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Distinct roles for JNK1 and JNK2 in regulating JNK activity and c-Jun-dependent cell proliferation.
It is found that Jnk2-/- fibroblasts exit G1 and enter S phase earlier than wild-type counterparts, while JnK1-/- cells show the inverse phenotype, and mechanistic insights into the distinct roles of different JNK isoforms are provided. Expand
Defective neural tube morphogenesis and altered apoptosis in the absence of both JNK1 and JNK2
These results assign both pro- and anti-apoptotic functions for JNK1 and JNK2 in the development of the fetal brain. Expand
JNK2 is required for efficient T-cell activation and apoptosis but not for normal lymphocyte development
JNK2 functions in a cell-type-specific and stimulus-dependent manner, being required for apoptosis of immature thymocytes induced by anti-CD3 antibody but not for apoptotic induced byAnti-Fas antibody, UVC or dexamethasone, and is not required for activation-induced cell death of mature T cells. Expand
JNK1 modulates osteoclastogenesis through both c-Jun phosphorylation-dependent and -independent mechanisms
Genetic evidence is provided that JNK1 activation modulates osteoclastogenesis through both c-Jun-phosphorylation-dependent and -independent mechanisms. Expand
C-Jun Nh2-Terminal Kinase (Jnk)1 and Jnk2 Have Similar and Stage-Dependent Roles in Regulating T Cell Apoptosis and Proliferation
The reduced JNK dose results in defective c-Jun NH2-terminal phosphorylation in thymocytes but not in peripheral T cells, in which nuclear factors of activated T cells (NK-ATs)–DNA binding activity is affected; JNK1 and JNK2 control similar functions during T cell maturation through differential targeting of distinct substrates. Expand
Regulation of ES cell differentiation by functional and conformational modulation of p53
It is demonstrated that functional inactivation of p53 allows differentiating cells to escape from apoptosis, and it is suggested that the conformational switch could regulate the inactivation process. Expand
Functional Crosstalk between Type I and II Interferon through the Regulated Expression of STAT1
Small "priming" quantities of type I interferon enhance cellular responses to type II interferon by maintaining basal levels of STAT1, explaining the observed crosstalk between these two cytokines.
Therapeutic targeting of p53: all mutants are equal, but some mutants are more equal than others
This Review proposes a categorization of the major classes of p53 mutants based on their functionality in tumour suppression and response to therapy, and suggests that the mutations across TP53 form a 'rainbow of mutants', with varying degrees of functionality and different pathobiological consequences. Expand
Trp53-dependent DNA-repair is affected by the codon 72 polymorphism
The data highlight the functional differences between the Trp53 polymorphic variants, and suggest that their expression status may influence cancer risk. Expand
Cancer-derived p53 mutants suppress p53-target gene expression—potential mechanism for gain of function of mutant p53
It is shown that stable down-regulation of mutant p53 expression resulted in reduced cellular colony growth in human cancer cells, which was found to be due to the induction of apoptosis, demonstrating another mechanism through which p53 mutants could promote cellular growth. Expand