polyclonal primary antibodies for aqp1  (Boster Bio)

Journal: Particle and Fibre Toxicology

Article Title: Inhaled gold nanoparticles cause cerebral edema and upregulate endothelial aquaporin 1 expression, involving caveolin 1 dependent repression of extracellular regulated protein kinase activity

doi: 10.1186/s12989-019-0324-2

Figure Lengend Snippet: Au-NPs induced aquaporin-1 (AQP1) protein expression in bEnd.3 cells. a / b The bEnd.3 cells (an immortalized mouse cerebral endothelial cell line) were exposed to Au-NPs (or Au-MPs) and the expression level of AQP1 was detected by western blots. Representative images showed an increase of AQP1 protein level in Au-NP-treated groups, whereas AQP1 protein level remained unaffected in Au-MP-treated groups. a concentration-dependent treatment; cells were incubated with 10, 50, 100 and 500 ng/mL Au-NPs for 24 h. b time-dependent treatment; cells were incubated with 500 ng/mL Au-NPs for 3, 6, 12, and 24 h. (* p < 0.05, ** p < 0.01, and *** p < 0.001 indicates statistically significant difference from the control group; N = 11). c Representative images of immunofluorescent staining, the Au-NP-induced AQP1 and the nucleus was manifested by red and blue fluorescence, respectively. A gain of red fluorescence in cell membrane and cytosol was observed in Au-NP-treated bEnd.3 cells (500 ng/mL; 24 h), as compared to control. d Transendothelial permeability assay was performed as described in Materials and Methods. Au-NP treatment (500 ng/mL; 24 h) made bEnd.3 cell more permeable to water. (* p < 0.05, indicates statistically significant difference from the control group; N = 12)

Article Snippet: After Au-NP treatment (500 ng/mL; 24 h), the cells were fixed in 4% paraformaldehyde, permeabilized with 0.1% Triton X-100 for 5 min at room temperature, and incubated with blocking serum for 30 min. Next, the cells were incubated overnight (4 °C) with a primary AQP1 antibody (1:50; Bioss Antibodies, Woburn, MA, catalog. bs-1506R) and then with a fluorescein isothiocyanate (FITC)-conjugated secondary antibody (1:1000) at room temperature for 1 h in the dark.

Techniques: Expressing, Western Blot, Concentration Assay, Incubation, Staining, Fluorescence, Permeability

Journal: Particle and Fibre Toxicology

Article Title: Inhaled gold nanoparticles cause cerebral edema and upregulate endothelial aquaporin 1 expression, involving caveolin 1 dependent repression of extracellular regulated protein kinase activity

doi: 10.1186/s12989-019-0324-2

Figure Lengend Snippet: Au-NP treatment rapidly changed the phosphorylating status of FAK, AKT and ERK, and subsequently contributing to Au-NP-mediated AQP1 accumulation. bEnd.3 cells were incubated with 500 ng/mL Au-NPs for 15, 30 and 60 min, and the phosphorylating status of FAK, AKT, ERK, and Cav1 was measured by western blots. a Representative images showed an augmentation of FAK and AKT phosphorylation; a reduction of ERK and Cav1 phosphorylation in Au-NP-treated groups in time-dependent manner, as compared to control. Also, Au-NP treatment caused an accumulation of Cav1 protein level. Quantified data was gained by densitometry analysis, followed by a normalized process to their total form. b phospho-FAK, ( c ) phospho-AKT, ( d ) phospho-ERK, ( e ) Cav1 and ( f ) phospho-Cav1. (* p < 0.05, ** p < 0.01, and *** p < 0.001 indicates statistically significant difference from the control group; N > 10). g Cells were pre-incubated with 10 μM U0126 (ERK inhibitor), 10 μM GDC-0068 (pan-AKT inhibitor) and 10 μM PF-573228 (FAK inhibitor), subjected to a 12–16 h exposure of Au-NPs. Images and quantified data revealed that Au-NP-induced AQP1 expression was prevented while FAK and AKT inhibition, whereas an enhancement of AQP1 expression was presented in the presence of U0126. (* p < 0.05, ** p < 0.01, and *** p < 0.001 indicates statistically significant difference from the control group; ## p < 0.01, and ### p < 0.0001 indicates statistically significant difference from the Au-NP-treated group; N = 7)

Article Snippet: After Au-NP treatment (500 ng/mL; 24 h), the cells were fixed in 4% paraformaldehyde, permeabilized with 0.1% Triton X-100 for 5 min at room temperature, and incubated with blocking serum for 30 min. Next, the cells were incubated overnight (4 °C) with a primary AQP1 antibody (1:50; Bioss Antibodies, Woburn, MA, catalog. bs-1506R) and then with a fluorescein isothiocyanate (FITC)-conjugated secondary antibody (1:1000) at room temperature for 1 h in the dark.

