Small Heat Shock Protein Beta-1 (HSPB1) Is Upregulated and Regulates Autophagy and Apoptosis of Renal Tubular Cells in Acute Kidney Injury
Published 2015 View Full Article
- Home
- Publications
- Publication Search
- Publication Details
Title
Small Heat Shock Protein Beta-1 (HSPB1) Is Upregulated and Regulates Autophagy and Apoptosis of Renal Tubular Cells in Acute Kidney Injury
Authors
Keywords
Autophagic cell death, Apoptosis, Kidneys, Small interfering RNAs, Protein expression, Heat shock response, Oxidative stress, Transfection
Journal
PLoS One
Volume 10, Issue 5, Pages e0126229
Publisher
Public Library of Science (PLoS)
Online
2015-05-12
DOI
10.1371/journal.pone.0126229
References
Ask authors/readers for more resources
Related references
Note: Only part of the references are listed.- HMGB1-dependent and -independent autophagy
- (2014) Xiaofang Sun et al. Autophagy
- Emerging role of autophagy in kidney function, diseases and aging
- (2012) Tobias B. Huber et al. Autophagy
- Small heat shock proteins HSP27 (HspB1), αB-crystallin (HspB5) and HSP22 (HspB8) as regulators of cell death
- (2012) Julie Acunzo et al. INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
- Phosphorylation of HSP27 by Protein Kinase D Is Essential for Mediating Neuroprotection against Ischemic Neuronal Injury
- (2012) R. A. Stetler et al. JOURNAL OF NEUROSCIENCE
- Autophagy, mitochondria and oxidative stress: cross-talk and redox signalling
- (2011) Jisun Lee et al. BIOCHEMICAL JOURNAL
- High-Mobility Group Box 1 Is Essential for Mitochondrial Quality Control
- (2011) Daolin Tang et al. Cell Metabolism
- Autophagy Protects the Proximal Tubule from Degeneration and Acute Ischemic Injury
- (2011) T. Kimura et al. JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
- Chronic kidney disease worsens sepsis and sepsis-induced acute kidney injury by releasing High Mobility Group Box Protein-1
- (2011) Asada Leelahavanichkul et al. KIDNEY INTERNATIONAL
- HSP27/HSPB1 as an adaptive podocyte antiapoptotic protein activated by high glucose and angiotensin II
- (2011) Maria D Sanchez-Niño et al. LABORATORY INVESTIGATION
- Autophagy Is a Renoprotective Mechanism During in Vitro Hypoxia and in Vivo Ischemia-Reperfusion Injury
- (2010) Man Jiang et al. AMERICAN JOURNAL OF PATHOLOGY
- Autophagy in health and disease. 5. Mitophagy as a way of life
- (2010) Roberta A. Gottlieb et al. AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
- Methods in Mammalian Autophagy Research
- (2010) Noboru Mizushima et al. CELL
- Locally synthesized HSP27 in hepatocytes: Is it possibly a novel strategy against human liver ischemia/reperfusion injury?
- (2010) Sun-yi Ye et al. MEDICAL HYPOTHESES
- Immunohistochemical Study of Heat Shock Protein 27 with Respect to Survival and Regeneration of Proximal Tubular Cells after Uranyl Acetate-Induced Acute Tubular Injury in Rats
- (2010) Yoshihide Fujigaki et al. RENAL FAILURE
- Cisplatin-induced macroautophagy occurs prior to apoptosis in proximal tubules in vivo
- (2009) Kosuke Inoue et al. Clinical and Experimental Nephrology
- Mitochondrial Autophagy Promotes Cellular Injury in Nephropathic Cystinosis
- (2009) P. Sansanwal et al. JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
- Participation of autophagy in renal ischemia/reperfusion injury
- (2008) Chigure Suzuki et al. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Transduced human PEP-1-heat shock protein 27 efficiently protects against brain ischemic insult
- (2008) Jae J. An et al. FEBS Journal
- Hsp27 Inhibits Bax Activation and Apoptosis via a Phosphatidylinositol 3-Kinase-dependent Mechanism
- (2008) Andrea Havasi et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- Expression and function of the Delta-1/Notch-2/Hes-1 pathway during experimental acute kidney injury
- (2008) T. Kobayashi et al. KIDNEY INTERNATIONAL
- Mice that overexpress human heat shock protein 27 have increased renal injury following ischemia reperfusion
- (2008) Sean W.C. Chen et al. KIDNEY INTERNATIONAL
Publish scientific posters with Peeref
Peeref publishes scientific posters from all research disciplines. Our Diamond Open Access policy means free access to content and no publication fees for authors.
Learn MoreAsk a Question. Answer a Question.
Quickly pose questions to the entire community. Debate answers and get clarity on the most important issues facing researchers.
Get Started