Spred-1 negatively regulates allergen-induced airway eosinophilia and hyperresponsiveness. - Wikidata - awgldk - TriplyDB

Spred-1 negatively regulates allergen-induced airway eosinophilia and hyperresponsiveness.

Spred-1 negatively regulates allergen-induced airway eosinophilia and hyperresponsiveness.

http://www.wikidata.org/entity/Q38515481

about

Spred2 interaction with the late endosomal protein NBR1 down-regulates fibroblast growth factor receptor signaling Spred1 and TESK1--two new interaction partners of the kinase MARKK/TAO1 that link the microtubule and actin cytoskeleton RASopathies: unraveling mechanisms with animal models Interleukin-5 and IL-5 receptor in health and diseases Adipose tissue deficiency and chronic inflammation in diabetic Goto-Kakizaki rats The VASP-Spred-Sprouty domain puzzle.Spred1, a negative regulator of Ras-MAPK-ERK, is enriched in CNS germinal zones, dampens NSC proliferation, and maintains ventricular zone structure.Anti‑inflammatory effects of dihydromyricetin in a mouse model of asthma.Gene disruption of Spred-2 causes dwarfism.The Sprouty-related protein, Spred-1, localizes in a lipid raft/caveola and inhibits ERK activation in collaboration with caveolin-1.Regulation of CD4⁺ and CD8⁺ effector responses by Sprouty-1 Germline loss-of-function mutations in SPRED1 cause a neurofibromatosis 1-like phenotype.Identification of SPRED2 (sprouty-related protein with EVH1 domain 2) as a negative regulator of the hypothalamic-pituitary-adrenal axis.Spreds are essential for embryonic lymphangiogenesis by regulating vascular endothelial growth factor receptor 3 signaling.SPRED1 Interferes with K-ras but Not H-ras Membrane Anchorage and Signaling.TGF-beta modulates the functionality of tumor-infiltrating CD8+ T cells through effects on TCR signaling and Spred1 expression Diversity of polyproline recognition by EVH1 domains.IL-5- and eosinophil-mediated inflammation: from discovery to therapy.The signaling mechanism of eosinophil activation.Review and update of SPRED1 mutations causing Legius syndrome.Modeling RASopathies with Genetically Modified Mouse Models.The many ways tissue phagocytes respond to dying cells.The neuropeptide neuromedin U activates eosinophils and is involved in allergen-induced eosinophilia.Strand and Cell Type-specific Function of microRNA-126 in Angiogenesis Loss of SOCS3 in T helper cells resulted in reduced immune responses and hyperproduction of interleukin 10 and transforming growth factor-beta 1 Short-term roxithromycin treatment attenuates airway inflammation via MAPK/NF-κB activation in a mouse model of allergic asthma.Feedback regulation of RTK signaling in development.OCD-like behavior is caused by dysfunction of thalamo-amygdala circuits and upregulated TrkB/ERK-MAPK signaling as a result of SPRED2 deficiency.SPRED1, a RAS MAPK pathway inhibitor that causes Legius syndrome, is a tumour suppressor downregulated in paediatric acute myeloblastic leukaemia.SPREDs (Sprouty related proteins with EVH1 domain) promote self-renewal and inhibit mesodermal differentiation in murine embryonic stem cells.Rosmarinic Acid Attenuates Airway Inflammation and Hyperresponsiveness in a Murine Model of Asthma.Dihydroartemisinin suppresses ovalbumin-induced airway inflammation in a mouse allergic asthma model.Decreased Bronchial Eosinophilic Inflammation and Mucus Hypersecretion in Asthmatic Mice Lacking All Nitric Oxide Synthase Isoforms.Estrogen-induced miR-196a elevation promotes tumor growth and metastasis via targeting SPRED1 in breast cancer.Regulation of functional phenotypes of cord blood derived eosinophils by gamma-secretase inhibitor.miR126 positively regulates mast cell proliferation and cytokine production through suppressing Spred1.Craniofacial and oral alterations in patients with Neurofibromatosis 1

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P2860

Spred-1 negatively regulates allergen-induced airway eosinophilia and hyperresponsiveness.

http://www.wikidata.org/entity/Q38515481

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Akihiko Yoshimura

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Atsushi Nonami

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Byoung-gon Moon

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Fumihiko Ishikawa

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Hiromasa Inoue

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Kiyoshi Takatsu

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Koichiro Matsumoto

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Kouji Taniguchi

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Masato Kubo

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Mikiko Matsumura

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P2860

Eotaxin induces degranulation and chemotaxis of eosinophils through the activation of ERK2 and p38 mitogen-activated protein kinases

Regulation of eosinophilopoiesis in a murine model of asthma

sprouty encodes a novel antagonist of FGF signaling that patterns apical branching of the Drosophila airways

The JAK-binding protein JAB inhibits Janus tyrosine kinase activity through binding in the activation loop

SH2-B is required for both male and female reproduction

A critical cytoplasmic domain of the interleukin-5 (IL-5) receptor alpha chain and its function in IL-5-mediated growth signal transduction

Interleukin 5 synthesis by eosinophils: association with granules and immunoglobulin-dependent secretion

CIS3/SOCS-3 suppresses erythropoietin (EPO) signaling by binding the EPO receptor and JAK2

Decreased expression of membrane IL-5 receptor alpha on human eosinophils: I. Loss of membrane IL-5 receptor alpha on airway eosinophils and increased soluble IL-5 receptor alpha in the airway after allergen challenge

Interleukin-5, eosinophils, and disease

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