A5101566507- Genetic Neurodegenerative Diseases
- Mitochondrial Function and Pathology
- Muscle Physiology and Disorders
- Ubiquitin and proteasome pathways
- CRISPR and Genetic Engineering
- Plant tissue culture and regeneration
- Photosynthetic Processes and Mechanisms
- Seed and Plant Biochemistry
- Nanoparticles: synthesis and applications
- Light effects on plants
- Plant Molecular Biology Research
- Plant Reproductive Biology
- Plant Genetic and Mutation Studies
- Insect behavior and control techniques
- Genetics and Neurodevelopmental Disorders
- Plant Micronutrient Interactions and Effects
- DNA Repair Mechanisms
- Nitrogen and Sulfur Effects on Brassica
- Transgenic Plants and Applications
- Forensic Entomology and Diptera Studies
- Phytase and its Applications
- Chromosomal and Genetic Variations
- Insect Resistance and Genetics
- Genetically Modified Organisms Research
- Diptera species taxonomy and behavior
National Public Health Laboratory
2025
The University of Texas Medical Branch at Galveston
2019-2022
Indian Institute of Technology Kharagpur
2015-2018
Indian Institute of Technology Indore
2015
How huntingtin (HTT) triggers neurotoxicity in Huntington’s disease (HD) remains unclear. We report that HTT forms a transcription-coupled DNA repair (TCR) complex with RNA polymerase II subunit A (POLR2A), ataxin-3, the enzyme polynucleotide-kinase-3'-phosphatase (PNKP), and cyclic AMP-response element-binding (CREB) protein (CBP). This senses facilitates damage during transcriptional elongation, but its functional integrity is impaired by mutant HTT. Abrogated PNKP activity results...
DNA damage repair genes are modifiers of disease onset in Huntington's (HD), but how this process intersects with associated pathways remains unclear. Here we evaluated the mechanistic contributions protein inhibitor activated STAT-1 (PIAS1) HD mice and patient-derived induced pluripotent stem cells (iPSCs) find a link between PIAS1 pathways. We show that is component transcription-coupled complex, includes end processing enzyme polynucleotide kinase-phosphatase (PNKP), SUMO E3 ligase for...
Intestinal myiasis is a type of resulting from the accidental consumption Clogmia albipunctata larvae. This generally displays symptoms such as nausea, vomiting, abdominal distention and discomfort, loss appetite, weight loss, intermittent diarrhea. It rare form with relatively scarce literature in Nepal. We report probably first case human intestinal caused by A 39-year-old nondiabetic female, Brahmin belonging to khas/arya ethnicity presented complaints perianal itching, occasional...
SUMMARY Persistent DNA double-strand breaks (DSBs) are enigmatically implicated in neurodegenerative diseases including Huntington’s disease (HD), the inherited late-onset disorder caused by CAG repeat elongations Huntingtin (HTT). Here we combine biochemistry, computation and molecular cell biology to unveil a mechanism whereby HTT coordinates Transcription-Coupled Non-Homologous End-Joining (TC-NHEJ) complex. joins TC-NHEJ proteins PNKP, Ku70/80, XRCC4 with chromatin remodeler...
SUMMARYThe function of huntingtin (HTT) is enigmatic in that the native protein provides neuroprotection while mutant HTT (mHTT) carrying an expanded stretch glutamines triggers neurotoxicity Huntington’s disease (HD). We recently reported forms a transcription-coupled DNA repair (TCR) complex with RNA polymerase and enzyme polynucleotide-kinase-3'-phosphatase (PNKP). This resolves lesions during transcription to maintain genome integrity, mHTT impairs activity this complex, resulting lesion...