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710 results on '"Pandita, Tej K."'

2. Ubiquitin specific peptidase 37 and PCNA interaction promotes osteosarcoma pathogenesis by modulating replication fork progression

Author

Chauhan, Ravi, Gupta, Ashna, Malhotra, Lakshay, Bhat, Ajaz A., Pandita, Raj K., Masoodi, Tariq, Dagar, Gunjan, Sadida, Hana Q., Al-Marzooqi, Sara K., Batra, Atul, Bakhshi, Sameer, Sharma, Mehar Chand, Tanwar, Pranay, Khan, Shah Alam, Samath, Ethayathulla Abdul, Uddin, Shahab, Akil, Ammira S. Al-Shabeeb, Haris, Mohammad, Macha, Muzafar A., Pandita, Tej K., and Singh, Mayank

Published
2023
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3. EXO5-DNA structure and BLM interactions direct DNA resection critical for ATR-dependent replication restart

Author

Hambarde, Shashank, Tsai, Chi-Lin, Pandita, Raj K, Bacolla, Albino, Maitra, Anirban, Charaka, Vijay, Hunt, Clayton R, Kumar, Rakesh, Limbo, Oliver, Le Meur, Remy, Chazin, Walter J, Tsutakawa, Susan E, Russell, Paul, Schlacher, Katharina, Pandita, Tej K, and Tainer, John A

Subjects
Biochemistry and Cell Biology, Biological Sciences, Genetics, Human Genome, Generic health relevance, Ataxia Telangiectasia Mutated Proteins, Cell Line, Cell Line, Tumor, DNA, DNA Damage, DNA Helicases, DNA Mutational Analysis, DNA Repair, DNA Replication, DNA-Binding Proteins, Exonucleases, Genomic Instability, HEK293 Cells, HeLa Cells, Humans, Mutation, Oncogenes, Phosphorylation, RecQ Helicases, Up-Regulation, Hela Cells, ATR phosphorylation, Bloom, Fanconi anemia, SCE, exonuclease, fork restart, genetic instability, interstrand crosslink repair, replication stress, sister chromatid exchange, tumor proliferation, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Stalled DNA replication fork restart after stress as orchestrated by ATR kinase, BLM helicase, and structure-specific nucleases enables replication, cell survival, and genome stability. Here we unveil human exonuclease V (EXO5) as an ATR-regulated DNA structure-specific nuclease and BLM partner for replication fork restart. We find that elevated EXO5 in tumors correlates with increased mutation loads and poor patient survival, suggesting that EXO5 upregulation has oncogenic potential. Structural, mechanistic, and mutational analyses of EXO5 and EXO5-DNA complexes reveal a single-stranded DNA binding channel with an adjacent ATR phosphorylation motif (T88Q89) that regulates EXO5 nuclease activity and BLM binding identified by mass spectrometric analysis. EXO5 phospho-mimetic mutant rescues the restart defect from EXO5 depletion that decreases fork progression, DNA damage repair, and cell survival. EXO5 depletion furthermore rescues survival of FANCA-deficient cells and indicates EXO5 functions epistatically with SMARCAL1 and BLM. Thus, an EXO5 axis connects ATR and BLM in directing replication fork restart.

Published
2021

6. Cyclin-dependent kinases in cancer: Role, regulation, and therapeutic targeting

Author

Gupta, Ashna, primary, Dagar, Gunjan, additional, Chauhan, Ravi, additional, Sadida, Hana Q., additional, Almarzooqi, Sara K., additional, Hashem, Sheema, additional, Uddin, Shahab, additional, Macha, Muzafar A., additional, Akil, Ammira S. Al-Shabeeb, additional, Pandita, Tej K., additional, Bhat, Ajaz A., additional, and Singh, Mayank, additional

Published
2023
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7. Role of the Histone Acetyl Transferase MOF and the Histone Deacetylase Sirtuins in Regulation of H4K16ac During DNA Damage Repair and Metabolic Programming: Implications in Cancer and Aging

