fkbp11 (Bioss)
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fkbp11
Fkbp11, supplied by Bioss, used in various techniques. Bioz Stars score: 90/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/fkbp11/product/Bioss
Average 90 stars, based on 2 article reviews
Fkbp11, supplied by Bioss, used in various techniques. Bioz Stars score: 90/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/fkbp11/product/Bioss
Average 90 stars, based on 2 article reviews
fkbp11 - by Bioz Stars,
2026-02
90/100 stars
Images
1) Product Images from "Weighted Gene Co-expression Network Analysis Identifies FKBP11 as a Key Regulator in Acute Aortic Dissection through a NF-kB Dependent Pathway"
Article Title: Weighted Gene Co-expression Network Analysis Identifies FKBP11 as a Key Regulator in Acute Aortic Dissection through a NF-kB Dependent Pathway
Journal: Frontiers in Physiology
doi: 10.3389/fphys.2017.01010
Figure Legend Snippet: PCR primers for quantitative real-time PCR.
Techniques Used: Sequencing
Figure Legend Snippet: Top 10 hub genes identified in PPI network for DEGs.
Techniques Used: Sequencing, Binding Assay
Figure Legend Snippet: Expression and localization of FKBP11 in clinical aorta samples. (A) Representative immunoblots (upper panel) and bar graphs (lower panel) showing FKBP11 expression levels in whole aorta tissue lysates from AAD patients and control group. (B) Representative EVG staining of the aortic wall in the control group and AAD group. Distorted and deficient elastic fibers (dark blue staining) can be easily seen in AAD group, scale bar: 100 μm. (C) FKBP11 is strongly expressed in AAD group and in an endothelium prone manner. Exemplary immunohistochemical staining of aortic paraffin embedded tissue sections from control (left) and AAD (right) group; FKBP11 antigen detected by HRP-DAB reaction, brown; hematoxylin counterstain, blue; scale bar: 100 μm. (D) Double immunofluorescent staining showed co-localization of FKBP11 with endothelial marker CD31, not α-SMA (a smoot muscle cell marker) nor Mac-2 (a macrophage marker). And it showed that FKBP11 expression increased mainly on the endothelium of the AAD group. FKBP11 staining (red), nuclear staining DAPI (blue), specific cell marker (CD31, α-SMA and Mac-2) staining (green); scale bar: 100 μm. CON, control healthy donor, open bars; AADm patient with acute aortic dissection, black bars. Mean ± SEM of 6 subjects per group (A-C) ; * P < 0.05 ( A , student t -test).
Techniques Used: Expressing, Western Blot, Staining, Immunohistochemical staining, Marker, Dissection
Figure Legend Snippet: The correlation between FKBP11 and MMP9 expression in infiltrated macrophages under AAD. (A) Representative immune-blots (upper panel) and bar graphs (lower panel) showing MMP9 expression levels in whole aorta tissue lysates from AAD patients and control group. (B) Exemplary immune-histochemical staining of aortic paraffin embedded tissue sections from healthy donors and AAD patients; left, IgG control; middle, healthy donor; right, AAD patient; MMP9 antigen detected by HRP-DAB reaction, brown; hematoxylin counterstain, blue; scale bar: 100 μm. (C) Double immunofluorescent staining showed co-localization of MMP9 with macrophage marker Mac-2. It showed that the expression of MMP9 in infiltrated macrophages increased in AAD group. MMP9 staining (red), nuclear stain DAPI (blue), macrophage marker (Mac-2) staining (green); scale bar: 100 μm. CON, control healthy donor, open bars; AAD, patient with acute aortic dissection, black bars. Mean ± SEM of 6 subjects per group (A–C) ; * P < 0.05 ( A , student t -test).
