Abstract:
:The production of reactive oxygen species is a normal part of cell physiology, but many internal and external stimuli are able to trigger the production of excess levels of oxidants that are potentially damaging. The threat of oxidative damage is particularly significant to DNA, as damaged bases can interfere with replication to generate lasting mutations. Signalling through the JNK pathway is a key cellular response to oxidative damage. Depending on the intensity and duration of the damage signal, JNK signalling can lead to distinct alternative responses including DNA repair, anti-oxidant production or cell death. These responses are highly relevant to cancer therapy, as tumours are often under oxidative stress that produces elevated JNK levels and therapy often involves inducing DNA damage with the intention of driving cell death. In this review we examine the causes and consequences of JNK activation that relate to oxidative DNA damage, with a focus on the potential therapeutic implications.
journal_name
Curr Drug Targetsjournal_title
Current drug targetsauthors
Shaukat Z,Liu D,Hussain R,Khan M,Gregory SLdoi
10.2174/1389450116666150126111055subject
Has Abstractpub_date
2016-01-01 00:00:00pages
154-63issue
2eissn
1389-4501issn
1873-5592pii
CDT-EPUB-64819journal_volume
17pub_type
杂志文章,评审abstract::The hedgehog signal transduction network is a critical regulator of metazoan development. Inappropriate activation of this network is implicated in several different cancers, including breast. Genetic evidence in mice as well as molecular biological studies in human cells clearly indicate that activated signaling can ...
journal_title:Current drug targets
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abstract::Acute myeloid leukemia (AML) was the first malignancy for which immunotherapy, in the form of allogeneic hematopoietic stem cell transplantation (allo-HSCT), was integrated into the standard of care. Allo-HSCT however is an imperfect therapy associated with significant morbidity and mortality while offering only incom...
journal_title:Current drug targets
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journal_title:Current drug targets
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journal_title:Current drug targets
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journal_title:Current drug targets
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journal_title:Current drug targets
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journal_title:Current drug targets
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journal_title:Current drug targets
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journal_title:Current drug targets
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journal_title:Current drug targets
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abstract::As early as 1940, Abraham and Chain described "an enzyme able to destroy penicillin". In the late 1940's, penicillin-resistant strains of Staphylococcus aureus were found to be a clinical problem. They produced a penicillinase that could hydrolyze the amide bond in the β-lactam ring. Later, an enzyme mediated by an R-...
journal_title:Current drug targets
pub_type: 历史文章,杂志文章,评审
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journal_title:Current drug targets
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journal_title:Current drug targets
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abstract::The use of imatinib, second and third generation ABL tyrosine kinase inhibitors (TKI) (i.e. dasatinib, nilotinib, bosutinib and ponatinib) made CML a clinically manageable and, in a small percentage of cases, a cured disease. TKI therapy also turned CML blastic transformation into a rare event; however, disease progre...
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journal_title:Current drug targets
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abstract::Various herpes- and poxviruses contain DNA sequences encoding proteins with homology to cellular chemokine receptors, which belong to the family of G protein-coupled receptors (GPCRs). Since GPCRs play a crucial role in cellular communication and chemokine receptors play a prominent role in the immune system, the vira...
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