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c-Jun N-terminal kinase (JNK)-mediated modulation of brain mitochondria function: new target proteins for JNK signalling in mitochondrion-dependent apoptosis.
JNK-dependent phosphorylation of mitochondrial proteins including, but not limited to, Bcl-2/Bcl-x(L) may represent a potential of the modulation of mitochondrial function during apoptosis.
Protein synthesis and protein phosphorylation during heat stress, recovery, and adaptation
A large number of phosphorylation changes are induced by severe heat stress and occur with kinetics similar to the inhibition of protein synthesis, but, under mild heat stress conditions, these initiation factor phosphorylated changes do not occur.
Regulated phosphorylation and low abundance of HeLa cell initiation factor eIF-4F suggest a role in translational control. Heat shock effects on eIF-4F.
Heterogeneous nuclear ribonucleoprotein A1 binds to the transcription-regulatory region of mouse hepatitis virus RNA.
- H. P. Li, X. Zhang, R. Duncan, L. Comai, M. Lai
- BiologyProceedings of the National Academy of Sciences…
- 2 September 1997
The purified hnRNP A1 is a cellular factor that regulates the RNA-dependent RNA transcription of the virus and is determined to be heterogeneous nuclear ribonucleoprotein (hnRNP) A1, an abundant, primarily nuclear protein.
Identification and quantitation of levels of protein synthesis initiation factors in crude HeLa cell lysates by two-dimensional polyacrylamide gel electrophoresis.
Evaluation of isoelectric focusing running conditions during two-dimensional isoelectric focusing/sodium dodecyl sulfate-polyacrylamide gel electrophoresis: variation of gel patterns with changing…
Inhibition of Hsp90 function delays and impairs recovery from heat shock
- R. Duncan
- BiologyThe FEBS journal
- 1 October 2005
It is suggested that a multicomponent protein chaperone complex involving both Hsp90 and Hsp70 signals the cessation of heat shock protein synthesis, the restoration of normal translation, and likely the establishment of thermotolerance.
Heme and lipid peroxides in hemoglobin-modified low-density lipoprotein mediate cell survival and adaptation to oxidative stress.
It is concluded that Hb-catalyzed reactions may modulate vascular cell survival and oxidative stress adaptation due to the presence of peroxides and heme, thus providing a possible mechanism for the evolution of atherosclerotic and hemorrhagic lesions.
Modification of protein synthesis initiation factors and the shut-off of host protein synthesis in adenovirus-infected cells.
Hepatitis C virus IRES-dependent translation is insensitive to an eIF2alpha-independent mechanism of inhibition by interferon in hepatocyte cell lines.
HCV IRES-driven translation was resistant to IFN-induced, eIF2alpha-independent inhibition in human hepatoma cells that are frequently used in studies on HCV replication, and may present a new potential mechanism of viral resistance toIFN treatment during the early steps of virus infection.