A5043487129- DNA Repair Mechanisms
- Carcinogens and Genotoxicity Assessment
- RNA modifications and cancer
- Cancer-related Molecular Pathways
- RNA Research and Splicing
- Shoulder Injury and Treatment
- Myofascial pain diagnosis and treatment
- Epigenetics and DNA Methylation
- DNA and Nucleic Acid Chemistry
- Genetics, Aging, and Longevity in Model Organisms
- Biomedical and Chemical Research
- Neuroscience and Neuropharmacology Research
- Acute Myeloid Leukemia Research
- Pregnancy and preeclampsia studies
- Phytochemicals and Medicinal Plants
- Mitochondrial Function and Pathology
- Biochemical Analysis and Sensing Techniques
- Diagnosis and treatment of tuberculosis
- Circadian rhythm and melatonin
- Tuberculosis Research and Epidemiology
- GABA and Rice Research
- PARP inhibition in cancer therapy
- Medicinal Plants and Neuroprotection
- Gestational Diabetes Research and Management
- Chromosomal and Genetic Variations
Weizmann Institute of Science
2014-2022
University of Hyderabad
2008-2016
Jawaharlal Nehru Technological University, Hyderabad
2011-2014
Jawaharlal Nehru Technological University, Kakinada
2014
University Grants Commission
2011-2012
Kasturba Medical College, Manipal
1993
Abstract Background Genomic instability promotes evolution and heterogeneity of tumors. Unraveling its mechanistic basis is essential for the design appropriate therapeutic strategies. In a previous study, we reported an unexpected oncogenic property p21 WAF1/Cip1 , showing that chronic expression in p53-deficient environment causes genomic by deregulation replication licensing machinery. Results We now demonstrate can further fuel suppressing repair capacity low- high-fidelity pathways deal...
Abstract Cells cope with replication-blocking lesions via translesion DNA synthesis (TLS). TLS is carried out by low-fidelity polymerases that replicate across lesions, thereby preventing genome instability at the cost of increased point mutations. Here we perform a two-stage siRNA-based functional screen for mammalian genes and identify 17 validated genes. One genes, NPM1 , frequently mutated in acute myeloid leukaemia (AML). We show (nucleophosmin) regulates interaction catalytic core...
TENT4A (PAPD7) is a non-canonical poly(A) polymerase, of which little known. Here, we show that regulates multiple biological pathways and focuses on its multilayer regulation translesion DNA synthesis (TLS), in error-prone polymerases bypass unrepaired lesions. We mRNA stability and/or translation polymerase η RAD18 E3 ligase, guides the to replication stalling sites monoubiquitinates PCNA, thereby enabling recruitment damaged sites. Remarkably, addition effect via controlling tail,...
Abstract Background Genomic instability promotes evolution and heterogeneity of tumors. Unraveling its mechanistic basis is essential to design appropriate therapeutic strategies. In a recent study we reported an unexpected oncogenic property p21 WAF1/Cip1 showing that chronic expression, in p53-deficient environment, causes genomic by deregulating the replication licensing machinery. Results Extending on this work now demonstrate can further fuel suppressing repair capacity low high...
Abstract TENT4A (PAPD7) is a non-canonical poly(A) polymerase, of which little known. Here we focus on its multilayer regulation translesion DNA synthesis (TLS), in lesions are bypassed by error-prone polymerases. We show that regulates mRNA stability and/or translation polymerase η and RAD18 E3 ligase, guides the to replication stalling sites, monoubiquitinates PCNA, thereby enabling recruitment polymerases damaged sites. Remarkably, addition effect via controlling tail, indirectly tumor...