Author

Pandita, Tej K, Hunt, Clayton R., Singh, Vipin, Adhikary, Santanu, Pandita, Shruti, Roy, Siddhartha, Ramos, Kenneth, Das, Chandrima, Harris, J. Robin, Series Editor, Kundu, Tapas K., Advisory Editor, Korolchuk, Viktor, Advisory Editor, Bolanos-Garcia, Victor, Advisory Editor, Marles-Wright, Jon, Advisory Editor, Kundu, Tapas Kumar, editor, and Das, Chandrima, editor

Published
2022
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12. Correction: The Role of the Mammalian DNA End-processing Enzyme Polynucleotide Kinase 3’-Phosphatase in Spinocerebellar Ataxia Type 3 Pathogenesis

Author

Chatterjee, Arpita, primary, Saha, Saikat, additional, Chakraborty, Anirban, additional, Silva-Fernandes, Anabela, additional, Mandal, Santi M., additional, Neves-Carvalho, Andreia, additional, Liu, Yongping, additional, Pandita, Raj K., additional, Hegde, Muralidhar L., additional, Hegde, Pavana M., additional, Boldogh, Istvan, additional, Ashizawa, Tetsuo, additional, Koeppen, Arnulf H., additional, Pandita, Tej K., additional, Maciel, Patricia, additional, Sarkar, Partha S., additional, and Hazra, Tapas K., additional

Published
2024
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13. Classical non-homologous end-joining pathway utilizes nascent RNA for error-free double-strand break repair of transcribed genes.

Author

Chakraborty, Anirban, Tapryal, Nisha, Venkova, Tatiana, Horikoshi, Nobuo, Pandita, Raj K, Sarker, Altaf H, Sarkar, Partha S, Pandita, Tej K, and Hazra, Tapas K

Subjects
Humans, Escherichia coli, RNA Polymerase II, DNA-Binding Proteins, RNA, Small Interfering, RNA, Reproducibility of Results, Transcription, Genetic, Gene Expression Regulation, Bacterial, Lac Operon, Plasmids, DNA Breaks, Double-Stranded, Ribonuclease H, HEK293 Cells, DNA End-Joining Repair
Abstract

DNA double-strand breaks (DSBs) leading to loss of nucleotides in the transcribed region can be lethal. Classical non-homologous end-joining (C-NHEJ) is the dominant pathway for DSB repair (DSBR) in adult mammalian cells. Here we report that during such DSBR, mammalian C-NHEJ proteins form a multiprotein complex with RNA polymerase II and preferentially associate with the transcribed genes after DSB induction. Depletion of C-NHEJ factors significantly abrogates DSBR in transcribed but not in non-transcribed genes. We hypothesized that nascent RNA can serve as a template for restoring the missing sequences, thus allowing error-free DSBR. We indeed found pre-mRNA in the C-NHEJ complex. Finally, when a DSB-containing plasmid with several nucleotides deleted within the E. coli lacZ gene was allowed time to repair in lacZ-expressing mammalian cells, a functional lacZ plasmid could be recovered from control but not C-NHEJ factor-depleted cells, providing important mechanistic insights into C-NHEJ-mediated error-free DSBR of the transcribed genome.

Published
2016

15. Lysine acetyltransferase 8 is involved in cerebral development and syndromic intellectual disability

Author

Li, Lin, Ghorbani, Mohammad, Weisz-Hubshman, Monika, Rousseau, Justine, Thiffaul, Isabelle, Schnur, Rhonda E., Breen, Catherine, Oegema, Renske, Weiss, Marjan M.M., Waisfisz, Quinten, Welner, Sara, Kingston, Helen, Hills, Jordan A., Boon, Elles M.J., Basel-Salmon, Lina, Konen, Osnat, Goldberg-Stern, Hadassa, Bazak, Lily, Tzur, Shay, Jin, Jianliang, Bi, Xiuli, Bruccoleri, Michael, McWalter, Kirsty, Cho, Megan T., Scarano, Maria, Schaefer, G. Bradley, Brooks, Susan S., Hughes, Susan Starling, van Gassen, K.L.I., van Hagen, Johanna M., Pandita, Tej K., Agrawal, Pankaj B., Campeau, Philippe M., and Yang, Xiang- Jiao

