scispace - formally typeset
G

Gary A. Silverman

Researcher at Washington University in St. Louis

Publications -  139
Citations -  13136

Gary A. Silverman is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Serpin & Gene. The author has an hindex of 41, co-authored 131 publications receiving 12186 citations. Previous affiliations of Gary A. Silverman include University of Pittsburgh & Washington & Jefferson College.

Papers
More filters
Journal ArticleDOI

Worming our way to novel drug discovery with the Caenorhabditis elegans proteostasis network, stress response and insulin-signaling pathways

TL;DR: Evidence is provided for the close association between the IIS and the PN pathways, and the authors believe that high-throughput screening campaigns, which target the C. elegans IIS pathway, may identify drugs that are efficacious in treating numerous conformational diseases.
Journal ArticleDOI

The Caenorhabditis elegans muscle specific serpin, SRP-3, neutralizes chymotrypsin-like serine peptidases.

TL;DR: A comparative genomics study using Caenorhabditis elegans as a model organism suggested that C. elegans expressed at least two inhibitory-type serpins with nonoverlapping expression and inhibitory profiles, and found that these profiles share significant similarities with the profiles of clade B intracellular serpin members in higher vertebrates.
Journal ArticleDOI

Selective conservation of the RSL-encoding, proteinase inhibitory-type, clade L serpins in Caenorhabditis species.

TL;DR: The clade L serpin repertoire of Caenorhabditis elegans and other nematode species was sought to define and it was found that unlike their RSL-encoding paralogues, the relatively high percentage of non-RSL encoding serpins in C. elegans was a vestige of recent duplication events and these latter genes were unlikely to serve essential functions in CaenOrhabditIS species.
Journal ArticleDOI

An 18q− Syndrome Breakpoint Resides between the Duplicated Serpins SCCA1 and SCCA2 and Arises Via a Cryptic Rearrangement With Satellite III DNA

TL;DR: DNA sequence analysis suggested that the terminal deficiency in this 18q-syndrome patient arose via illegitimate (non-homologous) recombination, raising the possibility that a subset of chromosomal aberrations appearing cytogenetically and molecularly as simple terminal truncations or deletions are caused by small (<1000 kb) cryptic rearrangements.
Journal ArticleDOI

SERPINB12 Is a Slow-Binding Inhibitor of Granzyme A and Hepsin.

TL;DR: The clade B/intracellular serpins protect cells from peptidase-mediated injury by forming covalent complexes with their targets and may function as an endogenous inhibitor of these peptidases.