Area of General Research Interest:
Developmental biology of extracellular proteases, extracellular matrix,
arthritis, ADAMTS proteases, versican, fibrillins, musculoskeletal biology,
cardiovascular biology.
Current Program:
- ADAMTS proteases in limb, craniofacial, musculoskeletal and cardiovascular
development
- Mechanisms of cartilage destruction in arthritis
- Molecular mechanisms of inherited connective tissue and eye disorders
- Proteolysis of versican
- Fibrillin-1 networks and cellular regulation
Personnel:
- Hannah Bader, PhD ( Research Fellow )
- Noriko Hattori, MD, PhD (Research Fellow)
- Luis Gabriel, MD (Research Fellow)
- Lauren W. Wang, MS (Lead Research Technologist)
- Courtney Nelson, BS (Research Technician)
- Shweta Singh, BS (Research Technician)
- James Wylie, MS (Medical Student)
- Jason Ho, MS (Medical Student)
The laboratory has an opening for a post-doctoral fellow with a career
interest and background in extracellular matrix, proteases, cell biology
or developmental biology. Please send applications, a curriculum vitae
and the names and contact information (telephone and email) of three
references to: aptes@ccf.org
Collaborators:
- Christine B. Kern, Medical University of South Carolina, SC
- Robert Haltiwanger, Stony Brook University, NY
Project descriptions :
- Proteoglycan turnover by ADAMTS proteases and its biological implications:
Several ADAMTS proteases cleave the core proteins of aggrecan
and versican and are relevant to musculoskeletal and cardiovascular
disease. This project investigates versican and aggrecan turnover
in musculoskeletal, craniofacial and cardiovascular phenotypes of
ADAMTS deficient mice, and the mechanisms of versican turnover by
ADAMTS proteases. The project utilizes single and combinatorial mouse
mutants, conditional gene targeting in mice, biochemistry and cell
biology techniques.
- ADAMTS molecules, fibrillin-1 networks and cell regulation: Several
ADAMTS family members, e.g., ADAMTS10, ADAMTS17, ADAMTSL4, and ADAMTSL2,
are mutated in disorders associated with fibrillin-1, a critical component
of an extracellular network that regulates TGF-beta. These human and
animal mutations have highlighted the potential role of ADAMTS proteins
in fibrillin-rich tissues such as the zonule of the eye, and in regulating
skeletal growth and skin/organ fibrosis. The project utilizes single
and combinatorial mouse mutants, protein chemistry, intermolecular
interaction assays and cell biology techniques to investigate important
questions in this area.
Funding for our research is currently provided by the National Institutes
of Health and the National Marfan Foundation.
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