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The c-Jun amino-terminal kinase (JNK) is a member of the stress-activated group of mitogen-activated protein (MAP) kinases that are implicated in the control of cell growth. A murine cytoplasmic protein that binds specifically to JNK [the JNK interacting protein-1 (JIP-1)] was characterized and cloned. JIP-1 caused cytoplasmic retention of JNK and(More)
The leukemogenic tyrosine kinase fusion protein Bcr-Abl activates a Ras-dependent pathway required for transformation. To examine subsequent signal transduction events we measured the effect of Bcr-Abl on two mitogen-activated protein kinase (MAPK) cascades--the extracellular signal-regulated kinase (ERK) pathway and the Jun N-terminal kinase (JNK) pathway.(More)
The CRKL adaptor protein was recently identified as a substrate for the BCR-ABL tyrosine kinase in patients with chronic myelogenous leukemia, but its function is unknown. Here we report that CRKL is phosphorylated when overexpressed, activates RAS and JUN kinase signaling pathways, and transforms fibroblasts in a RAS-dependent fashion. We examined the(More)
We develop a general game-theoretic framework for reasoning about strategic agents performing possibly costly computation. In this framework, many traditional game-theoretic results (such as the existence of a Nash equilibrium) no longer hold. Nevertheless, we can use the framework to provide psychologically appealing explanations to observed behavior in(More)
I characterize the implications of the common prior assumption for finite orders of beliefs about beliefs at a state and show that in finite models, the only such implications are those stemming from the weaker assumption of a common support. More precisely, given any finite N and any finite partitions model where priors have the same support, there is(More)
Using chronic myelogenous leukemia (CML) as a model, we tested the hypothesis that cytokine-independent growth of leukemia cells results from aberrant activation of cytokine signaling pathways. The STAT5 (signal transducer and activator of transcription) protein, which is activated transiently in normal myeloid cells by cytokines such as GM-CSF(More)
Market behavior is the central topic of economics. Yet while economists have a good understanding of the behavior of well-functioning markets, we have little to say about market fragility, market resiliency, and market collapse. Research emerging at the frontier between computer science and economics offers new ways of addressing this important issue.(More)
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