Assignment&lt;footref rid="foot01"&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/footref&gt; of the Aquaporin-8 water channel gene (AQP8) to human chromosome 16p12

Viggiano, Luigi; Rocchi, Mariano; Svelto, María; Calamita, Giuseppe

doi:10.1159/000015260

Cited by 14 publications

(7 citation statements)

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“…The human AQP3 and AQP7 genes are also composed of six exons (Ishibashi et al, 1998) but four out of five splice sites do not correspond to those of Aqp8. This is consistent with previous phylogenetic analyses suggesting a different evolutionary pathway for Aqp8 compared to that of the other mammalian AQPs (Koyama et al, 1997;Viggiano et al, 1999). The fact that the first intron does not conform to the GT-AG rule by ending with the dinucleotide GG instead of the canonical AG at its 3)-end seems not to affect its correct splicing since no alternative splicing or truncations were identified in the Aqp8 cDNAs cloned by us or other investigators (Ma et al, 1997).…”

Section: Discussionsupporting

confidence: 91%

“…Indeed the 7F region has been reported to be syntenic, in centromere-telomere orientation, with human chromosomes 11p15, 16p12 → p11.2, and 10q25 → q26 (DeBry et al, 1996; Web database: http://www3.ncbi.nlm.nih.gov/Homology/). We have recently reported the mapping of the human AQP8 gene at 16p12 (Viggiano et al, 1999). The mapping results on human and mouse are therefore in perfect agreement and strongly suggest that the two loci are homologous.…”

Section: Discussionsupporting

confidence: 57%

“…The mouse AQP8 was also found to transport urea (Ma et al, 1997) although this feature is not observed in rat AQP8 (Koyama et al, 1997). Although the predicted AQP8 polypeptide is topologically and biochemically similar to those of the other mammalian AQPs, AQP8 features a distinct phylogenesis (Koyama et al, 1997;Viggiano et al, 1999). Tissue distribution of AQP8 suggests important roles for this water channel in processes such as the secretion of pancreatic juice, saliva and bile, fecal dehydration, sperm maturation and fertilization and the transport of fluid across the placenta.…”

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confidence: 96%

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Cloning, structural organization and chromosomal localization of the mouse Aquaporin-8 water channel gene <i>(Aqp8)</i>

Calamita

Spalluto²,

Mazzone³

et al. 1999

Cytogenet Genome Res

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The gene encoding the mouse Aquaporin-8 water channel protein (Aqp8) was cloned and its genomic structure was defined. Aqp8 consists of six exons with boundaries at amino acids 1–4, 5–87, 88–129, 130–201, 202–246 and 247–261 which partially correspond to those of other known aquaporin genes. All splice sites conform to the GT–AG rule except the first one which is GT–GG. Primer extension and RNase protection analyses using mouse liver RNA demonstrated three initiation transcription sites located 385, 156 and 146 bp upstream from the translational start codon. No defined TATA box was found in the 5′-flanking region where numerous CAAT motifs and one GATA box were identified. Fluorescence in situ hybridization localized the Aqp8 locus to mouse chromosome 7F3. The 7F region is syntenic with human chromosomes 11, 16 and 10. These results (i) reveal marked structural distinction between the Aqp8 gene and the other known mammalian aquaporin genes, (ii) may now permit the molecular characterization of Aqp8 expression and (iii) represent a fundamental step for the construction of a target vector to generate transgenic Aqp8 knockout mice.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 57%

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confidence: 96%

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Cloning, structural organization and chromosomal localization of the mouse Aquaporin-8 water channel gene <i>(Aqp8)</i>

Calamita

Spalluto²,

Mazzone³

et al. 1999

Cytogenet Genome Res

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“…It is important to elucidate their tumorspecific expression patterns and to reveal their potential functions besides sole water transport in the different organs and tumor entities. AQP8 gene encodes 261 amino acids that situates in chromosome 16 p12 (Viggiano et al, 1999), only participating in water metabolism. AQP8 is involved in the pathogenesis of inflammatory disease Zhao et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Aquaporin 8 Involvement in Human Cervical Cancer SiHa Migration via the EGFR-Erk1/2 Pathway

