Mouse Aquaporin 1 ELISA Kit

Name: Mouse Aquaporin 1 ELISA Kit
SKU: DEIA-BJ2365
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

Serum, plasma, cell culture supernatants, body fluid and tissue homogenate

Species Reactivity

Mouse

Detection Method

Sandwich ELISA

Intended Use

Mouse Aquaporin 1 ELISA Kit kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of the Aquaporin 1. This ELISA kit is for research use only, not for therapeutic or diagnostic applications.

Contents of Kit

1. MICROTITER PLATE: 96 wells
2. ENZYME CONJUGATE: 6.0 mL or 10 ml
3. STANDARD A-F: 1 vial each
4. SUBSTRATE A: 6 mL
5. SUBSTRATE B: 6 mL
6. STOP SOLUTION: 6 mL
7. WASH SOLUTION (100 x): 10 mL
8. BALANCE SOLUTION: 3 mL

Storage

All components of this kit are stable at 2-8°C until the kit's expiration date.

Detection Range

5-100 ng/mL

Sensitivity

0.1 ng/mL

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

MicroRNA-29a increased the intestinal membrane permeability of colonic epithelial cells in irritable bowel syndrome rats

ONCOTARGET

Authors: Chao, Guanqun; Wang, Yingying; Zhang, Shuo; Yang, Weilin; Ni, Zheying; Zheng, Xuliang

Abstract

Background: The whole pathogenesis of diarrhea-predominant irritable bowel syndrome(IBS-D) is poorly understood. Our goal was to evaluate the expression change of microRNA-29a(miR-29a) in colonic epithelial cells in IBS rats and clarify the mechanism of miR-29a increasing the intestinal membrane permeability through aquaporins(AQPs). Methods: The IBS-D rats models were induced by rectal distention pressure combining with extremities constraint. The colonic epithelial cells were divided into four groups. A: normal group. B: IBS-D control group. C: IBS-D + miR-29a NC. D: IBS-D + miR-29a antagomir. The expression of miR-29a, the concentration of the K+ and Lactate Dehydrogenase(LDH) and the expression of AQPs were detected. Results: The miR-29a expression increased in IBS-D control group(2.090 +/- 0.022) compared with the control group(1.00 +/- 0.031) (P<0.001) while it decreased in IBS-D+ miR-29a antagomir group(1.403 +/- 0.042) compared with IBS-D control group(P< 0.001). The K+ decreased in IBS-D control group(1.305 +/- 0.289) compared with the control group(2.171 +/- 0.204)(P<0.05) while it increased in IBS-D+ miR-29a antagomir group(1.813 +/- 0.102)(P<0.05) compared with IBS-D control group. The LDH increased in IBS-D control group(4153.440 +/- 177.365) compared with the control group(1434.573 +/- 96.111)(P<0.001) while it decreased in IBS-D+ miR-29a antagomir group(2700.473 +/- 275.414) compared with IBS-D control group (P<0.01). The expression of AQP1, AQP3 and AQP8 decreased in IBS-D control group(0.132 +/- 0.010,0.110 +/- 0.005,0.108 +/- 0.007) compared with the control group (P< 0.001) while it increased in IBS-D+ miR-29a antagomir group( 0.197 +/- 0.005,0.182 +/- 0.011,0.194 +/- 0.003) compared with IBS-D control group(P<0.001). The IBS-D+ miR-29a negative control(NC) group, a comparison with IBS-D+ miR-29a antagomir group, each date showed the similar trend to the IBS-D control group. Conclusions: MiR-29a increased the intestinal membrane permeability of colonic epithelial cells by reducing the AQPs expression in IBS-D rats.

pH-mediated upregulation of AQP1 gene expression through the Spi-B transcription factor

BMC MOLECULAR BIOLOGY

Authors: Zhai, Yihui; Xu, Hong; Shen, Qian; Schaefer, Franz; Schmitt, Claus P.; Chen, Jing; Liu, Haimei; Liu, Jialu; Liu, Jiaojiao

Abstract

Background: Bicarbonate-based peritoneal dialysis (PD) fluids enhance the migratory capacity and damage-repair ability of human peritoneal mesothelial cells by upregulating AQP1. However, little is known about the underlying molecular mechanisms. Results: Here we used HEK-293T cells to investigate the effect of pH on AQP1 gene transcription levels. We found that AQP1 mRNA levels increases with pH. Transfection of HEK-293T cells with luciferase reporter vectors containing different regions of the AQP1 promoter identified an upstream region in the AQP1 gene between - 2200 and - 2300 bp as an enhancer required for pH-mediated regulation of AQP1 expression. Site-directed mutagenesis of this specific promoter region revealed a critical region between - 2257 and - 2251 bp, and gene knock-down experiments and ChIP assays suggested that the Spi-B transcription factor SPIB is involved in pH-mediated regulation of AQP1 expression. Conclusions: We identified an upstream region in the AQP1 gene and the transcription factor SPIB that are critically involved in pH-mediated regulation of AQP1 expression. These findings provide the basis for further studies on the pH-and buffer-dependent effects of PD fluids on peritoneal membrane integrity and function.