Transcriptional Regulation of the Proteostatic Network
The mechanisms that maintain proteome folding and function (proteostasis), become ineffective during normal aging, contributing to the onset and progression of neurodegenerative protein misfolding diseases- including Alzheimer’s Disease. Proteostasis is sustained through integrated processes involving coordinated regulation of protein synthesis, folding, and degradation in response to diverse signals.
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Sumoylation and Aging
The mechanisms that maintain proper function and folding of the proteome (proteostasis) decline during normal aging, which facilitates the onset and progression of neurodegenerative protein misfolding diseases, including Alzheimer’s Disease. The functional integrity of the proteome is safeguarded from stress through the combined action of a cohort of transcription factors, each primed to respond to specific forms of proteotoxic stress. During aging, these responses decline and ultimately precipitate a collapse of proteostasis. C. elegans is an excellent model to study the molecular mechanisms involved in this complex process.
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Integration of Longevity Signals by the Myc-family of Transcription Factors
We discovered a vital role for the Myc family of transcription factors in regulating transcriptional programs that set the progression of aging in C. elegans. Myc and the related Myc family members have well known roles in diverse biological contexts, but our discovery directly links the Myc family to aging. In C. elegans two heterodimeric complexes have opposing roles in aging and transcriptional control (homologous to mammalian Myc-Mondo and Mad complexes).
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