Brian B. Ratliff

Molecular Biology · 2016

A researcher in the Science corpus: 1 paper; trusts 5 researchers and is trusted by 0 researchers here, as inferred from the citation graph.

Subfields

Whom Brian B. Ratliff trusts overall

Their strongest outbound trust, strongest first, inferred from their citations.

  1. J. Matés
  2. Michael Schieber
  3. Jian-Mei Li
  4. Natalie Gleyzer
  5. J. Forbes
  6. S. Ryter
  7. B. Lassègue
  8. R. Guzy
  9. Navdeep S. Chandel
  10. A. Shah

Papers from Brian B. Ratliff's perspective

Ordered by how strongly the researchers Brian B. Ratliff trusts endorse each paper. Same corpus, a different order for every researcher.

  1. Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage (Nature)
  2. ATP Activates a Reactive Oxygen Species-dependent Oxidative Stress Response and Secretion of Proinflammatory Cytokines in Macrophages* (Journal of Biological Chemistry)
  3. Mitochondrial complex III is required for hypoxia-induced ROS production and cellular oxygen sensing. (Cell Metabolism)
  4. Control of Mitochondrial Transcription Specificity Factors (TFB1M and TFB2M) by Nuclear Respiratory Factors (NRF-1 and NRF-2) and PGC-1 Family Coactivators (Molecular and Cellular Biology)
  5. Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology. (American Journal of Physiology. Regulatory Integrative and Comparative Physiology)
  6. Novel gp91phox Homologues in Vascular Smooth Muscle Cells: nox1 Mediates Angiotensin II-Induced Superoxide Formation and Redox-Sensitive Signaling Pathways (Circulation Research)
  7. Resveratrol improves mitochondrial function and protects against metabolic disease by activating SIRT1 and PGC-1alpha. (Cell)
  8. Secondary prevention with antioxidants of cardiovascular disease in endstage renal disease (SPACE): randomised placebo-controlled trial. (The Lancet)
  9. Mechanisms of Cell Death in Oxidative Stress (Antioxidants and Redox Signaling)
  10. HMGB1 promotes recruitment of inflammatory cells to damaged tissues by forming a complex with CXCL12 and signaling via CXCR4 (Journal of Experimental Medicine)

Their papers