Subjects
Thermo Fisher Scientific Inc., Brain, Epigenetic inheritance, Lysine, Apoptosis, Scientific equipment industry, Acylation, Disabilities, Autism, Seizures (Medicine), Epilepsy, Diseases, Health care industry
Abstract

Epigenetic integrity is critical for many eukaryotic cellular processes. An important question is how different epigenetic regulators control development and influence disease. Lysine acetyltransferase 8 (KAT8) is critical for acetylation of histone H4 at lysine 16 (H4K16), an evolutionarily conserved epigenetic mark. It is unclear what roles KAT8 plays in cerebral development and human disease. Here, we report that cerebrum-specific knockout mice displayed cerebral hypoplasia in the neocortex and hippocampus, along with improper neural stem and progenitor cell (NSPC) development. Mutant cerebrocortical neuroepithelia exhibited faulty proliferation, aberrant neurogenesis, massive apoptosis, and scant H4K16 propionylation. Mutant NSPCs formed poor neurospheres, and pharmacological KAT8 inhibition abolished neurosphere formation. Moreover, we describe KAT8 variants in 9 patients with intellectual disability, seizures, autism, dysmorphisms, and other anomalies. The variants altered chromobarrel and catalytic domains of KAT8, thereby impairing nucleosomal H4K16 acetylation. Valproate was effective for treating epilepsy in at least 2 of the individuals. This study uncovers a critical role of KAT8 in cerebral and NSPC development, identifies 9 individuals with KAT8 variants, and links deficient H4K16 acylation directly to intellectual disability, epilepsy, and other developmental anomalies., Introduction Hundreds of epigenetic regulators have been identified and characterized, but much less is known about their pathophysiological roles. Lysine acetyltransferases (KATs) form a prominent group of chromatin regulators, catalyze [...]

Published
2020
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19. A homozygous FANCM frameshift pathogenic variant causes male infertility

Author

Yin, Hao, Ma, Hui, Hussain, Sajjad, Zhang, Huan, Xie, Xuefeng, Jiang, Long, Jiang, Xiaohua, Iqbal, Furhan, Bukhari, Ihtisham, Jiang, Hanwei, Ali, Asim, Zhong, Liangwen, Li, Tao, Fan, Suixing, Zhang, Beibei, Gao, Jianing, Li, Yang, Nazish, Jabeen, Khan, Teka, Khan, Manan, Zubair, Muhammad, Hao, Qiaomei, Fang, Hui, Huang, Jun, Huleihel, Mahmoud, Sha, Jiahao, Pandita, Tej K., Zhang, Yuanwei, and Shi, Qinghua

Published
2019
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20. Ssb1 and Ssb2 cooperate to regulate mouse hematopoietic stem and progenitor cells by resolving replicative stress

Author

Shi, Wei, Vu, Therese, Boucher, Didier, Biernacka, Anna, Nde, Jules, Pandita, Raj K., Straube, Jasmin, Boyle, Glen M., Al-Ejeh, Fares, Nag, Purba, Jeffery, Jessie, Harris, Janelle L., Bain, Amanda L., Grzelak, Marta, Skrzypczak, Magdalena, Mitra, Abhishek, Dojer, Norbert, Crosetto, Nicola, Cloonan, Nicole, Becherel, Olivier J., Finnie, John, Skaar, Jeffrey R., Walkley, Carl R., Pandita, Tej K., Rowicka, Maga, Ginalski, Krzysztof, Lane, Steven W., and Khanna, Kum Kum

Published
2017
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24. Abstract 335: Ubiquitin Specific Peptidase 37promotes Osteosarcoma oncogenesis by interacting with PCNA and impacting constitutive replication fork movement.

