Angelica Barreto-Galvez

ORCID: 0000-0002-3731-6741
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About
Contact & Profiles
Research Areas
  • DNA Repair Mechanisms
  • Genomics and Chromatin Dynamics
  • T-cell and Retrovirus Studies
  • Genetics and Neurodevelopmental Disorders
  • Occupational and environmental lung diseases
  • CRISPR and Genetic Engineering
  • Protein Degradation and Inhibitors
  • RNA Interference and Gene Delivery
  • Research in Cotton Cultivation
  • Epigenetics and DNA Methylation
  • Disaster Response and Management
  • Histone Deacetylase Inhibitors Research
  • Injury Epidemiology and Prevention
  • Chromosomal and Genetic Variations
  • Vector-Borne Animal Diseases

Rutgers, The State University of New Jersey
2019-2025

Rutgers Cancer Institute of New Jersey
2019-2025

Johnson University
2019-2022

Significance Common fragile sites (CFSs) are normal loci that genetically unstable under and oncogenic replication stress. Pol eta has been proposed to play a key role in CFS replication. Here, we show the absence of eta, at five specific is perturbed, with fork pausing observed several sites. Sequence analysis showed certain pause associated presence non-B DNA motifs, while others not. Importantly, located within regions increased genetic variation healthy human populations could be...

10.1073/pnas.2106477118 article EN cc-by Proceedings of the National Academy of Sciences 2021-11-23

The replicative polymerase delta is inefficient copying repetitive DNA sequences. Error-prone translesion polymerases have been shown to switch with high-fidelity help navigate DNA. We and others demonstrated the importance of one such polymerase, Eta (pol eta), in facilitating replication at genomic regions called common fragile sites (CFS), which are difficult-to-replicate that hypersensitive stress. However, mechanistic basis for pol eta's role CFS and(or) other currently unclear....

10.1101/2025.01.06.631600 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2025-01-08

Abstract Mutations in the epigenetic regulator and global transcriptional activator, E1A binding protein (EP300), is being increasingly reported aggressive hematological malignancies including adult T-cell leukemia/lymphoma (ATLL). However, mechanistic contribution of EP300 dysregulation to cancer initiation progression are currently unknown. Independent inhibition human cells results differential expression genes involved regulating cell cycle, DNA replication damage response. Nevertheless,...

10.1101/2023.04.29.538781 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-04-29
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