNA. ( E ) demonstrates the colloidal stability of liposomes loaded with Bcar3 siRNA in PBS. ( F ) shows the time-lapse IVIS imaging depicting the mouse’s response to intratracheally injected liposomes labeled with DiR at different time points. ( G ) presents ex vivo IVIS images of the main organs of mice. ( H ) displays immunofluorescence images illustrating the distribution of Vimentin + cells (red), CD68 + cells (red), and DiO-labeled liposomes (green) in the mouse lungs. ( I ) presents the flow cytometry of liposome distribution in the lungs. ( J and K ) show immunofluorescent staining of CD68 (green) and Bcar3 (red), and Bcar3 (green) and a-SMA (red) in mice exposed to BLM followed by intravenous injection of liposomes containing Bcar3 siRNA. ( L ) presents the Western blot results of Bcar3 in mice exposed to BLM followed by intravenous injection of liposomes containing Bcar3 siRNA. Mean±SEM. *p<0.05.

Journal: International Journal of Nanomedicine

Article Title: Localized Administration of Bcar3 siRNA via Nano-Self-Assembly to Treat Idiopathic Pulmonary Fibrosis by Disrupting Macrophage-Fibroblast Crosstalk

doi: 10.2147/IJN.S444470

Figure Lengend Snippet: The distribution pattern of Bcar3 siRNA liposomes following intratracheal administration. ( A ) shows the preparation of liposomes loaded with Bcar3 siRNA. ( B ) presents the zeta potential, PDI, hydrodynamic diameter, and entrapment efficiency of liposomes (Bcar3 siRNA-loaded or empty). ( C ) displays a representative TEM image of liposomes loaded with Bcar3 siRNA. ( D ) shows the hydrodynamic diameter distribution of liposomes loaded with Bcar3 siRNA. ( E ) demonstrates the colloidal stability of liposomes loaded with Bcar3 siRNA in PBS. ( F ) shows the time-lapse IVIS imaging depicting the mouse’s response to intratracheally injected liposomes labeled with DiR at different time points. ( G ) presents ex vivo IVIS images of the main organs of mice. ( H ) displays immunofluorescence images illustrating the distribution of Vimentin + cells (red), CD68 + cells (red), and DiO-labeled liposomes (green) in the mouse lungs. ( I ) presents the flow cytometry of liposome distribution in the lungs. ( J and K ) show immunofluorescent staining of CD68 (green) and Bcar3 (red), and Bcar3 (green) and a-SMA (red) in mice exposed to BLM followed by intravenous injection of liposomes containing Bcar3 siRNA. ( L ) presents the Western blot results of Bcar3 in mice exposed to BLM followed by intravenous injection of liposomes containing Bcar3 siRNA. Mean±SEM. *p<0.05.

Techniques: Liposomes, Zeta Potential Analyzer, Imaging, Injection, Labeling, Ex Vivo, Immunofluorescence, Flow Cytometry, Staining, Western Blot

The protective effects of intratracheal injection of liposomes containing Bcar3 siRNA in pulmonary fibrosis mice. ( A ) shows the FITC (top), H&E (middle), and Masson (bottom) staining of the lung tissues following FITC simulation. Magnification 200×. ( B ) presents a bar graph illustrating hydroxyproline levels in following FITC stimulation. ( C ) displays the RT-PCR data of Bcar3, Acta2, Col1a1 , and Fn1 following FITC stimulation. ( D ) shows the Western blot results of fibronectin, Collagen 1, a-SMA, and Bcar3 in mice exposed to FITC. ( E ) illustrates Western blot results of Arg1 and CD206 in mice exposed to FITC. ( F ) shows H&E (up) and Masson (down) staining of the lungs in after BLM stimulation. ( G ) presents a bar graph revealing the semi-quantitative Ashcroft scores of fibrosis severity. Magnification 200×. ( H ) shows a bar graph of hydroxyproline levels in the lungs following BLM stimulation. ( I ) presents the Western blot results of fibronectin, Collagen 1, a-SMA, and Bcar3 in mice exposed to BLM. ( J ) illustrates the Western blot results of Arg1 and CD206 following BLM stimulation. Mean±SEM. *p<0.05; **p<0.01; ***p<0.001.