Author

Chauhan, Ravi, primary, Malhotra, Lakshay, additional, Gupta, Ashna, additional, Bhat, Ajaz, additional, Dagar, Gunjan, additional, Masoodi, Tariq, additional, Macha, Muzafar A., additional, Samath, Ethayathulla Abdul, additional, Batra, Atul, additional, Sharma, Mehar Chand, additional, Haris, Mohammad, additional, Akil, Ammira Al-Shabeeb, additional, Pandita, Tej K., additional, Uddin, Shahab, additional, and Singh, Mayank, additional

Published
2023
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27. Supplemental Figures from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis

Author

Valerio, Daria G., primary, Xu, Haiming, primary, Chen, Chun-Wei, primary, Hoshii, Takayuki, primary, Eisold, Meghan E., primary, Delaney, Christopher, primary, Cusan, Monica, primary, Deshpande, Aniruddha J., primary, Huang, Chun-Hao, primary, Lujambio, Amaia, primary, Zheng, YuJun George, primary, Zuber, Johannes, primary, Pandita, Tej K., primary, Lowe, Scott W., primary, and Armstrong, Scott A., primary

Published
2023
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28. Supplementary Table 1-3 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition

Author

Gadhikar, Mayur A., primary, Zhang, Jiexin, primary, Shen, Li, primary, Rao, Xiayu, primary, Wang, Jing, primary, Zhao, Mei, primary, Kalu, Nene N., primary, Johnson, Faye M., primary, Byers, Lauren A., primary, Heymach, John, primary, Hittelman, Walter N., primary, Udayakumar, Durga, primary, Pandita, Raj K., primary, Pandita, Tej K., primary, Pickering, Curtis R., primary, Redwood, Abena B., primary, Piwnica-Worms, Helen, primary, Schlacher, Katharina, primary, Frederick, Mitchell J., primary, and Myers, Jeffrey N., primary

Published
2023
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29. Data from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition

Author

Gadhikar, Mayur A., primary, Zhang, Jiexin, primary, Shen, Li, primary, Rao, Xiayu, primary, Wang, Jing, primary, Zhao, Mei, primary, Kalu, Nene N., primary, Johnson, Faye M., primary, Byers, Lauren A., primary, Heymach, John, primary, Hittelman, Walter N., primary, Udayakumar, Durga, primary, Pandita, Raj K., primary, Pandita, Tej K., primary, Pickering, Curtis R., primary, Redwood, Abena B., primary, Piwnica-Worms, Helen, primary, Schlacher, Katharina, primary, Frederick, Mitchell J., primary, and Myers, Jeffrey N., primary

Published
2023
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30. Supplemental table S1 from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis

Author

Valerio, Daria G., primary, Xu, Haiming, primary, Chen, Chun-Wei, primary, Hoshii, Takayuki, primary, Eisold, Meghan E., primary, Delaney, Christopher, primary, Cusan, Monica, primary, Deshpande, Aniruddha J., primary, Huang, Chun-Hao, primary, Lujambio, Amaia, primary, Zheng, YuJun George, primary, Zuber, Johannes, primary, Pandita, Tej K., primary, Lowe, Scott W., primary, and Armstrong, Scott A., primary

Published
2023
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31. Figure S5 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition

Author

Gadhikar, Mayur A., primary, Zhang, Jiexin, primary, Shen, Li, primary, Rao, Xiayu, primary, Wang, Jing, primary, Zhao, Mei, primary, Kalu, Nene N., primary, Johnson, Faye M., primary, Byers, Lauren A., primary, Heymach, John, primary, Hittelman, Walter N., primary, Udayakumar, Durga, primary, Pandita, Raj K., primary, Pandita, Tej K., primary, Pickering, Curtis R., primary, Redwood, Abena B., primary, Piwnica-Worms, Helen, primary, Schlacher, Katharina, primary, Frederick, Mitchell J., primary, and Myers, Jeffrey N., primary

