The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Pemphigus vulgaris-IgG causes a rapid depletion of desmoglein 3 (Dsg3) from the Triton X-100 soluble pools, leading to the formation of Dsg3-depleted desmosomes in a human squamous carcinoma cell line, DJM-1 cells.

In this study, we examined desmoglein (Dsg) 3 and other desmosomal molecules after pemphigus vulgaris (PV)-immunoglobulin G (IgG) binding to the Dsg3 on the cell surface in DJM-1 cells, a human squamous cell carcinoma cell line. After cells were incubated with PV-IgG for various time periods (0, 5, 10, 20, 30, 60 min, or 30 h), cells were fractionated into phosphate-buffered saline soluble (cytosol), phosphate-buffered saline insoluble-Triton X-100 soluble (membrane), and Triton X-100 insoluble (cytoskeleton) fractions, and subjected to immunoblotting and immunofluorescence microscopy using antibodies against Dsgl, Dsg3, plakoglobin, desmoplakin 1, and cytokeratins. Immunoblot analysis with PV-IgG revealed that Dsg3 was already dramatically depleted from the membrane fraction 20 min after PV-IgG treatment, whereas no reduction of Dsg3 was detected in the cytoskeleton fraction as examined by immunoblotting. A 30 h incubation with PV-IgG, however, caused a marked disappearance of Dsg3, but not other desmosomal molecules, from cytoskeleton fractions. Furthermore, double-staining immunofluorescence microscopy revealed that Dsg3 was depleted from the desmosomes whereas Dsg1, desmoplakin 1, plakoglobin, and keratin filaments were bound to desmosomes. These results provide a novel interpretation for a better understanding of mechanisms for blistering in PV; i.e., a possibility that PV-IgG generates the formation of aberrant desmosomes, which are lacking in Dsg3, but not other desmosomal constituents.[1]

References

 
WikiGenes - Universities