Contact

Location: STRF 2.292.3

Department

Cell Systems and Anatomy

Karl A. Rodriguez, PhD

Assistant Professor

Personal Statement:

My long-term research goal is to understand the role of molecular chaperones in protein homeostasis and how proteostasis influences healthspan and longevity. Molecular chaperones, namely heat shock proteins (HSPs), play a key role in maintaining protein quality, preventing protein unfolding and aggregation and influencing the rates of protein degradation via either the proteasome or autophagy. During aging, most organisms have a greater load of damaged or misfolded proteins to target for degradation. This condition is exacerbated by a decline in the efficacy of proteolytic machinery and leads to an accrual of the aggregation-prone cytotoxic proteins that underlie several age-associated pathologies (e.g., Alzheimer’s disease, Parkinson’s disease, sarcopenia). As such, the loss of protein homeostasis is considered to be one of the ‘hallmarks of aging’.

I have recently discovered that heat shock protein 25kDa (HSP25) correlated with maximum lifespan potential in rodent muscle and liver tissue. The mechanisms and regulatory processes by which HSP25 is responds to stress within a cell and this regulation influences both cellular and organ health and lifespan is unknown and presents a gap of knowledge in the field of chaperone biology. In Project I, we will investigate the role of HSP25 on longevity and protein homeostasis using primarily the Caenorhabditis elegans worm model system. In Project II, my laboratory will pursue the mechanism behind HSP25 regulation and its potential role in proteolytic mechanisms during stress using vertebrate cell culture and tissues. Finally, in Project III we will examine the physiological ramifications of changes in HSP25 expression focusing on its role in muscle function in vertebrate animals.


Education

Year Degree Discipline Institution
2002 PhD Molecular Medicine University of Texas Health Science Center at San Antonio
San Antonio, TX

Research

Research Area: Biology of Aging

Sub-Field of Study: Protein Homeostatis

Specific Field of Study: Neurodegenrative Disease

Relevant Diseases: Alzheimer’s Disease and related dementias, Parkinson’s disease, Huntington’s disease, any age-related disease

Research Techniques: C. elegans research (genetics, RNAi), microscopy (including confocal, two-photon), cell culture, biochemistry, molecular biology

Description of Research: During aging, most organisms have a greater load of damaged or misfolded proteins to target for degradation. This condition is exacerbated by a decline in the efficacy of proteolytic machinery and leads to an accrual of the aggregation-prone cytotoxic proteins that underlie several age-associated pathologies (e.g., Alzheimer’s disease, Parkinson’s disease, sarcopenia). We study these pathologies in the lab using the C. elegans worm as a model organism.