Outputs (5)

The AP-1 transcription factor c-Jun is required for efficient axonal regeneration (2004)
Journal Article
Raivich, G., Bohatschek, M., Da Costa, C., Iwata, O., Galiano, M., Hristova, M., Nateri, A. S., Makwana, M., Riera-Sans, L., Wolfer, D. P., Lipp, H. P., Aguzzi, A., Wagner, E. F., & Behrens, A. (2004). The AP-1 transcription factor c-Jun is required for efficient axonal regeneration. Neuron, 43(1), 57-67. https://doi.org/10.1016/j.neuron.2004.06.005

Nerve injury triggers numerous changes in the injured neurons and surrounding nonneuronal cells that ultimately result in successful target reinnervation or cell death. c-Jun is a component of the heterodimeric AP-1 transcription factor, and c-Jun is... Read More about The AP-1 transcription factor c-Jun is required for efficient axonal regeneration.

Advances in the understanding of susceptibility to treatment-related acute myeloid leukaemia (2004)
Journal Article
Seedhouse, C., & Russell, N. (2004). Advances in the understanding of susceptibility to treatment-related acute myeloid leukaemia. British Journal of Haematology, 137(6), 513-529. https://doi.org/10.1111/j.1365-2141.2007.06613.x

Treatment-related acute myeloid leukaemia (t-AML) is a devastating complication following exposure to the cytotoxic and genotoxic agents used to treat a primary malignancy. Whilst the incidence of t-AML is rising, it still only occurs in a minority o... Read More about Advances in the understanding of susceptibility to treatment-related acute myeloid leukaemia.

Clonal haemopoiesis may occur after conventional chemotherapy and is associated with accelerated telomere shortening and defects in the NQO1 pathway; possible mechanisms leading to an increased risk of t-AML/MDS (2004)
Journal Article
Fern, L., Pallis, M., Carter, G. I., Seedhouse, C., Russell, N., & Byrne, J. (2004). Clonal haemopoiesis may occur after conventional chemotherapy and is associated with accelerated telomere shortening and defects in the NQO1 pathway; possible mechanisms leading to an increased risk of t-AML/MDS. British Journal of Haematology, 126(1), 63-71. https://doi.org/10.1111/j.1365-2141.2004.05006.x

The molecular pathogenesis of therapy-related acute myeloid leukaemia/myelodysplastic syndrome (t-AML/MDS) remains uncertain. However, clonal haemopoiesis may develop following stem cell transplantation and precede the development of t-AML/MDS. Moreo... Read More about Clonal haemopoiesis may occur after conventional chemotherapy and is associated with accelerated telomere shortening and defects in the NQO1 pathway; possible mechanisms leading to an increased risk of t-AML/MDS.

Polymorphisms in Genes Involved in Homologous Recombination Repair Interact to Increase the Risk of Developing Acute Myeloid Leukemia (2004)
Journal Article
Seedhouse, C., Faulkner, R., Ashraf, N., Das-Gupta, E., & Russell, N. (2004). Polymorphisms in Genes Involved in Homologous Recombination Repair Interact to Increase the Risk of Developing Acute Myeloid Leukemia. Clinical Cancer Research, 10(8), 2675–2680. https://doi.org/10.1158/1078-0432.CCR-03-0372

Purpose: Double-strand break repair via homologous recombination is essential in maintaining genetic integrity. RAD51 and XRCC3 are involved in the repair of DNA by this pathway, and polymorphisms have been identified in both the RAD51 (RAD51-G135C)... Read More about Polymorphisms in Genes Involved in Homologous Recombination Repair Interact to Increase the Risk of Developing Acute Myeloid Leukemia.

The Ubiquitin Ligase SCF Fbw7 Antagonizes Apoptotic JNK Signaling (2004)
Journal Article
Nateri, A. S., Riera-Sans, L., Da Costa, C., & Behrens, A. (2004). The Ubiquitin Ligase SCF Fbw7 Antagonizes Apoptotic JNK Signaling. Science, 303(5662), 1374-1378. https://doi.org/10.1126/science.1092880

Jun N-terminal kinases (JNKs) are essential for neuronal microtubute assembly and apoptosis. Phosphorylation of the activating protein 1 (AP1) transcription factor c-Jun, at multiple sites within its transactivation domain, is required for JNK-induce... Read More about The Ubiquitin Ligase SCF Fbw7 Antagonizes Apoptotic JNK Signaling.