Filter By:

Journal Check one or more journals to show results from those journals only.

Choose more journals

Article type Check one or more article types to show results from those article types only.
Subject Check one or more subjects to show results from those subjects only.
Date Choose a date option to show results from those dates only.

Custom date range

Clear all filters
Sort by:
Showing 1–4 of 4 results
Advanced filters: Author: Prajakta Ghatpande Clear advanced filters
  • Prabhakar et al. demonstrate in rats with mitomycin C-caused pulmonary veno-occlusive disease activation of protein kinase R (PKR) and the integrated stress response (ISR), leading to the depletion of VE-cadherin and RAD51 from endothelial junctions, endothelial barrier disruption and vascular remodeling. Inhibiting the PKR–ISR axis protects against mitomycin C-induced endothelial damage.

    • Amit Prabhakar
    • Rahul Kumar
    • Akiko Hata
    Research
    Nature Cardiovascular Research
    Volume: 3, P: 799-818
  • Bone morphogenetic protein (BMP) receptors are single pass transmembrane serine/threonine kinases that form tetrameric complexes comprised of two type I and two type II BMP receptors. Here the authors characterize a structure of an active type I/type II kinase tetramer providing insight into molecular mechanism driving ligand-induced signaling.

    • Christopher Agnew
    • Pelin Ayaz
    • Natalia Jura
    ResearchOpen Access
    Nature Communications
    Volume: 12, P: 1-17
  • Hematopoietic stem and progenitor cells are generated first from the vascular endothelium of the dorsal aorta and then the fetal liver but what regulates this switch is unknown. Here, the authors show that changing miRNA biogenesis and leukotriene B4 signaling in mice modulates this switch in the niche.

    • Xuan Jiang
    • John S. Hawkins
    • Akiko Hata
    ResearchOpen Access
    Nature Communications
    Volume: 8, P: 1-14
  • Sanna Vattulainen-Collanus et al. report that mutations in the BMPR2 gene, which is associated with pulmonary arterial hypertension, result in a deficit of RAD51 and altered DNA repair and replication. They were able to rescue the RAD51-deficient phenotype by restoring BMPR2 activity in cell culture.

    • Sanna Vattulainen-Collanus
    • Mark Southwood
    • Akiko Hata
    ResearchOpen Access
    Communications Biology
    Volume: 1, P: 1-15