Conditional ablation of mature olfactory sensory neurons mediated by diphtheria toxin receptor

2005 ◽  
Vol 34 (1-2) ◽  
pp. 37-47 ◽  
Author(s):  
Huaiyang Chen ◽  
Kenji Kohno ◽  
Qizhi Gong
Keyword(s):  
Sensory Neurons ◽  
Diphtheria Toxin ◽  
Olfactory Sensory Neurons ◽  
Diphtheria Toxin Receptor ◽  
Toxin Receptor

scholarly journals CD206+ macrophage is an accelerator of endometriotic-like lesion via promoting angiogenesis in the endometriosis mouse model

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yosuke Ono ◽  
Osamu Yoshino ◽  
Takehiro Hiraoka ◽  
Erina Sato ◽  
Akiko Furue ◽  
...  
Keyword(s):  
Mouse Model ◽  
Diphtheria Toxin ◽  
Immunohistochemical Study ◽  
Mrna Levels ◽  
Cytokines And Chemokines ◽  
Diphtheria Toxin Receptor ◽  
Endothelial Cell Marker ◽  
Toxin Receptor ◽  
Group A

AbstractIn endometriosis, M2 MΦs are dominant in endometriotic lesions, but the actual role of M2 MΦ is unclear. CD206 positive (+) MΦ is classified in one of M2 type MΦs and are known to produce cytokines and chemokines. In the present study, we used CD206 diphtheria toxin receptor mice, which enable to deplete CD206+ cells with diphtheria toxin (DT) in an endometriosis mouse model. The depletion of CD206+ MΦ decreased the total weight of endometriotic-like lesions significantly (p < 0.05). In the endometriotic-like lesions in the DT group, a lower proliferation of endometriotic cells and the decrease of angiogenesis were observed. In the lesions, the mRNA levels of VEGFA and TGFβ1, angiogenic factors, in the DT group significantly decreased to approximately 50% and 30% of control, respectively. Immunohistochemical study revealed the expressions of VEGFA and an endothelial cell marker CD31 in lesions of the DT group, were dim compared to those in control. Also, the number of TGFβ1 expressing MΦ was significantly reduced compared to control. These data suggest that CD206+ MΦ promotes the formation of endometriotic-like lesions by inducing angiogenesis around the lesions.

Expression cloning of a diphtheria toxin receptor: Identity with a heparin-binding EGF-like growth factor precursor

Cell ◽  
1992 ◽  
Vol 69 (6) ◽  
pp. 1051-1061 ◽  
Author(s):  
Joseph G. Naglich ◽  
James E. Metherall ◽  
David W. Russell ◽  
Leon Eidels
Keyword(s):  
Growth Factor ◽  
Diphtheria Toxin ◽  
Expression Cloning ◽  
Heparin Binding ◽  
Diphtheria Toxin Receptor ◽  
Toxin Receptor

Diphtheria toxin receptor–mediated conditional and targeted cell ablation in transgenic mice

10.1038/90795 ◽  
2001 ◽  
Vol 19 (8) ◽  
pp. 746-750 ◽  
Author(s):  
Michiko Saito ◽  
Takao Iwawaki ◽  
Choji Taya ◽  
Hiromichi Yonekawa ◽  
Munehiro Noda ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Diphtheria Toxin ◽  
Cell Ablation ◽  
Diphtheria Toxin Receptor ◽  
Toxin Receptor

Endocytic mechanisms responsible for uptake of GPI-linked diphtheria toxin receptor

1999 ◽  
Vol 112 (22) ◽  
pp. 3899-3909 ◽  
Author(s):  
G. Skretting ◽  
M.L. Torgersen ◽  
B. van Deurs ◽  
K. Sandvig
Keyword(s):  
Protein Synthesis ◽  
Cell Surface ◽  
Hela Cells ◽  
Diphtheria Toxin ◽  
Surface Receptors ◽  
Caveolin 1 ◽  
Ultrastructural Studies ◽  
Diphtheria Toxin Receptor ◽  
Early Endosomes ◽  
Toxin Receptor

We have here used diphtheria toxin as a tool to investigate the type of endocytosis used by a glycosylphosphatidylinositol-linked molecule, a glycosylphosphatidylinositol-linked version of the diphtheria toxin receptor that is able to mediate intoxication. The receptor is expressed in HeLa cells where clathrin-dependent endocytosis can be blocked by overexpression of mutant dynamin. Diphtheria toxin intoxicates cells by first binding to cell-surface receptors, then the toxin is endocytosed, and upon exposure to low endosomal pH, the toxin enters the cytosol where it inhibits protein synthesis. Inhibition of protein synthesis by the toxin can therefore be used to probe the entry of the glycosylphosphatidylinositol-linked receptor into an acidic compartment. Furthermore, degradation of the toxin can be used as an indicator of entry into the endosomal/lysosomal compartment. The data show that although expression of mutant dynamin inhibits intoxication mediated via the wild-type receptors, mutant dynamin does not affect intoxication or endocytosis and degradation of diphtheria toxin bound to the glycosylphosphatidylinositol-linked receptor. Confocal microscopy demonstrated that diphtheria toxin is transported to vesicles containing EEA1, a marker for early endosomes. Biochemical and ultrastructural studies of the HeLa cells used reveal that they have very low levels of caveolin-1 and that they contain very few if any caveolae at the cell surface. Furthermore, the endocytic uptake of diphtheria toxin bound to the glycosylphosphatidylinositol-linked receptor was not reduced by methyl-beta-cyclodextrin or by nystatin which both disrupt caveolar structure and functions. Thus, uptake of a glycosylphosphatidylinositol-linked protein, in this case the diphtheria toxin receptor, into the endosomal/lysosomal system can occur independently of both caveolae and clathrin-coated vesicles.

scholarly journals Diphtheria toxin receptor.

1993 ◽  
Vol 48 (5) ◽  
pp. 685-692 ◽  
Author(s):  
Eisuke MEKADA
Keyword(s):  
Diphtheria Toxin ◽  
Diphtheria Toxin Receptor ◽  
Toxin Receptor

scholarly journals Induction of Toxin Sensitivity in Insect Cells by Infection with Baculovirus Encoding Diphtheria Toxin Receptor

1995 ◽  
Vol 270 (28) ◽  
pp. 16879-16885 ◽  
Author(s):  
Elsa M. Valdizan ◽  
Evgenij V. Loukianov ◽  
Sjur Olsnes
Keyword(s):  
Diphtheria Toxin ◽  
Insect Cells ◽  
Diphtheria Toxin Receptor ◽  
Toxin Receptor ◽  
Toxin Sensitivity

scholarly journals Diphtheria Toxin Receptor Complex.

1996 ◽  
Vol 51 (3) ◽  
pp. 853-862
Author(s):  
Eisuke MEKADA ◽  
Yuji SHISHIDO ◽  
Kailash D. SHARMA
Keyword(s):  
Diphtheria Toxin ◽  
Receptor Complex ◽  
Diphtheria Toxin Receptor ◽  
Toxin Receptor
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