Photoinhibition of photosystem II in vivo is preceded by down-regulation through light-induced acidification of the lumen: Consequences for the mechanism of photoinhibition in vivo

Planta ◽  
1993 ◽  
Vol 189 (3) ◽  
pp. 359-368 ◽  
Author(s):  
Klaas J. van Wijk ◽  
Philip R. van Hasselt
Keyword(s):  
Photosystem Ii ◽  
Down Regulation

NF-κB Down–regulation and PARP Cleavage by novel 3-α-butyryloxy-β-boswellic Acid Results in Cancer Cell Specific Apoptosis and in vivo Tumor Regression

2013 ◽  
Vol 13 (5) ◽  
pp. 777-790 ◽  
Author(s):  
Yasrib Qurishi ◽  
Abid Hamid ◽  
Parduman R. Sharma ◽  
Zahoor A. Wani ◽  
Dilip M. Mondhe ◽  
...  
Keyword(s):  
Cancer Cell ◽  
Tumor Regression ◽  
Parp Cleavage ◽  
Boswellic Acid ◽  
Down Regulation

scholarly journals LINGO-1 shRNA protects the brain against ischemia/reperfusion injury by inhibiting the activation of NF-κB and JAK2/STAT3

Human Cell ◽  
2021 ◽  
Author(s):  
Jiaying Zhu ◽  
Zhu Zhu ◽  
Yipin Ren ◽  
Yukang Dong ◽  
Yaqi Li ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Nuclear Translocation ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Glucose Deprivation ◽  
Artery Occlusion ◽  
Mice Model ◽  
Down Regulation

AbstractLINGO-1 may be involved in the pathogenesis of cerebral ischemia. However, its biological function and underlying molecular mechanism in cerebral ischemia remain to be further defined. In our study, middle cerebral artery occlusion/reperfusion (MACO/R) mice model and HT22 cell oxygen–glucose deprivation/reperfusion (OGD/R) were established to simulate the pathological process of cerebral ischemia in vivo and in vitro and to detect the relevant mechanism. We found that LINGO-1 mRNA and protein were upregulated in mice and cell models. Down-regulation LINGO-1 improved the neurological symptoms and reduced pathological changes and the infarct size of the mice after MACO/R. In addition, LINGO-1 interference alleviated apoptosis and promoted cell proliferation in HT22 of OGD/R. Moreover, down-regulation of LINGO-1 proved to inhibit nuclear translocation of p-NF-κB and reduce the expression level of p-JAK2 and p-STAT3. In conclusion, our data suggest that shLINGO-1 attenuated ischemic injury by negatively regulating NF-KB and JAK2/STAT3 pathways, highlighting a novel therapeutic target for ischemic stroke.

Diverging signaling events control the pathway of GPVI down-regulation in vivo

Blood ◽  
2007 ◽  
Vol 110 (2) ◽  
pp. 529-535 ◽  
Author(s):  
Tamer Rabie ◽  
David Varga-Szabo ◽  
Markus Bender ◽  
Rastislav Pozgaj ◽  
Francois Lanza ◽  
...  
Keyword(s):  
Platelet Reactivity ◽  
Severe Thrombocytopenia ◽  
Ectodomain Shedding ◽  
Down Regulation ◽  
Therapeutic Implications ◽  
Glycoprotein Vi ◽  
Coronary Artery Thrombosis ◽  
Activation Motif

Abstract Coronary artery thrombosis is often initiated by platelet activation on collagen-rich subendothelial layers in the disrupted atherosclerotic plaque. The activating platelet collagen receptor glycoprotein VI (GPVI) noncovalently associates with the Fc receptor γ-chain (FcRγ), which signals through its immunoreceptor-tyrosine–based activation motif (ITAM) via the adaptor LAT leading to the activation of phospholipase Cγ2 (PLCγ2). GPVI is a promising antithrombotic target as anti-GPVI antibodies induce the irreversible loss of the receptor from circulating platelets by yet undefined mechanisms in humans and mice and long-term antithrombotic protection in the latter. However, the treatment is associated with transient but severe thrombocytopenia and reduced platelet reactivity to thrombin questioning its clinical usefulness. Here we show that GPVI down-regulation occurs through 2 distinct pathways, namely ectodomain shedding or internalization/intracellular clearing, and that both processes are abrogated in mice carrying a point mutation in the FcRγ-associated ITAM. In mice lacking LAT or PLCγ2, GPVI shedding is abolished, but the receptor is irreversibly down-regulated through internalization/intracellular clearing. This route of GPVI loss is not associated with thrombocytopenia or altered thrombin responses. These results reveal the existence of 2 distinct signaling pathways downstream of the FcRγ-ITAM and show that it is possible to uncouple GPVI down-regulation from undesired side effects with obvious therapeutic implications.

