Over-expression of heat shock protein 70 protects neuronal cells against both thermal and ischaemic stress but with different efficiencies
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[1] S. Lindquist. The heat-shock response. , 1986, Annual review of biochemistry.
[2] D. Latchman,et al. The Cyclic AMP Response Element in the Calcitonin/Calcitonin Gene-related Peptide Gene Promoter Is Necessary but Not Sufficient for Its Activation by Nerve Growth Factor (*) , 1995, The Journal of Biological Chemistry.
[3] A. Leon,et al. Nerve Growth Factor Transcriptional Control of C-fos Promoter Transfected in Cultured Spinal Sensory Neurons Materials and Methods Preparation of Neuronal Cultures , 2022 .
[4] K. Mikoshiba,et al. ‘Ischemic tolerance’ phenomenon found in the brain , 1990, Brain Research.
[5] D. Latchman,et al. Nerve growth factor induces expression of immediate-early genes NGFI-A (Egr-1) and NGFI-B (nur 77) in adult rat dorsal root ganglion neurons. , 1994, Brain research. Molecular brain research.
[6] M. Barbe,et al. Hyperthermia protects against light damage in the rat retina. , 1988, Science.
[7] D. Lowenstein,et al. The stress protein response in cultured neurons: Characterization and evidence for a protective role in excitotoxicity , 1991, Neuron.
[8] S. Lindquist,et al. The heat-shock proteins. , 1988, Annual review of genetics.
[9] D. Latchman,et al. A Minimal CGRP Gene Promoter is Inducible by Nerve Growth Factor in Adult Rat Dorsal Root Ganglion Neurons But Not in PC12 Phaeochromocytoma Cells , 1995, The European journal of neuroscience.
[10] E. Gerner,et al. Effects of cycloheximide on thermotolerance expression, heat shock protein synthesis, and heat shock protein mRNA accumulation in rat fibroblasts , 1986, Molecular and cellular biology.
[11] D. Latchman,et al. Stable high level expression of a transfected human HSP70 gene protects a heart-derived muscle cell line against thermal stress. , 1994, Journal of molecular and cellular cardiology.
[12] M. Dereski,et al. Transient hyperthermia protects against subsequent forebrain ischemic cell damage in the rat , 1989, Neurology.
[13] D. Latchman,et al. Heat shock protects neuronal cells from programmed cell death by apoptosis , 1993, Neuroscience.
[14] G. Zupi,et al. Heat‐shock proteins produced by two human melanoma cell lines: Absence of correlation with thermosensitivity , 1984, International journal of cancer.
[15] D. Latchman,et al. The degree of protection provided to neuronal cells by a pre-conditioning stress correlates with the amount of heat shock protein 70 it induces and not with the similarity of the subsequent stress , 1995, Neuroscience Letters.
[16] D. Latchman,et al. Nerve growth factor induces the Oct‐2 transcription factor in sensory neurons with the kinetics of an immediate‐early gene , 1995, Journal of neuroscience research.
[17] L. Kedes,et al. A human beta-actin expression vector system directs high-level accumulation of antisense transcripts. , 1987, Proceedings of the National Academy of Sciences of the United States of America.
[18] T. Smith,et al. NADH measurements in adult rat myocytes during simulated ischemia. , 1991, The American journal of physiology.
[19] D. Leader,et al. Heat shock causes diverse changes in the phosphorylation of the ribosomal proteins of mammalian cells , 1984, FEBS letters.
[20] D. Latchman,et al. Heat Shock Proteins hsp90 and hsp70 Protect Neuronal Cells from Thermal Stress but Not from Programmed Cell Death , 1994, Journal of neurochemistry.
[21] W. Koroshetz,et al. Heat shock protects cultured neurons from glutamate toxicity , 1991, Neuron.
[22] D. Latchman,et al. Differential stress protein mRNA expression during early ischaemic preconditioning in the rabbit heart and its relationship to adenosine receptor function. , 1995, Journal of molecular and cellular cardiology.