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19 results on '"Singh, Divya Jyoti"'

4. Role of MBD4 Mutation in Neoplastic Evolution of Acute Myeloid Leukemia

Author

Kawashima, Naomi, primary, Jiang, Dongxu, additional, Singh, Divya Jyoti, additional, Grabowski, Dale, additional, Gurnari, Carmelo, additional, Kubota, Yasuo, additional, Aly, Mai, additional, Visconte, Valeria, additional, Griffin, Brittany L, additional, Haferlach, Torsten, additional, Maciejewski, Jaroslaw P., additional, and Jha, Babal K., additional

Published
2022
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5. Demonstration That Loss of TET2 Impairs DNA Mismatch Repair Resulting in Clonally Restricted Genomic Instability

Author

Jiang, Dongxu, primary, Pan, Feng, additional, Guan, Yihong, additional, Gu, Xiaorong, additional, Kawashima, Naomi, additional, Singh, Divya Jyoti, additional, Dima, Danai, additional, Qu, Guangbo, additional, Greenberg, Edward F, additional, Visconte, Valeria, additional, Mian, Omar, additional, Xu, Mingjiang, additional, Maciejewski, Jaroslaw P., additional, and Jha, Babal K., additional

Published
2022
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6. Heightened Endoplasmic-Reticulum Stress Is a Targetable Vulnerability of Malignant Plasma Cells in Multiple Myeloma

Author

Dima, Danai, primary, Hasipek, Metis, additional, Singh, Divya Jyoti, additional, Jiang, Dongxu, additional, Tiwari, Anand D., additional, Grabowski, Dale, additional, Parker, Yvonne, additional, Lindner, Daniel J., additional, Zhao, Jianjun, additional, Shain, Kenneth H., additional, Khouri, Jack, additional, Maciejewski, Jaroslaw P., additional, and Jha, Babal K., additional

Published
2022
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7. Multiple Myeloma Therapy: Emerging Trends and Challenges

Author

Dima, Danai, primary, Jiang, Dongxu, additional, Singh, Divya Jyoti, additional, Hasipek, Metis, additional, Shah, Haikoo S., additional, Ullah, Fauzia, additional, Khouri, Jack, additional, Maciejewski, Jaroslaw P., additional, and Jha, Babal K., additional

Published
2022
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12. Forward genetics combined with unsupervised classifications identified zebrafish mutants affecting biliary system formation

Author

Singh, Divya Jyoti, primary, Tuscano, Kathryn M., additional, Ortega, Karen L., additional, Dimri, Manali, additional, Tae, Kevin, additional, Lee, William, additional, Muslim, Muslim A., additional, Liu, Jay L., additional, Pierce, Lain X., additional, McClendon, Allyson, additional, Naegele, Gregory, additional, Gibson, Isabel, additional, Livesay, Jodi, additional, and Sakaguchi, Takuya F., additional

Published
2021
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16. Photoactivated Chlorophyllin and Acetylcholinesterase/ Cytochrome Oxidase Activity in Fasciola gigantica cercaria Larvae.

Author

Kumar Singh, Dinesh and Singh, Divya jyoti

Subjects
*CHLOROPHYLLIN, *ACETYLCHOLINESTERASE, *CYTOCHROME oxidase, *FASCIOLA, *BIOINDICATORS
Abstract

