scholarly journals Arf-GEF localization and function at myosin-rich adherens junctions via coiled-coil heterodimerization with an adaptor protein

2019 ◽  
Vol 30 (26) ◽  
pp. 3090-3103 ◽  
Author(s):  
Shiyu Zheng ◽  
Junior J. West ◽  
Cao Guo Yu ◽  
Tony J. C. Harris
Keyword(s):  
Negative Feedback ◽  
Feedback Loop ◽  
Adherens Junctions ◽  
Coiled Coil ◽  
Adaptor Protein ◽  
Epithelial Morphogenesis ◽  
Negative Feedback Loop ◽  
Dorsal Closure ◽  
Stepping Stone ◽  
And Function

Epithelial morphogenesis often depends on regulation of actomyosin networks at adherens junctions. The Arf-GEF Steppke has been implicated in a negative feedback loop that locally down-regulates junctional actomyosin. We find that coiled-coil heterodimerization with the adaptor protein Stepping stone recruits Steppke to myosin-rich adherens junctions to facilitate tissue stretching during Drosophila dorsal closure.

scholarly journals The Drosophila serine protease homologue Scarface regulates JNK signalling in a negative-feedback loop during epithelial morphogenesis

Development ◽  
2010 ◽  
Vol 137 (13) ◽  
pp. 2177-2186 ◽  
Author(s):  
R. Rousset ◽  
S. Bono-Lauriol ◽  
M. Gettings ◽  
M. Suzanne ◽  
P. Speder ◽  
...  
Keyword(s):  
Serine Protease ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Epithelial Morphogenesis ◽  
Negative Feedback Loop

scholarly journals O-GlcNAcylation on LATS2 disrupts the Hippo pathway by inhibiting its activity

2020 ◽  
pp. 201913469 ◽  
Author(s):  
Eunah Kim ◽  
Jeong Gu Kang ◽  
Min Jueng Kang ◽  
Jae Hyung Park ◽  
Yeon Jung Kim ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Cancer Cells ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Hippo Pathway ◽  
Critical Role ◽  
Adaptor Protein ◽  
Negative Regulator ◽  
Negative Feedback Loop ◽  
The Hippo Pathway

The Hippo pathway controls organ size and tissue homeostasis by regulating cell proliferation and apoptosis. The LATS-mediated negative feedback loop prevents excessive activation of the effectors YAP/TAZ, maintaining homeostasis of the Hippo pathway. YAP and TAZ are hyperactivated in various cancer cells which lead to tumor growth. Aberrantly increased O-GlcNAcylation has recently emerged as a cause of hyperactivation of YAP in cancer cells. However, the mechanism, which induces hyperactivation of TAZ and blocks LATS-mediated negative feedback, remains to be elucidated in cancer cells. This study found that in breast cancer cells, abnormally increased O-GlcNAcylation hyperactivates YAP/TAZ and inhibits LATS2, a direct negative regulator of YAP/TAZ. LATS2 is one of the newly identified O-GlcNAcylated components in the MST-LATS kinase cascade. Here, we found that O-GlcNAcylation at LATS2 Thr436 interrupted its interaction with the MOB1 adaptor protein, which connects MST to LATS2, leading to activation of YAP/TAZ by suppressing LATS2 kinase activity. LATS2 is a core component in the LATS-mediated negative feedback loop. Thus, this study suggests that LATS2 O-GlcNAcylation is deeply involved in tumor growth by playing a critical role in dysregulation of the Hippo pathway in cancer cells.

scholarly journals Smad2/3 Activation Regulates Smad1/5/8 Signaling via a Negative Feedback Loop to Inhibit 3T3-L1 Adipogenesis

2021 ◽  
Vol 22 (16) ◽  
pp. 8472
Author(s):  
Senem Aykul ◽  
Jordan Maust ◽  
Vijayalakshmi Thamilselvan ◽  
Monique Floer ◽  
Erik Martinez-Hackert
Keyword(s):  
Negative Feedback ◽  
Feedback Loop ◽  
Negative Feedback Loop ◽  
Adipose Tissues ◽  
Family Growth ◽  
Simultaneous Activation ◽  
Adipocyte Hypertrophy ◽  
Adipocyte Development ◽  
Energy Surplus

Adipose tissues (AT) expand in response to energy surplus through adipocyte hypertrophy and hyperplasia. The latter, also known as adipogenesis, is a process by which multipotent precursors differentiate to form mature adipocytes. This process is directed by developmental cues that include members of the TGF-β family. Our goal here was to elucidate, using the 3T3-L1 adipogenesis model, how TGF-β family growth factors and inhibitors regulate adipocyte development. We show that ligands of the Activin and TGF-β families, several ligand traps, and the SMAD1/5/8 signaling inhibitor LDN-193189 profoundly suppressed 3T3-L1 adipogenesis. Strikingly, anti-adipogenic traps and ligands engaged the same mechanism of action involving the simultaneous activation of SMAD2/3 and inhibition of SMAD1/5/8 signaling. This effect was rescued by the SMAD2/3 signaling inhibitor SB-431542. By contrast, although LDN-193189 also suppressed SMAD1/5/8 signaling and adipogenesis, its effect could not be rescued by SB-431542. Collectively, these findings reveal the fundamental role of SMAD1/5/8 for 3T3-L1 adipogenesis, and potentially identify a negative feedback loop that links SMAD2/3 activation with SMAD1/5/8 inhibition in adipogenic precursors.

scholarly journals HIC1 and miR-23~27~24 clusters form a double-negative feedback loop in breast cancer

2016 ◽  
Vol 24 (3) ◽  
pp. 421-432 ◽  
Author(s):  
Yanbo Wang ◽  
Hongwei Liang ◽  
Geyu Zhou ◽  
Xiuting Hu ◽  
Zhengya Liu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Negative Feedback Loop ◽  
Double Negative
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