scholarly journals Molecular mechanisms of EGF signaling-dependent regulation of pipe, a gene crucial for dorsoventral axis formation in Drosophila

2011 ◽  
Vol 222 (1) ◽  
pp. 1-17 ◽  
Author(s):  
Martin Technau ◽  
Meike Knispel ◽  
Siegfried Roth
Keyword(s):  
Molecular Mechanisms ◽  
Axis Formation ◽  
Dorsoventral Axis ◽  
Egf Signaling

scholarly journals Self-Regulatory Circuits in Dorsoventral Axis Formation of the Short-Germ Beetle Tribolium castaneum

2008 ◽  
Vol 14 (4) ◽  
pp. 605-615 ◽  
Author(s):  
Rodrigo Nunes da Fonseca ◽  
Cornelia von Levetzow ◽  
Patrick Kalscheuer ◽  
Abidin Basal ◽  
Maurijn van der Zee ◽  
...  
Keyword(s):  
Tribolium Castaneum ◽  
Axis Formation ◽  
Dorsoventral Axis ◽  
Regulatory Circuits

Conservation and Divergence in Molecular Mechanisms of Axis Formation

2001 ◽  
Vol 35 (1) ◽  
pp. 407-437 ◽  
Author(s):  
Sabbi Lall ◽  
Nipam H. Patel
Keyword(s):  
Molecular Mechanisms ◽  
Axis Formation

scholarly journals The adaptor protein NumbL is involved in the control of glucolipotoxicity-induced pancreatic beta cell apoptosis

2020 ◽  
Author(s):  
Halesha D. Basavarajappa ◽  
Jose M. Irimia ◽  
Patrick T. Fueger
Keyword(s):  
Cell Death ◽  
Beta Cell ◽  
Beta Cells ◽  
Cell Apoptosis ◽  
Molecular Mechanisms ◽  
Pancreatic Beta Cell ◽  
Adaptor Protein ◽  
Beta Cell Apoptosis ◽  
Beta Cell Death ◽  
Egf Signaling

AbstractAvoiding loss of functional beta cell mass is critical for preventing or treating diabetes. Currently, the molecular mechanisms underlying beta cell death are partially understood, and there is a need to identify new targets for developing novel therapeutics to treat diabetes. Previously, our group established that Mig6, an inhibitor of EGF signaling, mediates beta cell death under diabetogenic conditions. The objective of this study was to clarify the mechanisms linking diabetogenic stimuli to beta cell death by investigating Mig6-interacting proteins. Using co-immunoprecipitation and mass spectrometry, we evaluated the binding partners of Mig6 under both normal glucose (NG) and glucolipotoxic (GLT) conditions in beta cells. We identified that Mig6 interacts dynamically with NumbL; whereas Mig6 associates with NumbL under NG, this interaction is disrupted under GLT conditions. Further, we demonstrate that siRNA-mediated suppression of NumbL expression in beta cells prevented apoptosis under GLT conditions by blocking activation of NF-κB signaling. Using co-immunoprecipitation experiments we observed that NumbL’s interactions with TRAF6, a key component of NFκB signaling, are increased under GLT conditions. The interactions among Mig6, NumbL, and TRAF6 are dynamic and context-dependent. We propose a model wherein these interactions activate pro-apoptotic NF-κB signaling while blocking pro-survival EGF signaling under diabetogenic conditions, leading to beta cell apoptosis. These findings indicate that NumbL should be further investigated as a candidate anti-diabetic therapeutic target.

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