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Journal ArticleDOI

Proinflammatory cytokines downregulate connexin 43-gap junctions via the ubiquitin-proteasome system in rat spinal astrocytes

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TLDR
Results indicate that a JNK-dependent ubiquitin-proteasome system is induced under an inflammatory condition that disrupts astrocytic gap junction expression and function, leading to astroCytic dysfunction and the maintenance of the neuroinflammatory state.
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This article is published in Biochemical and Biophysical Research Communications.The article was published on 2015-09-04. It has received 35 citations till now. The article focuses on the topics: Connexin & Epoxomicin.

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Journal ArticleDOI

Connexins and their channels in inflammation.

TL;DR: A state-of-the-art overview of the effects of inflammation on connexin signaling is provided and a better understanding of the importance of con Nexin signaling in inflammation may open up towards clinical perspectives.
Journal ArticleDOI

Regulation of gap junction intercellular communication by connexin ubiquitination: physiological and pathophysiological implications

TL;DR: An overview of the advances made in understanding the roles of connexin ubiquitination in the regulation of gap junction intercellular communication is provided and the emerging physiological and pathophysiological implications of these processes are discussed.
Journal ArticleDOI

Astroglia in Sepsis Associated Encephalopathy.

TL;DR: In humans pathophysiology of SAE is complicated by frequent presence of comorbidities, as well as age-related remodelling of the brain tissue with senescence of astroglia; these confounding factors further impact upon SAE progression and neurological deficits.
Book ChapterDOI

Role of Hemichannels in CNS Inflammation and the Inflammasome Pathway.

TL;DR: This review considers the CNS immune system from the perspective that modulating connexin hemichannel opening can prevent tissue damage arising from excessive and uncontrolled inflammation.
Journal ArticleDOI

Regulation of connexins by the ubiquitin system: Implications for intercellular communication and cancer.

TL;DR: Current understanding of the role of the ubiquitin system in the regulation of connexins is provided and how the malfunction of these processes may contribute to the loss of intercellular communication via gap junctions during carcinogenesis is discussed.
References
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Journal ArticleDOI

The Ubiquitin-Proteasome Proteolytic Pathway: Destruction for the Sake of Construction

TL;DR: It is clear now that degradation of cellular proteins is a highly complex, temporally controlled, and tightly regulated process that plays major roles in a variety of basic pathways during cell life and death as well as in health and disease.
Journal ArticleDOI

Astrocyte dysfunction in neurological disorders: a molecular perspective

TL;DR: An improved understanding of astrocyte biology and heterogeneity and the involvement of these cells in pathogenesis offers the potential for developing novel strategies to treat neurological disorders.
Journal ArticleDOI

Diversity of degradation signals in the ubiquitin–proteasome system

TL;DR: This work focuses on different strategies of degron recognition by the ubiquitin system, and contrast regulatory degrons that are subject to signalling-dependent modification with those that are controlled by protein folding or assembly, as frequently occurs during protein quality control.
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T-cell infiltration and signaling in the adult dorsal spinal cord is a major contributor to neuropathic pain-like hypersensitivity.

TL;DR: Data reveal that T-cell infiltration and activation in the dorsal horn of the spinal cord following peripheral nerve injury contribute to the evolution of neuropathic pain-like hypersensitivity, and shows that IFNγ signaling is required for full expression of adult neuropathic hypersensitivity.
Journal ArticleDOI

Degradation of connexin43 gap junctions involves both the proteasome and the lysosome.

TL;DR: Results implicate both the proteasome and the lysosome in the degradation of connexin43-containing gap junctions in rat heart-derived BWEM cells.
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