Inhibition of overactivated p38 MAPK can restore hematopoiesis in myelodysplastic syndrome progenitors. - Wikidata - awgldk - TriplyDB

Inhibition of overactivated p38 MAPK can restore hematopoiesis in myelodysplastic syndrome progenitors.

Inhibition of overactivated p38 MAPK can restore hematopoiesis in myelodysplastic syndrome progenitors.

http://www.wikidata.org/entity/Q35848761

about

Protein-arginine methyltransferase 1 suppresses megakaryocytic differentiation via modulation of the p38 MAPK pathway in K562 cells Signal transduction inhibitors in treatment of myelodysplastic syndromes Deregulation of innate immune and inflammatory signaling in myelodysplastic syndromes Thrombocytopenia in MDS: epidemiology, mechanisms, clinical consequences and novel therapeutic strategies.Cytosine methylation dysregulation in neonates following intrauterine growth restriction.Vitamin D3-driven signals for myeloid cell differentiation--implications for differentiation therapy Current therapy of myelodysplastic syndromes Molecular basis of crosstalk between oncogenic Ras and the master regulator of hematopoiesis GATA-2 Reactive oxygen species in normal and tumor stem cells.p38 MAPK inhibition reduces diabetes-induced impairment of wound healing Rigosertib as a selective anti-tumor agent can ameliorate multiple dysregulated signaling transduction pathways in high-grade myelodysplastic syndrome.The effects of p38 MAPK inhibition combined with G-CSF administration on the hematoimmune system in mice with irradiation injury.Inhibition of p38 mitogen-activated protein kinase promotes ex vivo hematopoietic stem cell expansion Differential effects of nitrostyrene derivatives on myelopoiesis involve regulation of C/EBPα and p38MAPK activity.A phase I study of oral ARRY-614, a p38 MAPK/Tie2 dual inhibitor, in patients with low or intermediate-1 risk myelodysplastic syndromes.Protein kinase R as mediator of the effects of interferon (IFN) gamma and tumor necrosis factor (TNF) alpha on normal and dysplastic hematopoiesis Inhibition of p38 MAPK attenuates ionizing radiation-induced hematopoietic cell senescence and residual bone marrow injury Mitigation of ionizing radiation-induced bone marrow suppression by p38 inhibition and G-CSF administration.Differential Effects of p38, MAPK, PI3K or Rho Kinase Inhibitors on Bacterial Phagocytosis and Efferocytosis by Macrophages in COPD.Biology of the bone marrow microenvironment and myelodysplastic syndromes.Stem and progenitor cells in myelodysplastic syndromes show aberrant stage-specific expansion and harbor genetic and epigenetic alterations Inhibition of the TGF-beta receptor I kinase promotes hematopoiesis in MDS.Heme oxygenase-1 deficiency leads to disrupted response to acute stress in stem cells and progenitors.Impaired clearance of apoptotic cells leads to HMGB1 release in the bone marrow of patients with myelodysplastic syndromes and induces TLR4-mediated cytokine production.Distinct roles of stress-activated protein kinases in Fanconi anemia-type C-deficient hematopoiesis.MAPK signaling pathways in the regulation of hematopoiesis.Hematopoietic stem cell injury induced by ionizing radiation.Hematopoietic stem cell senescence and cancer therapy-induced long-term bone marrow injury.Immunological derangement in hypocellular myelodysplastic syndromes.Are T-cell dysfunctions the other side of the moon in the pathogenesis of myelodysplastic syndromes?The many faces of p38 mitogen-activated protein kinase in progenitor/stem cell differentiation.Interferon receptor signaling in malignancy: a network of cellular pathways defining biological outcomes.Monocytic cell differentiation from band-stage neutrophils under inflammatory conditions via MKK6 activation.The inflammatory microenvironment in MDS.Stem and progenitor cell alterations in myelodysplastic syndromes.Pexmetinib: A Novel Dual Inhibitor of Tie2 and p38 MAPK with Efficacy in Preclinical Models of Myelodysplastic Syndromes and Acute Myeloid Leukemia.Emerging biological therapies for the treatment of myelodysplastic syndromes.Lack of MK2 inhibits myofibroblast formation and exacerbates pulmonary fibrosis.Arsenic trioxide and proteasome inhibitor bortezomib synergistically induce apoptosis in leukemic cells: the role of protein kinase Cdelta.An exploratory, randomized, parallel-group, open-label, relative bioavailability study with an additional two-period crossover food-effect study exploring the pharmacokinetics of two novel formulations of pexmetinib (ARRY-614).

P2860

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P2860

Inhibition of overactivated p38 MAPK can restore hematopoiesis in myelodysplastic syndrome progenitors.

http://www.wikidata.org/entity/Q35848761

description

2006 nî lūn-bûn

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年论文

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2006年论文

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2006年论文

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name

Inhibition of overactivated p3 ...... splastic syndrome progenitors.

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Inhibition of overactivated p3 ...... splastic syndrome progenitors.

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type

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Inhibition of overactivated p3 ...... splastic syndrome progenitors.

@ast

Inhibition of overactivated p3 ...... splastic syndrome progenitors.

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prefLabel

Inhibition of overactivated p3 ...... splastic syndrome progenitors.

@ast

Inhibition of overactivated p3 ...... splastic syndrome progenitors.

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Inhibition of overactivated p3 ...... ysplastic syndrome progenitors

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Aaron N Nguyen

http://www.w3.org/2001/XMLSchema#string

Amit Verma

http://www.w3.org/2001/XMLSchema#string

Edwin Haghnazari

http://www.w3.org/2001/XMLSchema#string

Irene Kerr

http://www.w3.org/2001/XMLSchema#string

Jing Ying Ma

http://www.w3.org/2001/XMLSchema#string

Leonidas C Platanias

http://www.w3.org/2001/XMLSchema#string

Li Zhou

http://www.w3.org/2001/XMLSchema#string

Linda S Higgins

http://www.w3.org/2001/XMLSchema#string

Lubomir Sokol

http://www.w3.org/2001/XMLSchema#string

Mani Mohindru

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P2860

Induction of apoptosis by ASK1, a mammalian MAPKKK that activates SAPK/JNK and p38 signaling pathways

Engagement of Gab1 and Gab2 in erythropoietin signaling

International scoring system for evaluating prognosis in myelodysplastic syndromes

Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis

Mitogen-activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases

Efficacy of lenalidomide in myelodysplastic syndromes.

Myelodysplasia.

Cardiac muscle cell hypertrophy and apoptosis induced by distinct members of the p38 mitogen-activated protein kinase family.

Map kinase signaling pathways and hematologic malignancies.

Differentiation stage-specific activation of p38 mitogen-activated protein kinase isoforms in primary human erythroid cells

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