scholarly journals Stanniocalcin-1 acts in a negative feedback loop in the prosurvival ERK1/2 signaling pathway during oxidative stress

Oncogene ◽  
2009 ◽  
Vol 28 (18) ◽  
pp. 1982-1992 ◽  
Author(s):  
A Nguyen ◽  
A C M Chang ◽  
R R Reddel
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Negative Feedback Loop

scholarly journals A Negative Feedback Loop Between NAMPT and TGF-β Signaling Pathway in Colorectal Cancer Cells

2021 ◽  
Vol Volume 14 ◽  
pp. 187-198
Author(s):  
Xiaoqun Lv ◽  
Jinguo Zhang ◽  
Jun Zhang ◽  
Wencai Guan ◽  
Weifang Ren ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Negative Feedback Loop ◽  
Colorectal Cancer Cells

scholarly journals DOPA Homeostasis by Dopamine: A Control-Theoretic View

2021 ◽  
Vol 22 (23) ◽  
pp. 12862
Author(s):  
Rune Kleppe ◽  
Qaiser Waheed ◽  
Peter Ruoff
Keyword(s):  
Oxidative Stress ◽  
Experimental Data ◽  
Negative Feedback ◽  
Neural Activity ◽  
Feedback Loop ◽  
Feedback Inhibition ◽  
Zero Order ◽  
Negative Feedback Loop ◽  
Zero Order Kinetics ◽  
The Brain

Dopamine (DA) is an important signal mediator in the brain as well as in the periphery. The term “dopamine homeostasis” occasionally found in the literature refers to the fact that abnormal DA levels can be associated with a variety of neuropsychiatric disorders. An analysis of the negative feedback inhibition of tyrosine hydroxylase (TH) by DA indicates, with support from the experimental data, that the TH-DA negative feedback loop has developed to exhibit 3,4-dihydroxyphenylalanine (DOPA) homeostasis by using DA as a derepression regulator. DA levels generally decline when DOPA is removed, for example, by increased oxidative stress. Robust DOPA regulation by DA further implies that maximum vesicular DA levels are established, which appear necessary for a reliable translation of neural activity into a corresponding chemical transmitter signal. An uncontrolled continuous rise (windup) in DA occurs when Levodopa treatment exceeds a critical dose. Increased oxidative stress leads to the successive breakdown of DOPA homeostasis and to a corresponding reduction in DA levels. To keep DOPA regulation robust, the vesicular DA loading requires close to zero-order kinetics combined with a sufficiently high compensatory flux provided by TH. The protection of DOPA and DA due to a channeling complex is discussed.

scholarly journals Patterning on the move: the effects of Hh morphogen source movement on signaling dynamics

2021 ◽  
Author(s):  
david G Miguez ◽  
Antonella G Iannini ◽  
diana garcia-morales ◽  
Fernando Casares
Keyword(s):  
Signaling Pathway ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Computational Models ◽  
Compound Eye ◽  
Temporal Dynamics ◽  
Negative Feedback Loop ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Signaling Dynamics

Morphogens of the Hh-family trigger gene expression changes of receiving cells in a concentration-dependent manner. The outputs of the pathway include regulation of cell identity, proliferation, death or metabolism, depending on the tissue or organ. This variety of responses relies on a conserved signaling pathway. Its internal logic includes a negative feedback loop involving the Hh receptor Ptc. In this paper, we use experiments and computational models to study and compare the different spatial signaling profiles downstream of Hh in several developing Drosophila organs. We show that the spatial distribution of Ptc and the activator form of the Gli transcription factor, CiA, in wing, antenna and ocellus show similar features, but markedly different from that in the compound eye (CE). We show that these two profile types represent two time points along the signaling dynamics, and that the interplay between the spatial displacement of the Hh source in the CE and the negative feedback loop maintains the receiving cells effectively in an earlier stage of signaling. These results indicate that the dynamics of the Hh source strongly influences the signaling profile Hh elicits in receiving cells, and show how the interaction between spatial and temporal dynamics of signaling and differentiation processes can contribute to the informational versatility of the conserved Hh signaling pathway.

Huwe1-Mediated Ubiquitylation of Dishevelled Defines a Negative Feedback Loop in the Wnt Signaling Pathway

2014 ◽  
Vol 7 (317) ◽  
pp. ra26-ra26 ◽  
Author(s):  
R. E. A. de Groot ◽  
R. S. Ganji ◽  
O. Bernatik ◽  
B. Lloyd-Lewis ◽  
K. Seipel ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Signaling Pathway ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Wnt Signaling Pathway ◽  
Negative Feedback Loop

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.

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