Objective: The effect of chlorophyllin (CHL), CHL + freeze dried cow urine (FCU) and FCU on acetylcholinesterase (AChE) and cytochrome oxidase activity in the nervous tissue of the host snail Lymnaea acuminata, and parasitic cercaria larvae of Fasciola gigantica were studied. Methods: Whole cercaria larvae and snail nervous tissue was homogenized and supernatant was used as an enzyme source. Enzyme activity was measured in 10-mm path length cuvette using incubation mixtures and change in optical density was recorded. Results: Sublethal 4 h LC50 40% and 80% of these formulations in sunlight and laboratory conditions caused no significant change in AChE activity in the nervous tissue of host snail. It was noted that sublethal in vivo 8 h exposure to 40% and 80% of 4 h LC50 of single and binary combination of CHL+FCU, CHL and FCU significantly altered the AChE and cytochrome oxidase activity in the cercaria larvae. Binary combinations of CHL+FCU in sunlight were more effective in inhibiting both the enzymes. Conclusion: The present study reported that enzymes AChE and cytochrome oxidase were inhibited by chlorophyllin formulations and thus causing the larval death inside the snail body without affecting the snail itself which is an important bioindicator of aquatic ecosytem. [ABSTRACT FROM AUTHOR]

Published
2018
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17. Methyl-CpG Binding Domain Protein MBD2 Is a Targetable Vulnerability in TET2Mutant Myeloid Neoplasia

Author

Jiang, Dongxu, Guan, Yihong, Ganguly, Shinjini, Balyimez, Aysegul, Muskara, Andrew, Singh, Divya Jyoti, Pagliuca, Simona, Vail, Daniel, Zhang, Yahan, Durkin, Jill, Kawashima, Naomi, Gu, Xiaorong, Gurnari, Carmelo, Maciejewski, Jaroslaw P., Mian, Omar, and Jha, Babal K.

Abstract

Background & Significance.Epigenetic dysregulation leading to acquired disorganization of CpG methylation (mCpG) is a hallmark of cancer in general and myeloid neoplasia (MN) in particular. TET dioxygenases (TET1, TET2 and TET3) progressively oxidize 5-methyl cytosine (mC) to facilitate CpG demethylation, a process critical to efficient transcription, lineage differentiation, and proliferation. Loss of function TET2mutation ( TET2 MT), the predominant TET in HSPCs, isone of the most common genetic lesions in MN and often occurs early in MDS/AML as a founder lesion. It is frequently observed in clonal hematopoiesis of indeterminate potential (CHIP) 1,2, a prodromal condition linked with increased risk of MN, coronary heart disease 3, and pulmonary arterial hypertension 4. TET2 MTresults in abnormal accumulation of mC in the genome resulting in loss of lineage plasticity due to transcriptional repression of differentiation-promoting genes and tumor suppressor genes (TSGs), contributing to a volatile pre-neoplastic state. Indeed, the accumulation of mC at otherwise unmethylated promoter- and enhancer-associated CpGs is a hallmark cancer 2,5. The epigenetic reader mCpG binding domain protein 2 (MBD2) specifically recognizes mCpG, thereby modulating regional gene transcription 6. This modulation occurs through the recruitment of co-repressor complexes which deliver enzymatic machinery to reorganize chromatin into compact, inaccessible, and stably silenced regions. This tightly regulated process, required for normal development and cell lineage differentiation, is hijacked by malignant cells to maintain a pro-oncogenic transcriptional program. Therefore, MBD2 inhibition may restore the normal hematopoiesis in TET2 MTHSPCs and may represent a selective therapeutic target.

Published
2023
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18. Loss of Function MBD4Mutation Impairs DNA Repair in Association with TET2 in Acute Myeloid Leukemia

Author

Kawashima, Naomi, Jiang, Dongxu, Vail, Daniel, Singh, Divya Jyoti, Gu, Xiaorong, Schlanger, Simon, Gurnari, Carmelo, Kubota, Yasuo, Stewart, Brittany L, Visconte, Valeria, Maciejewski, Jaroslaw P., and Jha, Babal K.

Abstract

Background:Methyl-CpG binding domain 4 (MBD4) is a known DNA glycosylase involved in critical steps of base excision repair (BER) and DNA mismatch repair (MMR) and is essential for reducing genotoxic stress in normal cells. MBD4 binds to 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC) - oxidation products of TET2 dioxygenases - and may initiate a multi-step BER/MMR around mCpG/hmCpG DNA.

Published
2023
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