A5025259805- Chronic Lymphocytic Leukemia Research
- Monoclonal and Polyclonal Antibodies Research
- CAR-T cell therapy research
- Lysosomal Storage Disorders Research
- Pharmacological Effects of Medicinal Plants
- Natural product bioactivities and synthesis
- Endoplasmic Reticulum Stress and Disease
- Autophagy in Disease and Therapy
- Cellular transport and secretion
- Glycosylation and Glycoproteins Research
- PI3K/AKT/mTOR signaling in cancer
- Lymphoma Diagnosis and Treatment
- Sphingolipid Metabolism and Signaling
- Protein Kinase Regulation and GTPase Signaling
- Pancreatitis Pathology and Treatment
- ATP Synthase and ATPases Research
- Virus-based gene therapy research
- Heat shock proteins research
- Advanced Materials and Mechanics
- Cytokine Signaling Pathways and Interactions
- Erythrocyte Function and Pathophysiology
- Macrophage Migration Inhibitory Factor
- Plant biochemistry and biosynthesis
- Cellular Mechanics and Interactions
- Nuclear Receptors and Signaling
Sanford Burnham Prebys Medical Discovery Institute
2011-2023
Pharmacyclics (United States)
2023
AbbVie (United States)
2023
Discovery Institute
2016
Vellore Institute of Technology University
2011
Indian Institute of Science Bangalore
2011
Hospital de Clínicas de Porto Alegre
2005-2011
St. Jude Children's Research Hospital
2004-2009
Universidade Federal do Rio Grande do Sul
2005-2008
Autophagy is a lysosomal degradation pathway that converts macromolecules into substrates for energy production during nutrient-scarce conditions such as those encountered in tumor microenvironments. Constitutive mitochondrial uptake of endoplasmic reticulum (ER) Ca 2+ mediated by inositol triphosphate receptors (IP 3 Rs) maintains cellular bioenergetics, thus suppressing autophagy. We show the ER membrane protein Bax inhibitor-1 (BI-1) promotes autophagy an IP R-dependent manner. By...
Autophagy is an evolutionarily conserved process for catabolizing damaged proteins and organelles in a lysosome-dependent manner. Dysregulation of autophagy may cause various diseases, such as cancer neurodegeneration. However, the relevance to diseases remains controversial because limited availability chemical modulators. Herein, authors developed fluorescence-based assay measuring activity protease, autophagin-1(Atg4B). The employs novel reporter substrate Atg4B composed natural (LC3B)...
Abstract Small molecule inhibitors of Bruton's tyrosine kinase (BTK) have been approved for the treatment multiple B-cell malignancies and are being evaluated autoimmune inflammatory diseases. Various BTK (BTKi) distinct potencies, selectivity profiles, binding modes within ATP-binding site. On basis latter feature, BTKis can be classified into those that occupy back-pocket, H3 pocket, hinge region only. Hypothesizing differing may differential impact on receptor (BCR) signaling pathway, we...
Endoplasmic reticulum (ER) stress occurs when unfolded proteins accumulate in the lumen of organelle, triggering signal transduction events that contribute either to cellular adaptation and recovery or alternatively dysfunction death. ER has been implicated numerous diseases. To identify novel modulators stress, we undertook a siRNA library screen kinome, revealing Interleukin-1 Receptor-Associated Kinase-2 (IRAK2) as contributor protein response (UPR) signaling stress-induced cell Knocking...
Infantile GM1 gangliosidosis is caused by the absence or reduction of lysosomal beta-galactosidase activity. Studies conducted in Brazil have indicated that it one most frequent storage disorders southern part country. To assess incidence this disorder, 390 blood donors were tested for presence two common mutations (1622-1627insG and R59H) GLB1 gene. Another group, consisting 26 patients, polymorphisms (R521C S532G), an attempt to elucidate whether there a founder effect. The frequencies...
We explored the effect of a novel synthetic triterpenoid compound cyano enone methyl boswellates (CEMB) on various prostate cancer and glioma cell lines. CEMB displayed concentration-dependent cytotoxic activity with submicromolar lethal dose 50% (LD(50)) values in 10 tumor lines tested. CEMB-induced cytotoxicity is accompanied by activation downstream effector caspases (caspases 3 7) upstream initiator involved both extrinsic (caspase 8) intrinsic 9) apoptotic pathways. By using short...
<div>Abstract<p>Small molecule inhibitors of Bruton's tyrosine kinase (BTK) have been approved for the treatment multiple B-cell malignancies and are being evaluated autoimmune inflammatory diseases. Various BTK (BTKi) distinct potencies, selectivity profiles, binding modes within ATP-binding site. On basis latter feature, BTKis can be classified into those that occupy back-pocket, H3 pocket, hinge region only. Hypothesizing differing may differential impact on receptor (BCR)...
GM1 gangliosidosis is an autosomal recessive disorder caused by the deficiency of lysosomal acid hydrolase beta-galactosidase (beta-Gal). It one most frequent storage disorders in Brazil, with estimated frequency 1:17,000. The enzyme secreted and can be captured deficient cells targeted to lysosomes. There no effective treatment for gangliosidosis. To determine efficiency expression vector correcting genetic defect gangliosidosis, we tested transfer beta-Gal gene (Glb1) fibroblasts culture...
<p>Supplemental Figure 2</p>
<p>Supplemental Figure 3</p>
<p>Supplemental methods</p>
<p>Back-pocket and H3 pocket binders but not hinge-only inhibit calcium flux in Ramos TMD8 cells</p>
<p>Supplemental Figure 4</p>
<div>Abstract<p>Small molecule inhibitors of Bruton's tyrosine kinase (BTK) have been approved for the treatment multiple B-cell malignancies and are being evaluated autoimmune inflammatory diseases. Various BTK (BTKi) distinct potencies, selectivity profiles, binding modes within ATP-binding site. On basis latter feature, BTKis can be classified into those that occupy back-pocket, H3 pocket, hinge region only. Hypothesizing differing may differential impact on receptor (BCR)...
<p>Back-pocket and H3 pocket binders but not hinge-only inhibit calcium flux in Ramos TMD8 cells</p>
<p>Supplemental Figure 3</p>
<p>Supplemental Figure 1</p>
<p>Supplemental methods</p>