Techniques: Incubation, Western Blot, Expressing, Inhibition

Journal: Particle and Fibre Toxicology

Article Title: Inhaled gold nanoparticles cause cerebral edema and upregulate endothelial aquaporin 1 expression, involving caveolin 1 dependent repression of extracellular regulated protein kinase activity

doi: 10.1186/s12989-019-0324-2

Figure Lengend Snippet: Caveolin-1 (Cav1) is a crucial factor in Au-NP-mediated AQP1 expression. a bEnd.3 cells with a silenced Cav1 (bEnd.3 Cav1-KD) was established as described in Materials and Methods. The mRNA and protein expression level of Cav1 and AQP1 was obviously down-regulated. b / c Both images and quantitative data proved Au-NP-mediated FAK and AKT phosphorylation (as well as ERK de-phosphorylation) were prevented in bEnd.3 Cav1-KD ( N = 6). d Au-NP-mediated AQP1 induction and ( e ) water permeability was also ameliorated in bEnd.3 Cav1-KD, as compared to wild-type (N = 6). These data manifested the requirement of Cav1 of bEnd.3 cell in respond to Au-NP stimulation. (* p < 0.05, ** p < 0.01, and *** p < 0.001 indicates statistically significant difference from the control group; ## p < 0.01, and ### p < 0.001 indicates statistically significant difference from the Au-NP-treated group)

Article Snippet: After Au-NP treatment (500 ng/mL; 24 h), the cells were fixed in 4% paraformaldehyde, permeabilized with 0.1% Triton X-100 for 5 min at room temperature, and incubated with blocking serum for 30 min. Next, the cells were incubated overnight (4 °C) with a primary AQP1 antibody (1:50; Bioss Antibodies, Woburn, MA, catalog. bs-1506R) and then with a fluorescein isothiocyanate (FITC)-conjugated secondary antibody (1:1000) at room temperature for 1 h in the dark.

Techniques: Expressing, De-Phosphorylation Assay, Permeability

Journal: Particle and Fibre Toxicology

Article Title: Inhaled gold nanoparticles cause cerebral edema and upregulate endothelial aquaporin 1 expression, involving caveolin 1 dependent repression of extracellular regulated protein kinase activity

doi: 10.1186/s12989-019-0324-2

Figure Lengend Snippet: Inhaled Au-NPs upregulated AQP1 expression in cerebral microvessels in vivo. a Representative images showed an increase in immunoreactivity against AQP1 in microvessels of brain tissues, whereas the stained CD31 (an endothelial biomarker) was without significant differences. b The quantitative data was determined by the measurement of the length of AQP1-positive microvessels. (** p < 0.01, and *** p < 0.001 indicates statistically significant difference from the control group, N = 4)

Article Snippet: After Au-NP treatment (500 ng/mL; 24 h), the cells were fixed in 4% paraformaldehyde, permeabilized with 0.1% Triton X-100 for 5 min at room temperature, and incubated with blocking serum for 30 min. Next, the cells were incubated overnight (4 °C) with a primary AQP1 antibody (1:50; Bioss Antibodies, Woburn, MA, catalog. bs-1506R) and then with a fluorescein isothiocyanate (FITC)-conjugated secondary antibody (1:1000) at room temperature for 1 h in the dark.

Techniques: Expressing, In Vivo, Staining, Biomarker Assay

Journal: Veterinary Sciences

Article Title: Clinical Spatial Distribution of Aquaporin-1 in Camel Cornea Using Assistive AI Applications

doi: 10.3390/vetsci13050425

Figure Lengend Snippet: Representative photomicrographs of the camel cornea. Panels (C1, MD1, MV1) show H&E-stained sections illustrating epithelial thickness in the central (C), middle dorsal (MD), and middle ventral (MV) regions (scale bar: 100 µm). Panels (C2, MD2, MV2) depict the stromal layer and Descemet’s membrane in the same regions following H&E staining. Panels (C3, MD3, MV3) demonstrate AQP1 immunoreactivity within the corneal epithelium and keratocytes of the anterior stroma, with variable staining intensity across regions (black arrows; scale bar: 50 µm). Panels (C4, MD4, MV4) show AQP1 localization in the posterior stroma and endothelium, where immunostaining is primarily confined to keratocytes and endothelial cells (black arrows; scale bar: 50 µm).

