Anti-AQP1 monoclonal antibody, clone 7D11

Background: Irritable bowel syndrome (IBS) is one of the most common gastrointestinal (GI) disorders. The cAMP-PKA pathway plays a key role in mediating cell responses to various stimuli both of which might play an important role in IBS. Objective: Our research aimed to detect the mechanism of IBS rat models via the cAMP-PKA pathway so as to further detect the mechanisms of IBS. Methods: IBS rats were built by stress and conditioned stimulus. The study was divided into 3 groups (a control group, a model group, and a forskolin group). The expressions of AQP1, AQP3, AQP8, and CREB (Serl33) in the colons of rats were detected by immunohistochemistry. The expressions of AQP1, AQP3, AQP8, IL-1 beta, TGF beta, and TNF alpha in the colon were detected by the PCR technique. Results: The IBS rats were built successfully. The expressions of AQP1, AQP3, AQP8, and CREB (Serl33) were down-regulated in the colons of IBS rats and were up-regulated with the intervention of the activator of AMP (P<0.05). The expressions of IL-1 beta, TGF beta and TNF alpha were up-regulated in the colons of IBS rats and were down-regulated with the intervention of the activator of AMP (P<0.05). Conclusions: The release of inflammatory cytokines, the activation of the immune system and liquid water metabolic abnormalities are the mechanisms of IBS via the cAMP-PKA pathway.

In this study, an aquaporin protein, Aqp1, in Cryptococcus neoformans, which can lead either saprobic or parasitic lifestyles and causes life-threatening fungal meningitis was identified and characterized. AQP1 expression was rapidly induced (via the HOG pathway) by osmotic or oxidative stress. In spite of such transcriptional regulation, Aqp1 was found to be largely unnecessary for adaptation to diverse environmental stressors, regardless of the presence of the polysaccharide capsule. The latter is shown here to be a key environmental-stress protectant for C. neoformans. Furthermore, Aqp1 was not required for the development and virulence of C. neoformans. Deletion of AQP1 increased hydrophobicity of the cell surface. The comparative metabolic profiling analysis of the aqp1 mutant and AQP1-overexpressing strains revealed that deletion of AQP1 significantly increased cellular accumulation of primary and secondary metabolites, whereas overexpression of AQP1 depleted such metabolites, suggesting that this water channel protein performs a critical function in metabolic homeostasis. In line with this result, it was found that the aqp1 mutant (which is enriched with diverse metabolites) survived better than the wild type and a complemented strain, indicating that Aqp1 is likely to be involved in competitive fitness of this fungal pathogen.