Jordan J S VerPlank

PhD

Department of Primary Appointment:
School of Medicine
Anatomy, Physiology and Genetics
Location: Uniformed Services University of the Health Sciences, Bethesda, MD
Research Interests:
Protein Degradation, Ubiquitination, Proteostasis, Neurodegeneration
Email
jordan.verplank@usuhs.edu
Office Phone
(301) 295-1215
Department Website
Department of Anatomy, Physiology, and Genetics

Education

Postdoctoral Fellow (Biochemistry) - Advisor: Maria Laura Feltri, MD, State University of New York at Buffalo, 2021 - 2022
Postdoctoral Fellow (Cell Biology) - Advisor: Alfred Goldberg, PhD, Harvard Medical School, 2016-2020
PhD (Neuroscience) - Advisor: Lawrence Wrabetz, MD, State University of New York at Buffalo, 2011- 2016
BS (Biological Sciences) - Duquesne University, Pittsburgh, PA, 2011

Biography

In mammalian cells, the vast majority of proteins are degraded by the Ubiquitin Proteasome System. In this pathway, proteins to be degraded are attached to ubiquitin, and then destroyed by a large, multisubunit complex called the 26S proteasome. When this process is working efficiently, after ubiquitination, proteins are rapidly degraded. In aging, neurodegenerative diseases, and diseases in other tissues caused by mutant proteins that misfold and accumulate, the 26S proteasome becomes impaired and protein degradation slows. Consequently, un-degraded proteins - including the causative mutant protein- accumulate and contribute to disease progression. My lab is focused on understanding how protein breakdown by the 26S proteasome can be accelerated and decelerated, and on using this knowledge to develop new therapies for diseases that are presently without treatment.

Representative Bibliography

Biosketch Link
My PubMed Bibliography

Moore SM, Gawron J, Stevens M, Marziali LN, Buys ES, Milne GT, Feltri ML, VerPlank JJ. Pharmacologically increasing cGMP improves proteostasis and reduces neuropathy in mouse models of CMT1. Cellular and Molecular Life Sciences. 2024 Dec;81(1):434.

VerPlank JJS, Gawron JM, Silvestri NJ, Wrabetz L, Feltri ML. Knockout of PA200 improves proteasomal degradation and myelination in a proteotoxic neuropathy. Life Science Alliance. 2024 Apr 1;7(4).

VerPlank JJS, Gawron J, Silvestri NJ, Feltri ML, Wrabetz L, Goldberg AL. Raising cGMP restores proteasome function and myelination in mice with a proteotoxic neuropathy. Brain. 2022 Mar 29;145(1):168-178.

VerPlank JJS, Tyrkalska SD, Fleming A, Rubinsztein DC, Goldberg AL. cGMP via PKG activates 26S proteasomes and enhances degradation of proteins, including ones that cause neurodegenerative diseases. Proc Natl Acad Sci U S A. 2020 Jun 23;117(25):14220-14230.

VerPlank JJS, Lokireddy S, Zhao J, Goldberg AL. 26S Proteasomes are rapidly activated by diverse hormones and physiological states that raise cAMP and cause Rpn6 phosphorylation. Proc Natl Acad Sci U S A. 2019 Mar 5;116(10):4228-4237.

VerPlank JJS, Lokireddy S, Feltri ML, Goldberg AL, Wrabetz L. Impairment of protein degradation and proteasome function in hereditary neuropathies. Glia. 2018 Feb;66(2):379-395.

VerPlank JJS, Goldberg AL. Regulating protein breakdown through proteasome phosphorylation. Biochem J. 2017 Sep 24;474(19):3355-3371.