Techniques Used: Expressing, Staining, Marker, Dissection
Figure Legend Snippet: The pro-inflammatory function of FKBP11 and activation of NF-kB p65 subunit in endothelial cell. (A) Representative immunoblots (upper panel) and bar graph (lower panel) showed FKBP11 specific siRNA FKBP11-Si2 and FKBP11-Si3 but not FKBP11-Si1 can effectively suppress the protein expression as compared to the scrambled control NC-Si in EA.hy926 cells. (B–D) EA.hy926 cells were incubated with Ang II after transfected with FKBP11-Si2 or scrambled control NC-Si. (B) Cytofluorescent picture showed that Ang II promoted the nuclear localization of p-p65, while FKBP11 siRNA treatment could blunt it. Together, representative immunoblots (C) and bar graph (D) showing FKBP11-siRNA treatment could effectively suppress the phosphorylation and nuclear translocation of p65 and subsequently the expression of pro-inflammatory cytokines MCP1, VCAM1, ICAM1, and IL1-β. p-p65 staining (green); nuclear stain DAPI (blue); scale bar: 100 μm. (E) The interaction of FKBP11 and p-p65 was enhanced following Ang II treatment in EA.hy926 cells. Detection of p-p65 by immunoblotting following immunoprecipitation of FKBP11 from whole cell lysates of control (Con) cells or of cells after Ang II treatment (Ang II), left panel or vice versa, right panel; representative images of precipitated protein immunoblots (top) and respective input immunoblots (bottom). IgG controls for immunoprecipitation experiments were attached to the Supplementary Figure . CON: Control cells without treatment; Ang II: 1.0 × 10 −6 mol/L Angiotensin II treated cells; NC-Si, Scrambled SiRNA for FKBP11; FKBP11-Si, FKBP11 knockdown SiRNA. Mean value ± SEM of at least three independent experiments (A,D) ; * P < 0.05; ** P < 0.01 (ANOVA); Representative immunoblots of at least three independent experiments; (A,C,E) ; IB, immunoblot; IP, immunoprecipitation.
Techniques Used: Activation Assay, Western Blot, Expressing, Incubation, Transfection, Translocation Assay, Staining, Immunoprecipitation
Figure Legend Snippet: FKBP11 and monocyte transmigration through an endothelial cell monolayer. (A,B) EA.hy926 monolayer in the lower compartment was incubated without or with Ang II after transfected with FKBP11-Si RNA or NC–Si RNA for 24 h. Then 5 × 10 5 THP-1 cells were seeded into each upper compartment containing 100 μL serum-free RPMI medium. Images depicting crystal violet stained THP-1 cells which migrated across the membrane of transwell inserts (pore size 8 μm) to the lower side after incubation with conditioned media from the lower compartment for 12 h. Representative pictures are shown. (A) Migrated cells per high power field were quantified and the data were showed in bar graph (B) . (C,D) The same as in (A,B) , instead of EA.hy926 cell monolayer, HUVECs were applied. NC-Si: Scrambled SiRNA for FKBP11 treated endothelial cells; FKBP11-Si: FKBP11 knockdown SiRNA treated endothelial cells; NC-Si+Ang II: Scrambled SiRNA for FKBP11 and 1.0 × 10 −6 mol/L Angiotensin II treated endothelial cells; FKBP11-Si+AngII: FKBP11 knockdown SiRNA and 1.0 × 10 −6 mol/L Angiotensin II treated endothelial cells. Mean value ± SEM of at least three independent experiments (B,D) ; * P < 0.05; ** P < 0.01 (ANOVA); Scale bar: 200 μm.
Techniques Used: Transmigration Assay, Incubation, Transfection, Staining
Figure Legend Snippet: Proposed model of how FKBP11 affects the formation and progression of AAD. In response to environmental stress (such as Ang II), FKBP11 expression was induced in endothelium of the dissected aorta and it could provoke the pro-inflammatory state of the endothelial cells by interacting with NF-kB p65 subunit and promoting its nuclear translocation, and the produced pro-inflammatory cytokines further facilitated the circulating monocytes transmigrating through the endothelium to the middle layer of the aorta, where they differentiated into active macrophages and secreted MMPs and other ECM degrading proteins, finally promoted the formation and progression of aortic dissection.
Techniques Used: Expressing, Translocation Assay, Produced, Dissection