Article Snippet: Subsequently, the sections were incubated for 60 min with a rabbit polyclonal anti-human AQP1 primary antibody (1:1000; catalog no. GB11310, Servicebio, Woburn city, MA, USA).

Techniques: Staining, Membrane, Immunostaining

Journal: Veterinary Sciences

Article Title: Clinical Spatial Distribution of Aquaporin-1 in Camel Cornea Using Assistive AI Applications

doi: 10.3390/vetsci13050425

Figure Lengend Snippet: Representative photomicrographs of the camel cornea from the middle nasal (MN), middle temporal (MT), and peripheral dorsal (PD) regions. Panels (MN1, MT1, PD1) show H&E-stained sections illustrating epithelial thickness in the corresponding regions. In addition, vascular structures are visible in the peripheral dorsal region (PD2), likely associated with the limbal area (black arrows; scale bar: 100 µm). Panels (MN2, MT2, PD2) demonstrate the stromal layer and Descemet’s membrane in these regions following H&E staining. Panels (MN3, MT3, PD3) reveal AQP1 immunoreactivity within the corneal epithelium and keratocytes of the anterior stroma, with regional variation in staining intensity (black arrows; scale bar: 50 µm). Panels (MN4, MT4, PD4) illustrate AQP1 localization in the posterior stroma and endothelium, where staining is predominantly confined to keratocytes and endothelial cells (black arrows; scale bar: 50 µm).

Article Snippet: Subsequently, the sections were incubated for 60 min with a rabbit polyclonal anti-human AQP1 primary antibody (1:1000; catalog no. GB11310, Servicebio, Woburn city, MA, USA).

Techniques: Staining, Membrane

Journal: Veterinary Sciences

Article Title: Clinical Spatial Distribution of Aquaporin-1 in Camel Cornea Using Assistive AI Applications

doi: 10.3390/vetsci13050425

Figure Lengend Snippet: Representative photomicrographs of the camel cornea from the peripheral ventral (PV), peripheral nasal (PN), and peripheral temporal (PT) regions. Panels (PV1, PN1, PT1) show H&E-stained sections illustrating epithelial thickness in the respective regions (scale bar: 100 µm). Vascular structures are evident in the peripheral areas (PV2, PN2, PT2), likely corresponding to extensions of the limbal vasculature (black arrows). Panels (PV2, PN2, PT2) further demonstrate the stromal layer and Descemet’s membrane following H&E staining. Panels (PV3, PN3, PT3) display AQP1 immunoreactivity within the corneal epithelium and keratocytes of the anterior stroma, with noticeable regional differences in staining intensity (black arrows; scale bar: 50 µm). The strongest epithelial expression of AQP1 was observed in the peripheral nasal region (PN3), highlighted by white circles. Panels (PV4, PN4, PT4) illustrate AQP1 localization in the posterior stroma and endothelium, where staining is primarily confined to keratocytes and endothelial cells (black arrows; scale bar: 50 µm). Additionally, panel (PT5) shows the presence of brown melanin granules within the peripheral temporal region (black arrows; scale bar: 50 µm).

Article Snippet: Subsequently, the sections were incubated for 60 min with a rabbit polyclonal anti-human AQP1 primary antibody (1:1000; catalog no. GB11310, Servicebio, Woburn city, MA, USA).

Techniques: Staining, Membrane, Expressing

Journal: Veterinary Sciences

Article Title: Clinical Spatial Distribution of Aquaporin-1 in Camel Cornea Using Assistive AI Applications

doi: 10.3390/vetsci13050425

Figure Lengend Snippet: Immunohistochemical localization of AQP1 in camel corneal epithelium across different cellular layers, including superficial, intermediate (polyhedral), and basal cells. The columns represent the relative expression levels of AQP1 in the following corneal regions according to Area Fraction (%): central (C), middle dorsal (MD), middle nasal (MN), middle temporal (MT), middle ventral (MV), peripheral dorsal (PD), peripheral nasal (PN), peripheral temporal (PT), and peripheral ventral (PV). Data are presented as Mean ± SD (n = 6). Different superscript letters above bars indicate statistically significant differences between groups (One-way ANOVA followed by Tukey’s post hoc test, p < 0.05).

Article Snippet: Subsequently, the sections were incubated for 60 min with a rabbit polyclonal anti-human AQP1 primary antibody (1:1000; catalog no. GB11310, Servicebio, Woburn city, MA, USA).