Published
2023
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32. Extended supplementary procedures from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition

Author

Gadhikar, Mayur A., primary, Zhang, Jiexin, primary, Shen, Li, primary, Rao, Xiayu, primary, Wang, Jing, primary, Zhao, Mei, primary, Kalu, Nene N., primary, Johnson, Faye M., primary, Byers, Lauren A., primary, Heymach, John, primary, Hittelman, Walter N., primary, Udayakumar, Durga, primary, Pandita, Raj K., primary, Pandita, Tej K., primary, Pickering, Curtis R., primary, Redwood, Abena B., primary, Piwnica-Worms, Helen, primary, Schlacher, Katharina, primary, Frederick, Mitchell J., primary, and Myers, Jeffrey N., primary

Published
2023
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33. Supplemental experimental Procedures from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis

Author

Valerio, Daria G., primary, Xu, Haiming, primary, Chen, Chun-Wei, primary, Hoshii, Takayuki, primary, Eisold, Meghan E., primary, Delaney, Christopher, primary, Cusan, Monica, primary, Deshpande, Aniruddha J., primary, Huang, Chun-Hao, primary, Lujambio, Amaia, primary, Zheng, YuJun George, primary, Zuber, Johannes, primary, Pandita, Tej K., primary, Lowe, Scott W., primary, and Armstrong, Scott A., primary

Published
2023
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35. Data from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis

Author

Valerio, Daria G., primary, Xu, Haiming, primary, Chen, Chun-Wei, primary, Hoshii, Takayuki, primary, Eisold, Meghan E., primary, Delaney, Christopher, primary, Cusan, Monica, primary, Deshpande, Aniruddha J., primary, Huang, Chun-Hao, primary, Lujambio, Amaia, primary, Zheng, YuJun George, primary, Zuber, Johannes, primary, Pandita, Tej K., primary, Lowe, Scott W., primary, and Armstrong, Scott A., primary

Published
2023
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37. Supplementary Figures 1-5 from Single-Strand DNA-Binding Protein SSB1 Facilitates TERT Recruitment to Telomeres and Maintains Telomere G-Overhangs

Author

Pandita, Raj K., primary, Chow, Tracy T., primary, Udayakumar, Durga, primary, Bain, Amanda L., primary, Cubeddu, Liza, primary, Hunt, Clayton R., primary, Shi, Wei, primary, Horikoshi, Nobuo, primary, Zhao, Yong, primary, Wright, Woodring E., primary, Khanna, Kum Kum, primary, Shay, Jerry W., primary, and Pandita, Tej K., primary

Published
2023
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39. Data from Single-Strand DNA-Binding Protein SSB1 Facilitates TERT Recruitment to Telomeres and Maintains Telomere G-Overhangs

Author

Pandita, Raj K., primary, Chow, Tracy T., primary, Udayakumar, Durga, primary, Bain, Amanda L., primary, Cubeddu, Liza, primary, Hunt, Clayton R., primary, Shi, Wei, primary, Horikoshi, Nobuo, primary, Zhao, Yong, primary, Wright, Woodring E., primary, Khanna, Kum Kum, primary, Shay, Jerry W., primary, and Pandita, Tej K., primary

Published
2023
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45. Supplementary Figure Legend, Methods and Materials, Tables 1-2. from Single-Strand DNA-Binding Protein SSB1 Facilitates TERT Recruitment to Telomeres and Maintains Telomere G-Overhangs

Author

Pandita, Raj K., primary, Chow, Tracy T., primary, Udayakumar, Durga, primary, Bain, Amanda L., primary, Cubeddu, Liza, primary, Hunt, Clayton R., primary, Shi, Wei, primary, Horikoshi, Nobuo, primary, Zhao, Yong, primary, Wright, Woodring E., primary, Khanna, Kum Kum, primary, Shay, Jerry W., primary, and Pandita, Tej K., primary

Published
2023
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