Three paths to stress relief

Article Abstract:

The c-Abl, c-jun amino terminal kinase (JNK) and p53 pathways are activated in mammalian cells in response to genotoxic stress and selectively activate three different groups of mitogen activated protein (MAP) kinases. The MAP kinases namely; extracellular-signal-related kinases 1 and 2 JNK1 and JNK2, and p38; move into the nucleus and selectively activate different transcription factors. Ceramide could be a common activator of the three pathways. The cellular outcome depends on the balance between opposite signalling pathways.

Stress (Physiology), Enzyme activation, Genetic toxicology

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Reversal of apoptosis by the leukaemia-associated E2A-HLF chimaeric transcription factor

Article Abstract:

The introduction of the oncogenic E2A-hepatic leukaemia factor (HLF) protein into the murine pro-B lymphocytes reverses the apoptosis induced by both interleukin-3 and p-53. Human leukaemia cells containing the translocation t(17;19) die due to apoptosis when programmed to express the dominant-negative suppressor of the chimaeric oncoprotein E2A-HLF. This shows that the E2A-HLF influences cell survival more than cell growth. The E2A-HLF(dn) protein decreases growth rate and stability of control human leukaemia cells.

Observations, Proteins, Leukemia, Lymphocytes

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A BID for the pathway

Article Abstract:

The role of a protein BID, a known regulator of programmed cell-death, apoptosis, in the control of cell-cycle progression following DNA damage is discussed. The research done by Zinkel and Kamer has established that the apoptotic protein BID is a target of ATM and that it has an unanticipated role in controlling cell-cycle progression following DNA damage.

United States, Science & research, Cell cycle, Apoptosis

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