Shi¹,

Tuokan²,

Chen³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Overexpression of aquaporins (AQPs) has been reported in several human cancers. Epidermal growth factor receptor (EGFR)-extracellular signal-regulated kinases 1/2 (Erk1/2) are associated with tumorigenesis and cancer progression and may upregulate AQP expression. In this study, we demonstrated that EGF (epidermal growth factor) induces SiHa cells migration and AQP8 expression. Wound healing results showed that cell migration was increased by 2.79-1.50-fold at 24h and 48h after EGF treatment. AQP8 expression was significantly increased (3.33-fold) at 48h after EGF treatment in SiHa cells. An EGFR kinase inhibitor, PD153035, blocked EGFinduced AQP8 expression and cell migration and AQP8 expression was decreased from 1.59-fold (EGF-treated) to 0.43-fold (PD153035-treated) in SiHa. Furthermore, the MEK (MAPK (mitogen-activated protein kinase)/ Erk (extracellular signal regulated kinase)/Erk inhibitor U0126 also inhibited EGF-induced AQP8 expression and cell migration. AQP8 expression was decreased from 1.21-fold (EGF-treated) to 0.43-fold (U0126-treated). Immunofluorescence microscopy further confirmed the results. Collectively, our findings show that EGF induces AQP8 expression and cell migration in human cervical cancer SiHa cells via the EGFR/Erk1/2 signal transduction pathway.

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“…By combining information from published IBD linkage analysis and association studies with our Affymetrix microarray results (mapping and arraying strategy [6] ), we obtained several genes of interest. Among them, we found the significantly differentially regulated aquaporin-8 (AQP8) gene, which is located on chromosome 16p12.1 and thus within the IBD locus 8 [7] . Therefore, we focused on the analysis of this gene in the present study.…”

Section: Introductionmentioning

confidence: 99%

Aquaporin-8 expression is reduced in ileum and induced in colon of patients with ulcerative colitis

Zahn

Moehle²,

Langmann³

et al. 2007

WJG

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AIM:To study susceptibility genes which may play a potential role in the pathogenesis and etiology of inflammatory bowel disease (IBD). METHODS:To identify potential susceptibility genes we performed global gene expression profiling in patients with IBD and control specimens. For determination of an intrinsic gene expression profile in ulcerative colitis (UC) and Crohn's disease (CD) compared to normal subjects, mucosal biopsies of non-inflamed regions of the colon and the terminal ileum were subjected to DNA microarray analysis. Real-time RT-PCR and immunohistochemistry were used for verification of selected regulated candidate genes and a genetic analysis was performed. RESULTS:We could show that aquaporin-8 (AQP8) mRNA and protein levels were significantly increased in the colon of UC patients compared to controls. Genetic analysis of the six exons and the promoter region of AQP8, however, revealed no mutations or polymorphisms in IBD patients. CONCLUSION:Our results suggest that upregulation of AQP8 in the colon of UC patients represents a secondary phenomenon which may, due to altered water exchange of the distal intestinal mucosa, disturb the physiologic colonic mucus barrier and thus lead to chronic inflammation and ulceration.

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Assignment<footref rid="foot01"><sup>1</sup></footref> of the Aquaporin-8 water channel gene (AQP8) to human chromosome 16p12

Cited by 14 publications

References 10 publications

Cloning, structural organization and chromosomal localization of the mouse Aquaporin-8 water channel gene <i>(Aqp8)</i>

Cloning, structural organization and chromosomal localization of the mouse Aquaporin-8 water channel gene <i>(Aqp8)</i>

Aquaporin 8 Involvement in Human Cervical Cancer SiHa Migration via the EGFR-Erk1/2 Pathway

Aquaporin-8 expression is reduced in ileum and induced in colon of patients with ulcerative colitis

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