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The ATM-Chk2 and ATR-Chk1 pathways in DNA damage signaling and cancer.
Phosphorylation of HuR by Chk2 regulates SIRT1 expression.
Mutant p53 Drives Invasion by Promoting Integrin Recycling
Chk1 is required for spindle checkpoint function.
Chk1‐deficient tumour cells are viable but exhibit multiple checkpoint and survival defects
Chk1 is dispensable for normal cell division in somatic DT40 cells but is essential for DNA damage‐induced G2/M arrest and a subset of replication checkpoint responses, which promote tumour cell survival after perturbations of DNA structure or metabolism.
Akt: A Double-Edged Sword in Cell Proliferation and Genome Stability
Akt modifies both the response to and repair of genotoxic damage in complex ways that are likely to have important consequences for the therapy of tumors with deregulation of the PI3K-Akt-PTEN pathway.
Cells deficient in the FANC/BRCA pathway are hypersensitive to plasma levels of formaldehyde.
It is proposed that endogenous formaldehyde might have an effect on highly proliferating cells, such as bone marrow cells, as well as an etiology of cancer in Fanconi anemia patients because of the hypersensitivity to formaldehyde detected in DT40 mutants deficient in the BRCA/FANC pathway.
A new c-Jun N-terminal kinase (JNK)-interacting protein, Sab (SH3BP5), associates with mitochondria.
- C. Wiltshire, M. Matsushita, S. Tsukada, D. Gillespie, G. May
- BiologyThe Biochemical journal
- 1 November 2002
It is demonstrated that the most N-terminal KIM in Sab is essential for JNK binding, and that, as with c-Jun, physical interaction with JNK is necessary for Sab phosphorylation.
Loss of autophagy causes a synthetic lethal deficiency in DNA repair
It is reported here that inhibition of autophagy causes elevated proteasomal activity leading to enhanced degradation of checkpoint kinase 1 (Chk1), a pivotal factor for the error-free DNA repair process, homologous recombination (HR).