A5078697902- DNA Repair Mechanisms
- Genetic Neurodegenerative Diseases
- RNA modifications and cancer
- CRISPR and Genetic Engineering
- Ubiquitin and proteasome pathways
- CAR-T cell therapy research
- Genetics and Neurodevelopmental Disorders
- Cytokine Signaling Pathways and Interactions
- Cancer-related Molecular Pathways
- Microbial Metabolic Engineering and Bioproduction
- Bioinformatics and Genomic Networks
- Fungal and yeast genetics research
- Gene Regulatory Network Analysis
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Mitochondrial Function and Pathology
Advanced Centre for Treatment, Research and Education in Cancer
2025
Indian Institute of Technology Bombay
2019-2025
Baylor College of Medicine
2024
Tufts University
2009-2011
Abstract Trinucleotide repeats can form secondary structures, whose inappropriate repair or replication lead to repeat expansions. There are multiple loci within the human genome where expansion of trinucleotide leads disease. Although it is known that expanded accumulate double-strand breaks (DSBs), not which DSB pathways act on such lesions and whether inaccurate contribute Using Saccharomyces cerevisiae, we found CAG/CTG tracts 70 155 exhibited significantly elevated levels breakage...
Why cancer cells disproportionately accumulate polyubiquitinated proteotoxic proteins despite high proteasomal activity is an outstanding question. While mis-regulated ubiquitination a contributing factor, here we show that structurally-perturbed and sub-optimally functioning proteasome at the core of altered proteostasis in tumors. By integrating gene coexpression signatures subunits breast (BrCa) patient tissues with atomistic details 26S holocomplex, find transcriptional deregulation...
Repetitive DNA elements are mutational hotspots in the genome, and their instability is linked to various neurological disorders cancers. Although it known that expanded trinucleotide repeats can interfere with replication repair, cellular response these events has not been characterized. Here, we demonstrate an CAG/CTG repeat elicits a damage checkpoint budding yeast. Using microcolony single cell pedigree analysis, found cells carrying CAG frequently experience protracted division cycles,...
<h3>Background</h3> CAR-T cell efficacy in solid tumors is dampened by T-cell dysfunction, especially exhaustion, which driven chronic exposure to tumor antigens and the immunosuppressive, nutrient-limited microenvironment. Transcription factor (TF) overexpression or knockout are promising approaches enhance durability. However, given that a single genetic modulation unlikely sufficiently counter multiple triggers of efforts needed manipulate function engineering pairs TFs synergize...
<h3>Background</h3> A major barrier to the application of chimeric antigen receptor (CAR) T-cell therapy solid tumors is a dysfunctional state that T cells adopt upon chronic stimulation and exposure tumor microenvironment conditions. Modulation transcription factors promising avenue for imbuing CAR-T with dysfunction resistance, basic leucine zipper (bZIP) family (TFs) has several members roles in regulating dysfunction. Despite previous research, there remains uncertainty regarding role...