Techniques: Immunohistochemical staining, Expressing

Journal: Veterinary Sciences

Article Title: Clinical Spatial Distribution of Aquaporin-1 in Camel Cornea Using Assistive AI Applications

doi: 10.3390/vetsci13050425

Figure Lengend Snippet: Immunohistochemical distribution of AQP1 in the camel cornea, including the anterior and posterior stromal regions as well as the endothelium. The columns illustrate the relative expression levels of AQP1 across different corneal regions according to Area Fraction (%): central (C), middle dorsal (MD), middle nasal (MN), middle temporal (MT), middle ventral (MV), peripheral dorsal (PD), peripheral nasal (PN), peripheral temporal (PT), and peripheral ventral (PV). Data are presented as Mean ± SD (n = 6). Different superscript letters above bars indicate statistically significant differences between groups (One-way ANOVA followed by Tukey’s post hoc test, p < 0.05).

Article Snippet: Subsequently, the sections were incubated for 60 min with a rabbit polyclonal anti-human AQP1 primary antibody (1:1000; catalog no. GB11310, Servicebio, Woburn city, MA, USA).

Techniques: Immunohistochemical staining, Expressing

Journal: Veterinary Sciences

Article Title: Clinical Spatial Distribution of Aquaporin-1 in Camel Cornea Using Assistive AI Applications

doi: 10.3390/vetsci13050425

Figure Lengend Snippet: Proposed model for the spatial distribution of AQP1 water channels in the camel cornea in the three corneal layers, epithelium, stroma and endothelium. The green color shows AQP1 localization in the different corneal epithelial cell layers; superficial, polyhedral, and basal cell layers. The black color shows localization of AQP1 in keratocyte cells of stroma, while the red color clarifies the localization of AQP1 in corneal endothelium.

Article Snippet: Subsequently, the sections were incubated for 60 min with a rabbit polyclonal anti-human AQP1 primary antibody (1:1000; catalog no. GB11310, Servicebio, Woburn city, MA, USA).

Techniques:

Journal: Veterinary Sciences

Article Title: Clinical Spatial Distribution of Aquaporin-1 in Camel Cornea Using Assistive AI Applications

doi: 10.3390/vetsci13050425

Figure Lengend Snippet: Topographical map of AQP1 distribution across the nine corneal regions. The schematic represents the regional intensity of AQP1 expression in the epithelium (EPI), stroma (STR), and endothelium (EN) of the camel cornea. The AI-generated Area Fraction (AF %) data: (+) = Weak expression (AF < 2%), (++) = Moderate expression (AF = 2–4%), (+++) = Strong expression (AF = 4–6%) and (++++) = Very strong expression (AF > 6%).

Article Snippet: Subsequently, the sections were incubated for 60 min with a rabbit polyclonal anti-human AQP1 primary antibody (1:1000; catalog no. GB11310, Servicebio, Woburn city, MA, USA).

Techniques: Expressing, Generated

Journal: International Journal of Molecular Sciences

Article Title: Personalized Treatment Response Assessment for Rare Childhood Tumors Using Microcalorimetry–Exemplified by Use of Carbonic Anhydrase IX and Aquaporin 1 Inhibitors

doi: 10.3390/ijms20204984

Figure Lengend Snippet: Clinical presentation ( A ) The child presented with a large abdominal mass, which was not reduced in size after initial chemotherapy. The scar was a result of the initial surgical biopsy. ( B ) MRI of primary clear cell sarcoma of left kidney following chemotherapy. Despite few necrotic areas the tumor is largely intact and appears to be vital. ( C ) Large tumor after resection. Immuno-staining ( D AQP1 IHC, E : CAIX IHC, F : AQP1 and CAIX IF stainings) The response to the specific inhibitors corresponded with the protein expression profiles of AQP1 (mostly in vibrovascular septae and vessels and CAIX (most strongly within tumor nests). Microcalorimteric measurements ( G ) Microcalorimetric measurements showed a decrease metabolic activity under treatment with AQP and CAIX inhibitors compared to medium control. (Control – medium, Drug 1—AQP1 inhibitor TEA, Drug 2—FC8-325A, Drug 3—FC8-207A, Drug 4—FC12-520A).

Article Snippet: AQP1 and CAIX staining was performed according to the protocol using a primary polyclonal rabbit anti-AQP1 antibody (Merck Millipore, Sigma-Aldrich Chemie GmbH Buchs, Switzerland) at a dilution of 1:400 and antibody M75 (BioScience Slovakia, Bratislava, Slovak republic) at a dilution of 1:200.

Techniques: Immunostaining, Expressing, Activity Assay