Mice expressing BMPR2R899X transgene in smooth muscle develop pulmonary vascular lesions. - Wikidata - awgldk - TriplyDB

Mice expressing BMPR2R899X transgene in smooth muscle develop pulmonary vascular lesions.

Mice expressing BMPR2R899X transgene in smooth muscle develop pulmonary vascular lesions.

http://www.wikidata.org/entity/Q36977330

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Functional changes in pulmonary arterial endothelial cells associated with BMPR2 mutations Targeting BMP signalling in cardiovascular disease and anaemia The molecular genetics and cellular mechanisms underlying pulmonary arterial hypertension Microvascular repair: post-angiogenesis vascular dynamics The genetics of pulmonary arterial hypertension A brief overview of mouse models of pulmonary arterial hypertension: problems and prospects.Endoglin-mediated suppression of prostate cancer invasion is regulated by activin and bone morphogenetic protein type II receptors.Gene expression in lungs of mice lacking the 5-hydroxytryptamine transporter gene.Adenosine A2B receptor and hyaluronan modulate pulmonary hypertension associated with chronic obstructive pulmonary disease Development of pulmonary arterial hypertension in women: interplay of sex hormones and pulmonary vascular disease.Interaction between bone morphogenetic protein receptor type 2 and estrogenic compounds in pulmonary arterial hypertension Subcellular mechanisms in pulmonary arterial hypertension: combinatorial modalities that inhibit anterograde trafficking and cause bone morphogenetic protein receptor type 2 mislocalization.Altered gene expression in pulmonary tissue of tryptophan hydroxylase-1 knockout mice: implications for pulmonary arterial hypertension.Role of BMPR2 alternative splicing in heritable pulmonary arterial hypertension penetrance.BMPR2 mutation alters the lung macrophage endothelin-1 cascade in a mouse model and patients with heritable pulmonary artery hypertension.Bone Morphogenetic Protein (BMP) signaling in development and human diseases Modification of hemodynamic and immune responses to exposure with a weak antigen by the expression of a hypomorphic BMPR2 gene Pulmonary hypertension in women.Deletion of the sequence encoding the tail domain of the bone morphogenetic protein type 2 receptor reveals a bone morphogenetic protein 7-specific gain of function Physiologic and molecular consequences of endothelial Bmpr2 mutation.Paigen diet-fed apolipoprotein E knockout mice develop severe pulmonary hypertension in an interleukin-1-dependent manner.Rescuing the BMPR2 signaling axis in pulmonary arterial hypertension The genetics of pulmonary arterial hypertension in the post-BMPR2 era.Idiopathic and heritable PAH perturb common molecular pathways, correlated with increased MSX1 expression.Cytoskeletal defects in Bmpr2-associated pulmonary arterial hypertension Serotonin 2B Receptor Antagonism Prevents Heritable Pulmonary Arterial Hypertension.Metabolomic analysis of bone morphogenetic protein receptor type 2 mutations in human pulmonary endothelium reveals widespread metabolic reprogramming.Expression of mutant bone morphogenetic protein receptor II worsens pulmonary hypertension secondary to pulmonary fibrosis.Estrogen Metabolite 16α-Hydroxyestrone Exacerbates Bone Morphogenetic Protein Receptor Type II-Associated Pulmonary Arterial Hypertension Through MicroRNA-29-Mediated Modulation of Cellular Metabolism Raf/ERK drives the proliferative and invasive phenotype of BMPR2-silenced pulmonary artery endothelial cells.Right ventricular systolic pressure measurements in combination with harvest of lung and immune tissue samples in mice.Pulmonary Arterial Hypertension: A Current Perspective on Established and Emerging Molecular Genetic Defects.Endothelial HIF signaling regulates pulmonary fibrosis-associated pulmonary hypertension.The A2B adenosine receptor modulates pulmonary hypertension associated with interstitial lung disease.Bone Marrow-derived Cells Contribute to the Pathogenesis of Pulmonary Arterial Hypertension.The Endothelial Prolyl-4-Hydroxylase Domain 2/Hypoxia-Inducible Factor 2 Axis Regulates Pulmonary Artery Pressure in Mice.SMAD1 deficiency in either endothelial or smooth muscle cells can predispose mice to pulmonary hypertension A potential role for insulin resistance in experimental pulmonary hypertension Rho-kinase inhibition alleviates pulmonary hypertension in transgenic mice expressing a dominant-negative type II bone morphogenetic protein receptor gene.Defective pulmonary vascular remodeling in Smad8 mutant mice

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P2860

Mice expressing BMPR2R899X transgene in smooth muscle develop pulmonary vascular lesions.

http://www.wikidata.org/entity/Q36977330

description

2008 nî lūn-bûn

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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2008年论文

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2008年论文

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name

Mice expressing BMPR2R899X transgene in smooth muscle develop pulmonary vascular lesions.

@en

type

label

Mice expressing BMPR2R899X transgene in smooth muscle develop pulmonary vascular lesions.

@en

prefLabel

Mice expressing BMPR2R899X transgene in smooth muscle develop pulmonary vascular lesions.

@en

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AJPLUNG.90255.2008

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American Journal of Physiology - Lung Cellular and Molecular Physiology

P1476

Mice expressing BMPR2R899X transgene in smooth muscle develop pulmonary vascular lesions.

@en

P2093

Brian Ickes

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Daniel Crona

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Duncan Stewart

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James West

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Julie Harral

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

Karen Fagan

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

Kirk Lane

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Sebastian Albu

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Yupu Deng

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P2860

Functional analysis of bone morphogenetic protein type II receptor mutations underlying primary pulmonary hypertension

BMP4 induces HO-1 via a Smad-independent, p38MAPK-dependent pathway in pulmonary artery myocytes

The Physiological Principle of Minimum Work: I. The Vascular System and the Cost of Blood Volume

Identification of cofilin and LIM-domain-containing protein kinase 1 as novel interaction partners of 14-3-3 zeta

Direct signaling by the BMP type II receptor via the cytoskeletal regulator LIMK1

Insights into the kinetics of siRNA-mediated gene silencing from live-cell and live-animal bioluminescent imaging

The Gene Ontology (GO) project in 2006

Model-based analysis of oligonucleotide arrays: expression index computation and outlier detection

Downregulation of FUSE-binding protein and c-myc by tRNA synthetase cofactor p38 is required for lung cell differentiation

Bone morphogenetic proteins

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18723761

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2584890

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