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Open AccessJournal ArticleDOI

The Deubiquitinating Enzyme USP5 Modulates Neuropathic and Inflammatory Pain by Enhancing Cav3.2 Channel Activity

TLDR
Experiments reveal a cell signaling pathway that regulates T-type channel activity and their role in nociceptive signaling and reveal the role of USP5 in both inflammatory and neuropathic mouse models of mechanical hypersensitivity.
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This article is published in Neuron.The article was published on 2014-09-03 and is currently open access. It has received 192 citations till now. The article focuses on the topics: Ubiquitin ligase & Deubiquitinating enzyme.

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The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential

TL;DR: This review describes how use-dependent blockers of the different isoforms could selectively block calcium channels in particular pathologies, such as nociceptive neurons in pain states or in epileptic brain circuits, and describes how selectivity for different subtypes of calcium channels may be achieved in the future.
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Targeting voltage-gated calcium channels in neurological and psychiatric diseases

TL;DR: An overview of calcium channels as drug targets for nervous system disorders is provided, and potential challenges and opportunities for the development of new clinically effective calcium channel inhibitors are discussed.
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Role of Prelimbic GABAergic Circuits in Sensory and Emotional Aspects of Neuropathic Pain

TL;DR: It is found that peripheral nerve injury inhibits pyramidal cell firing in the prelimbic area of the prefrontal cortex as a result of feed-forward inhibition mediated by parvalbumin-expressing GABAergic interneurons, and this region is identified as a potential target for pain therapeutics.
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Voltage-Gated Ion Channels in the PNS: Novel Therapies for Neuropathic Pain?

TL;DR: Three voltage-gated ion channel families, CaV, HCN, and NaV, are focused on, first reviewing the preclinical data and then the human data where it exists, and altered expression, trafficking, and functioning of ion channels expressed by primary sensory neurons are proposed.
References
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Journal ArticleDOI

The formalin test in mice: dissociation between inflammatory and non-inflammatory pain

TL;DR: It is suggested that the early phase is due to a direct effect on nociceptors and that prostaglandins do not play an important role during this phase, and the late phase seems to be an inflammatory response with inflammatory pain that can be inhibited by anti‐inflammatory drugs.
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Breaking the chains: structure and function of the deubiquitinases.

TL;DR: DUBs are subject to multiple layers of regulation that modulate both their activity and their specificity, and due to their wide-ranging involvement in key regulatory processes, these enzymes might provide new therapeutic targets.
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A Genomic and Functional Inventory of Deubiquitinating Enzymes

TL;DR: An inventory of the deubiquitinating enzymes encoded in the human genome is presented and the literature concerning these enzymes is reviewed, with particular emphasis on their function, specificity, and the regulation of their activity.
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Molecular Physiology of Low-Voltage-Activated T-type Calcium Channels

TL;DR: The goal of this review is to provide a comprehensive description of T-type currents, their distribution, regulation, pharmacology, and cloning.
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WW domains of Nedd4 bind to the proline-rich PY motifs in the epithelial Na+ channel deleted in Liddle's syndrome.

TL;DR: The results demonstrate that the WW domains of rNedd4 bind to the PY motifs deleted from beta or gammaENaC in Liddle's syndrome patients, and suggest that Nedd4 may be a regulator (suppressor) of the epithelial Na+ channel.
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