Reprogramming control of a modular allosteric signaling switch.
Description
- Language(s)
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English
- Published
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2005.
- Summary
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Living cells exhibit amazing abilities for biocomputation: they sense environmental cues, translate this information into biological currency that can be transduced and, ultimately, produce an appropriate response. To accomplish this biocomputation, eukaryotic cells contain diverse and highly complex signaling circuits. A major question is how these circuits have evolved, as survival demands these processes be adaptable, allowing formation of new connections between environmental cues and cellular behaviors. Of particular interest are proteins in these networks that occupy key node positions--sites where multiple signals are integrated. Many node proteins have a component-based architecture: they are built from combinations of protein interaction domains and catalytic domains. Despite being built from simple modular domains, these proteins can display sophisticated behaviors such as allosteric gating and multi-input signal integration. This thesis addresses how complex behaviors can emerge from combinations of simple domains. I have taken two different but complementary approaches towards this aim, using the actin regulatory protein neuronal Wiskott-Aldrich Syndrome protein (N-WASP) as a model: (1) using simple domain recombination and insertion events to generate synthetic versions of N-WASP that show novel input/output behavior and (2) investigating how the pathogenic factors IcsA and EspFu are capable of reprogramming N-WASP's gated behavior through protein-protein interactions.
- Note
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Adviser: Lim, Wendell.
Source: Dissertation Abstracts International, Volume: 66-06, Section: B, page: 3114
- Physical Description
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xiv, 127 p. :
col. ill. ;
28 cm
Viewability