Journal: International Journal of Nanomedicine

Article Title: Localized Administration of Bcar3 siRNA via Nano-Self-Assembly to Treat Idiopathic Pulmonary Fibrosis by Disrupting Macrophage-Fibroblast Crosstalk

doi: 10.2147/IJN.S444470

Figure Lengend Snippet: The protective effects of intratracheal injection of liposomes containing Bcar3 siRNA in pulmonary fibrosis mice. ( A ) shows the FITC (top), H&E (middle), and Masson (bottom) staining of the lung tissues following FITC simulation. Magnification 200×. ( B ) presents a bar graph illustrating hydroxyproline levels in following FITC stimulation. ( C ) displays the RT-PCR data of Bcar3, Acta2, Col1a1 , and Fn1 following FITC stimulation. ( D ) shows the Western blot results of fibronectin, Collagen 1, a-SMA, and Bcar3 in mice exposed to FITC. ( E ) illustrates Western blot results of Arg1 and CD206 in mice exposed to FITC. ( F ) shows H&E (up) and Masson (down) staining of the lungs in after BLM stimulation. ( G ) presents a bar graph revealing the semi-quantitative Ashcroft scores of fibrosis severity. Magnification 200×. ( H ) shows a bar graph of hydroxyproline levels in the lungs following BLM stimulation. ( I ) presents the Western blot results of fibronectin, Collagen 1, a-SMA, and Bcar3 in mice exposed to BLM. ( J ) illustrates the Western blot results of Arg1 and CD206 following BLM stimulation. Mean±SEM. *p<0.05; **p<0.01; ***p<0.001.

Techniques: Injection, Liposomes, Staining, Reverse Transcription Polymerase Chain Reaction, Western Blot

The attenuation of fibrosis-related phenotypes in TGF-β-exposed hPCLS after treatment with liposomes containing Bcar3 siRNA. ( A ) shows Sirius red staining (bottom) and Masson staining (top) of fibrosis-related phenotypes in TGF-β-exposed hPCLS after treatment with liposomes containing Bcar3 siRNA. ( B ) presents the Western blot results of Bcar3, fibronectin, and Collagen 1 in hPCLS after treatment with TGF-β and liposomes containing Bcar3 siRNA. The left panel shows representative Western blot data, and the right panel presents the bar graph of Western blot data. ( C ) displays the Western blot results of CD206 in hPCLS after treatment with TGF-β and liposomes containing Bcar3 siRNA. The left panel shows representative Western blot data, and the right panel presents the bar graph of Western blot data. ( D ) shows the immunofluorescence of CD206 in hPCLS after treatment with TGF-β and liposomes containing Bcar3 siRNA. ( E ) depicts a schematic of the mechanism by which Bcar3 regulates pulmonary fibrosis. Mean±SEM. *p<0.05; **p<0.01.

Journal: International Journal of Nanomedicine

Article Title: Localized Administration of Bcar3 siRNA via Nano-Self-Assembly to Treat Idiopathic Pulmonary Fibrosis by Disrupting Macrophage-Fibroblast Crosstalk

doi: 10.2147/IJN.S444470

Figure Lengend Snippet: The attenuation of fibrosis-related phenotypes in TGF-β-exposed hPCLS after treatment with liposomes containing Bcar3 siRNA. ( A ) shows Sirius red staining (bottom) and Masson staining (top) of fibrosis-related phenotypes in TGF-β-exposed hPCLS after treatment with liposomes containing Bcar3 siRNA. ( B ) presents the Western blot results of Bcar3, fibronectin, and Collagen 1 in hPCLS after treatment with TGF-β and liposomes containing Bcar3 siRNA. The left panel shows representative Western blot data, and the right panel presents the bar graph of Western blot data. ( C ) displays the Western blot results of CD206 in hPCLS after treatment with TGF-β and liposomes containing Bcar3 siRNA. The left panel shows representative Western blot data, and the right panel presents the bar graph of Western blot data. ( D ) shows the immunofluorescence of CD206 in hPCLS after treatment with TGF-β and liposomes containing Bcar3 siRNA. ( E ) depicts a schematic of the mechanism by which Bcar3 regulates pulmonary fibrosis. Mean±SEM. *p<0.05; **p<0.01.

Techniques: Liposomes, Staining, Western Blot, Immunofluorescence

Review

bcar3 (Proteintech)

Structured Review

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1) Product Images from "mRNA‐Lipid Nanoparticle‐Mediated Restoration of PTPN14 Exhibits Antitumor Effects by Overcoming Anoikis Resistance in Triple‐Negative Breast Cancer"

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