Cathepsin S causes inflammatory pain via biased agonism of PAR2 and TRPV4.
about
Protease inhibition as new therapeutic strategy for GI diseasesSmall molecule dual-inhibitors of TRPV4 and TRPA1 for attenuation of inflammation and pain.Redefining the concept of protease-activated receptors: cathepsin S evokes itch via activation of MrgprsBiased ligand quantification in drug discovery: from theory to high throughput screening to identify new biased μ opioid receptor agonistsCathepsin S inhibition combines control of systemic and peripheral pathomechanisms of autoimmune tissue injury.TRPV4 as a therapeutic target for joint diseases.Molecular and cellular mechanisms that initiate pain and itch.Protein Kinase D and Gβγ Subunits Mediate Agonist-evoked Translocation of Protease-activated Receptor-2 from the Golgi Apparatus to the Plasma Membrane.Transient Receptor Potential Vanilloid 4 Ion Channel Functions as a Pruriceptor in Epidermal Keratinocytes to Evoke Histaminergic Itch.Design of a highly selective quenched activity-based probe and its application in dual color imaging studies of cathepsin S activity localization.ThermoTRPs and Pain.Sensitivity to wheat, gluten and FODMAPs in IBS: facts or fiction?Pathophysiological roles of proteases in gastrointestinal disease.Protease activated receptor 2 (PAR2) modulators: a patent review (2010-2015).Proteinases, Their Extracellular Targets, and Inflammatory Signaling.TRPV1 and TRPA1 in cutaneous neurogenic and chronic inflammation: pro-inflammatory response induced by their activation and their sensitization.Protease-Activated Receptor 2 contributes to Toxoplasma gondii-mediated gut inflammation.Neonatal immune challenge followed by adult immune challenge induces epigenetic-susceptibility to aggravated visceral hypersensitivity.Cathepsin S Is Involved in Th17 Differentiation Through the Upregulation of IL-6 by Activating PAR-2 after Systemic Exposure to Lipopolysaccharide from Porphyromonas gingivalis.Interferon-γ treatment in vitro elicits some of the changes in cathepsin S and antigen presentation characteristic of lacrimal glands and corneas from the NOD mouse model of Sjögren's Syndrome.Neutrophil Elastase Activates Protease-activated Receptor-2 (PAR2) and Transient Receptor Potential Vanilloid 4 (TRPV4) to Cause Inflammation and Pain.Antagonism of the proinflammatory and pronociceptive actions of canonical and biased agonists of protease-activated receptor-2.Integrating the GPCR transactivation-dependent and biased signalling paradigms in the context of PAR1 signalling.Potent Small Agonists of Protease Activated Receptor 2.Protease-Mediated Suppression of DRG Neuron Excitability by Commensal Bacteria.Endosomal signaling of the receptor for calcitonin gene-related peptide mediates pain transmission.Regulation of Pain and Itch by TRP Channels.Granulocyte-colony-stimulating factor (G-CSF) signaling in spinal microglia drives visceral sensitization following colitis.Distinct Gene Profiles of Bone Marrow-Derived Macrophages and Microglia During Neurotropic Coronavirus-Induced Demyelination.Protease-activated receptor-2 in endosomes signals persistent pain of irritable bowel syndrome
P2860
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P2860
Cathepsin S causes inflammatory pain via biased agonism of PAR2 and TRPV4.
description
2014 nî lūn-bûn
@nan
2014年の論文
@ja
2014年論文
@yue
2014年論文
@zh-hant
2014年論文
@zh-hk
2014年論文
@zh-mo
2014年論文
@zh-tw
2014年论文
@wuu
2014年论文
@zh
2014年论文
@zh-cn
name
Cathepsin S causes inflammatory pain via biased agonism of PAR2 and TRPV4.
@en
type
label
Cathepsin S causes inflammatory pain via biased agonism of PAR2 and TRPV4.
@en
prefLabel
Cathepsin S causes inflammatory pain via biased agonism of PAR2 and TRPV4.
@en
P2093
P2860
P50
P356
P1476
Cathepsin S causes inflammatory pain via biased agonism of PAR2 and TRPV4.
@en
P2093
Christoph Korbmacher
Dane D Jensen
Eduardo E Valdez-Morales
Erik Lindström
Ian Henderson
Matthew Metcalf
Nigel W Bunnett
Peishen Zhao
Peter McIntyre
Raquel Guerrero-Alba
P2860
P304
27215-27234
P356
10.1074/JBC.M114.599712
P407
P577
2014-08-12T00:00:00Z