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Article

Raf/ERK drives the proliferative and invasive phenotype of BMPR2-silenced pulmonary artery endothelial cells.

American journal of physiology. Lung cellular and molecular physiology - 15 Jan 2016

Awad Keytam S, Elinoff Jason M, Wang Shuibang, Gairhe Salina, Ferreyra Gabriela A, Cai Rongman, Sun Junfeng, Solomon Michael A, Danner Robert L

Abstract excerpt

A proliferative endothelial cell phenotype, inflammation, and pulmonary vascular remodeling are prominent features of pulmonary arterial hypertension (PAH). Bone morphogenetic protein type II receptor (BMPR2) loss-of-function is the most common cause of heritable PAH and has been closely linked to the formation of pathological plexiform lesions. Although some BMPR2 mutations leave ligand-dependent responses...

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Share to Bone Morphogenetic Protein Receptors, Type II
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Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Extracellular Signal-Regulated MAP Kinases

Share to Familial Primary Pulmonary Hypertension

Share to Hypertension, Pulmonary

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Source

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Identifiers

PMID: 26589479
DOI: 10.1152/ajplung.00303.2015
PMCID: PMC4719048

Genes

BMPR2
PAH

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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