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Jonathan K. Alder

Researcher at University of Pittsburgh

Publications -  69
Citations -  5444

Jonathan K. Alder is an academic researcher from University of Pittsburgh. The author has contributed to research in topics: Telomere & Idiopathic pulmonary fibrosis. The author has an hindex of 24, co-authored 49 publications receiving 4628 citations. Previous affiliations of Jonathan K. Alder include Johns Hopkins University School of Medicine & University of Utah.

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Telomerase Mutations in Families with Idiopathic Pulmonary Fibrosis

TL;DR: In this paper, the authors found that mutations in the genes encoding telomerase components can appear as familial idiopathic pulmonary fibrosis, which is a rare hereditary disorder associated with premature death from aplastic anemia and lung fibrosis.
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Short telomeres are a risk factor for idiopathic pulmonary fibrosis

TL;DR: Short telomeres are a signature in IIPs and likely play a role in their age-related onset, and the clustering of cryptogenic liver cirrhosis with IPF suggests that the telomere shortening can contribute to what appears clinically as idiopathic progressive organ failure in the lung and the liver.
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CD34+ hematopoietic stem-progenitor cell microRNA expression and function: a circuit diagram of differentiation control.

TL;DR: This work found 33 miRNAs expressed in CD34+ hematopoietic stem-progenitor cells (HSPCs) from normal human bone marrow and mobilized human peripheral blood stem cell harvests, and formulated a model for miRNA control of stages of heMatopoiesis in which many of the genes specifying hematopolietic differentiation are expressed by HSPCs, but are held in check by miRNAAs until differentiation occurs.
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Virulence-related surface glycoproteins in the yeast pathogen Candida glabrata are encoded in subtelomeric clusters and subject to RAP1- and SIR-dependent transcriptional silencing

TL;DR: The identification and analysis of the EPA gene family provides a compelling example in an ascomycete of chromatin-based silencing of natural subtelomeric genes and provides for the first time in a pathogen, molecular insight into the transcriptionalsilencing of large subtelomersic gene families.
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Telomere dysfunction causes alveolar stem cell failure

TL;DR: The data show that alveoloar progenitor senescence is sufficient to recapitulate the regenerative defects, inflammatory responses, and susceptibility to injury that are characteristic of telomere-mediated lung disease.