- Ubiquitin and proteasome pathways
- RNA and protein synthesis mechanisms
- Enzyme Structure and Function
- Endoplasmic Reticulum Stress and Disease
- Autophagy in Disease and Therapy
- RNA Research and Splicing
- Protein Structure and Dynamics
- Parkinson's Disease Mechanisms and Treatments
- DNA and Nucleic Acid Chemistry
- Bacterial Genetics and Biotechnology
- Mitochondrial Function and Pathology
- Magnesium in Health and Disease
- Protein Tyrosine Phosphatases
- RNA modifications and cancer
- Glycosylation and Glycoproteins Research
- Cellular transport and secretion
- Legionella and Acanthamoeba research
- Genetic Neurodegenerative Diseases
- Peptidase Inhibition and Analysis
- Biochemical and Molecular Research
- Bacteriophages and microbial interactions
- Parathyroid Disorders and Treatments
- ATP Synthase and ATPases Research
- Signaling Pathways in Disease
- Cancer-related gene regulation
McGill University
2015-2024
Bioénergétique et Ingénierie des Protéines
2012-2014
Milbank Memorial Fund
2012
Daegu Haany University
2012
The University of Tokyo
2011
National Institute of Immunology
2008
Ontario Institute for Cancer Research
2008
New York University
2008
University of California, Riverside
2007
National University of General San Martín
2005
Parkin Enhanced? Inactivation of parkin, an E3 ubiquitin ligase, is responsible for a familial form Parkinson's disease and may be involved in sporadic forms as well. Trempe et al. (p. 1451 , published online 9 May) present the crystal structure full-length parkin autoinhibited configuration. Guided by structure, mutations were designed that activated both vitro cells. Because neuroprotective, provides framework enhancing function therapeutic strategy disease.
Abstract Mutations in Parkin and PINK 1 cause an inherited early‐onset form of Parkinson's disease. The two proteins function together a mitochondrial quality control pathway whereby accumulates on damaged mitochondria activates to induce mitophagy. How kinase activity releases the auto‐inhibited ubiquitin ligase remains unclear. Here, we identify binding switch between phospho‐ubiquitin ( pU b) ubiquitin‐like domain (Ubl) as key element. By mutagenesis SAXS , show that b binds RING at site...
The influx of genomic sequence information has led to the concept structural proteomics, determination protein structures on a genome-wide scale. Here we describe an approach proteomics small proteins using NMR spectroscopy. Over 500 from several organisms were cloned, expressed, purified, and evaluated by NMR. Although there was variability among proteomes, overall 20% these found be readily amenable structure determination. sample preparation centralized in one facility, distributive used...
We have determined the solution structure of C-terminal quarter human poly(A)-binding protein (hPABP). The fragment contains a domain, PABC [for domain], which is also found associated with HECT family ubiquitin ligases. By using peptides derived from PABP interacting (Paip) 1, Paip2, and eRF3, we show that functions as peptide binding domain. use chemical shift perturbation analysis to identify site in major elements involved recognition. From comparative sequence PABC-binding peptides,...
Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is a childhood-onset neurological disease resulting from mutations in the SACS gene encoding sacsin, 4,579-aa protein unknown function. Originally identified as founder Québec, ARSACS now recognized worldwide. Prominent features include pyramidal spasticity and cerebellar ataxia, but underlying pathology pathophysiological mechanisms are unknown. We have generated an animal model for ARSACS, sacsin knockout mice, that display...
ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTAcid multimers of oligodeoxycytidine strands: Stoichiometry, base-pair characterization, and proton exchange propertiesJean Louis Leroy, Kalle Gehring, Abdelali Kettani, Maurice GueronCite this: Biochemistry 1993, 32, 23, 6019–6031Publication Date (Print):June 15, 1993Publication History Published online1 May 2002Published inissue 15 June 1993https://pubs.acs.org/doi/10.1021/bi00074a013https://doi.org/10.1021/bi00074a013research-articleACS...
The use of deuteration in concert with uniform 15N,13C-labeling has been critical for the chemical shift assignment several proteins and protein complexes over 30 kDa. Unfortunately, reduces number interproton distance restraints available structure determination, compromising precision accuracy NMR-derived structures determined from these samples. We have recently described an isotopic labeling strategy that addresses this problem by generating labeled uniformly 15N, 13C, extensively 2H...
Poly(A)-binding protein (PABP) stimulates translation initiation by binding simultaneously to the mRNA poly(A) tail and eukaryotic factor 4G (eIF4G). PABP activity is regulated PABP-interacting (Paip) proteins. Paip1 binds an unknown mechanism. Here, we describe interaction between eIF3, which direct, RNA independent, mediated via eIF3g (p44) subunit. Stimulation of in vivo was decreased upon deletion N-terminal sequence containing eIF3-binding domain silencing or several eIF3 subunits. We...