Adult-onset pulmonary fibrosis caused by mutations in telomerase

By Kalliopi Tsakiri, Jennifer T. Cronkhite, Phillip J. Kuan, Chao Xing, G. Raghu, J. Weissler, R. Rosenblatt, J. Shay, C. Garcia. Proceedings of the National Academy of Sciences of the United States of America, 2007

893 citations recorded by the source corpus.

Subfields: Physiology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/fca569563796c7a4acf91e6b06fe9118608e8cdb

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Physiology

1. M. Blasco
2. Peter M. Lansdorp
3. M. Armanios
4. G. Aubert

Citations in the corpus

• A census of human RNA-binding proteins (2014, background): “telRNAbinding developmental / cardiovascular/ pulmonary disease TERT coronary artery disease, dyskeratosis congenita, aplastic anemia missense mutation, frameshift (Armanios et al., 2007; Marrone et al., 2007; Tsakiri et al., 2007; Yamaguchi et al., 2005)”
• Mechanisms of fibrosis: therapeutic translation for fibrotic disease (2012, neutral): “Telomere shortening has been hypothesized to be an important contributor to the development of adult-onset and familial forms of pulmonary fibrosis 128,129 .”
• Short telomeres are a risk factor for idiopathic pulmonary fibrosis (2008, background): “Mutations in telomerase components, hTERT and hTR, underlie inheritance of IPF in 8–15% of individuals who have a documented family history (5, 6).”
• Telomere length, stem cells and aging. (2007, background): “This further expands the number of human diseases characterized by regeneration defects that are associated with telomerase defect”
• Telomeres and aging. (2008, background): “Recent studies have shown that mutations in the genes encoding telomerase components are also implicated in familial idiopathic pulmonary fibrosis (6, 209).”