GDNF and neurturin are target-derived factors essential for cranial parasympathetic neuron development

Development ◽  
2001 ◽  
Vol 128 (19) ◽  
pp. 3773-3782 ◽  
Author(s):  
Eri Hashino ◽  
Marlene Shero ◽  
Dirk Junghans ◽  
Hermann Rohrer ◽  
Jeffrey Milbrandt ◽  
...  
Keyword(s):  
Striate Muscle ◽  
Ciliary Ganglion ◽  
Neuron Development ◽  
Down Regulation ◽  
Eye Muscle ◽  
Ciliary Ganglion Neurons ◽  
Ganglion Neurons ◽  
Parasympathetic Neuron

During development, parasympathetic ciliary ganglion neurons arise from the neural crest and establish synaptic contacts on smooth and striate muscle in the eye. The factors that promote the ciliary ganglion pioneer axons to grow toward their targets have yet to be determined. Here, we show that glial cell line-derived neurotrophic factor (GDNF) and neurturin (NRTN) constitute target-derived factors for developing ciliary ganglion neurons. Both GDNF and NRTN are secreted from eye muscle located in the target and trajectory pathway of ciliary ganglion pioneer axons during the period of target innervation. After this period, however, the synthesis of GDNF declines markedly, while that of NRTN is maintained throughout the cell death period. Furthermore, both in vitro and in vivo function-blocking of GDNF at early embryonic ages almost entirely suppresses ciliary axon outgrowth. These results demonstrate that target-derived GDNF is necessary for ciliary ganglion neurons to innervate ciliary muscle in the eye. Since the down-regulation of GDNF in the eye is accompanied by down-regulation of GFRα1 and Ret, but not of GFRα2, in innervating ciliary ganglion neurons, the results also suggest that target-derived GDNF regulates the expression of its high-affinity coreceptors.

scholarly journals Soil Application of Effective Microorganisms (EM) Maintains Leaf Photosynthetic Efficiency, Increases Seed Yield and Quality Traits of Bean (Phaseolus vulgaris L.) Plants Grown on Different Substrates

2019 ◽  
Vol 20 (9) ◽  
pp. 2327 ◽  
Author(s):  
Marcello Iriti ◽  
Alessio Scarafoni ◽  
Simon Pierce ◽  
Giulia Castorina ◽  
Sara Vitalini
Keyword(s):  
Phaseolus Vulgaris ◽  
Photosystem Ii ◽  
Sandy Soil ◽  
Photosynthetic Efficiency ◽  
Quality Traits ◽  
Phaseolus Vulgaris L ◽  
Effective Microorganisms ◽  
Yield And Quality ◽  
Bean Plants

EM (effective microorganisms) is a biofertilizer consisting of a mixed culture of potentially beneficial microorganisms. In this study, we investigated the effects of EM treatment on leaf in vivo chlorophyll a fluorescence of photosystem II (PSII), yield, and macronutrient content of bean plants grown on different substrates (nutrient rich substrate vs. nutrient poor sandy soil) in controlled environmental conditions (pot experiment in greenhouse). EM-treated plants maintained optimum leaf photosynthetic efficiency two weeks longer than the control plants, and increased yield independent of substrate. The levels of seed nutritionally-relevant molecules (proteins, lipids, and starch) were only slightly modified, apart from the protein content, which increased in plants grown in sandy soil. Although EM can be considered a promising and environmentally friendly technology for sustainable agriculture, more studies are needed to elucidate the mechanism(s) of action of EM, as well as its efficacy under open field conditions.

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