Search Results - "Mertz, Tony"

Refine Results
  1. 1

    APOBEC3A is a prominent cytidine deaminase in breast cancer by Cortez, Luis M, Brown, Amber L, Dennis, Madeline A, Collins, Christopher D, Brown, Alexander J, Mitchell, Debra, Mertz, Tony M, Roberts, Steven A

    Published in PLoS genetics (01-12-2019)
    “…APOBEC cytidine deaminases are the second-most prominent source of mutagenesis in sequenced tumors. Previous studies have proposed that APOBEC3B (A3B) is the…”
    Get full text
    Journal Article
  2. 2

    APOBEC3A and APOBEC3B Preferentially Deaminate the Lagging Strand Template during DNA Replication by Hoopes, James I., Cortez, Luis M., Mertz, Tony M., Malc, Ewa P., Mieczkowski, Piotr A., Roberts, Steven A.

    Published in Cell reports (Cambridge) (16-02-2016)
    “…APOBEC family cytidine deaminases have recently been implicated as powerful mutators of cancer genomes. How APOBECs, which are ssDNA-specific enzymes, gain…”
    Get full text
    Journal Article
  3. 3

    Her2 amplification, Rel-A, and Bach1 can influence APOBEC3A expression in breast cancer cells by Dennis, Madeline, Hurley, Alyssa, Bray, Nicholas, Cordero, Cameron, Ilagan, Jose, Mertz, Tony M, Roberts, Steven A

    Published in PLoS genetics (28-05-2024)
    “…APOBEC-induced mutations occur in 50% of sequenced human tumors, with APOBEC3A (A3A) being a major contributor to mutagenesis in breast cancer cells. The…”
    Get full text
    Journal Article
  4. 4

    APOBEC-Induced Mutagenesis in Cancer by Mertz, Tony M, Collins, Christopher D, Dennis, Madeline, Coxon, Margo, Roberts, Steven A

    Published in Annual review of genetics (30-11-2022)
    “…The initiation, progression, and relapse of cancers often result from mutations occurring within somatic cells. Consequently, processes that elevate mutation…”
    Get full text
    Journal Article
  5. 5

    Colon cancer-associated mutator DNA polymerase δ variant causes expansion of dNTP pools increasing its own infidelity by Mertz, Tony M., Sharma, Sushma, Chabes, Andrei, Shcherbakova, Polina V.

    “…Significance Mutations affecting replicative DNA polymerases δ (Polδ) and ε (Polε) are linked to sporadic and hereditary colorectal cancer and sporadic…”
    Get full text
    Journal Article
  6. 6

    Single-stranded DNA binding proteins influence APOBEC3A substrate preference by Brown, Amber L., Collins, Christopher D., Thompson, Secily, Coxon, Margo, Mertz, Tony M., Roberts, Steven A.

    Published in Scientific reports (25-10-2021)
    “…The cytidine deaminase, APOBEC3A (A3A), is a prominent source of mutations in multiple cancer types. These APOBEC-signature mutations are non-uniformly…”
    Get full text
    Journal Article
  7. 7

    Genetic inhibitors of APOBEC3B-induced mutagenesis by Mertz, Tony M, Rice-Reynolds, Elizabeth, Nguyen, Ly, Wood, Anna, Cordero, Cameron, Bray, Nicholas, Harcy, Victoria, Vyas, Rudri K, Mitchell, Debra, Lobachev, Kirill, Roberts, Steven A

    Published in Genome research (01-09-2023)
    “…The cytidine deaminases APOBEC3A (A3A) and APOBEC3B (A3B) are prominent mutators of human cancer genomes. However, tumor-specific genetic modulators of…”
    Get full text
    Journal Article
  8. 8

    A reversible histone H3 acetylation cooperates with mismatch repair and replicative polymerases in maintaining genome stability by Kadyrova, Lyudmila Y, Mertz, Tony M, Zhang, Yu, Northam, Matthew R, Sheng, Ziwei, Lobachev, Kirill S, Shcherbakova, Polina V, Kadyrov, Farid A

    Published in PLoS genetics (01-10-2013)
    “…Mutations are a major driving force of evolution and genetic disease. In eukaryotes, mutations are produced in the chromatin environment, but the impact of…”
    Get full text
    Journal Article
  9. 9

    Risks at the DNA Replication Fork: Effects upon Carcinogenesis and Tumor Heterogeneity by Mertz, Tony M, Harcy, Victoria, Roberts, Steven A

    Published in Genes (22-01-2017)
    “…The ability of all organisms to copy their genetic information via DNA replication is a prerequisite for cell division and a biological imperative of life. In…”
    Get full text
    Journal Article Book Review
  10. 10

    DNA polymerase ζ-dependent lesion bypass in Saccharomyces cerevisiae is accompanied by error-prone copying of long stretches of adjacent DNA by Kochenova, Olga V, Daee, Danielle L, Mertz, Tony M, Shcherbakova, Polina V

    Published in PLoS genetics (01-03-2015)
    “…Translesion synthesis (TLS) helps cells to accomplish chromosomal replication in the presence of unrepaired DNA lesions. In eukaryotes, the bypass of most…”
    Get full text
    Journal Article
  11. 11
  12. 12

    DNA polymerases ζ and Rev1 mediate error-prone bypass of non-B DNA structures by Northam, Matthew R, Moore, Elizabeth A, Mertz, Tony M, Binz, Sara K, Stith, Carrie M, Stepchenkova, Elena I, Wendt, Kathern L, Burgers, Peter M J, Shcherbakova, Polina V

    Published in Nucleic acids research (01-01-2014)
    “…DNA polymerase ζ (Pol ζ) and Rev1 are key players in translesion DNA synthesis. The error-prone Pol ζ can also participate in replication of undamaged DNA when…”
    Get full text
    Journal Article
  13. 13

    cancer-associated DNA polymerase δ variant modeled in yeast causes a catastrophic increase in genomic instability by Daee, Danielle L, Mertz, Tony M, Shcherbakova, Polina V

    “…Accurate DNA synthesis by the replicative DNA polymerases α, δ, and ε is critical for genome stability in eukaryotes. In humans, over 20 SNPs were reported…”
    Get full text
    Journal Article
  14. 14

    Histone deacetylase complexes promote trinucleotide repeat expansions by Debacker, Kim, Frizzell, Aisling, Gleeson, Olive, Kirkham-McCarthy, Lucy, Mertz, Tony, Lahue, Robert S

    Published in PLoS biology (01-02-2012)
    “…Expansions of DNA trinucleotide repeats cause at least 17 inherited neurodegenerative diseases, such as Huntington's disease. Expansions can occur at…”
    Get full text
    Journal Article
  15. 15

    An impaired ubiquitin-proteasome system increases APOBEC3A abundance by Coxon, Margo, Dennis, Madeline A, Dananberg, Alexandra, Collins, Christopher D, Wilson, Hannah E, Meekma, Jordyn, Savenkova, Marina I, Ng, Daniel, Osbron, Chelsea A, Mertz, Tony M, Goodman, Alan G, Duttke, Sascha H, Maciejowski, John, Roberts, Steven A

    Published in NAR cancer (01-12-2023)
    “…Apolipoprotein B messenger RNA (mRNA) editing enzyme, catalytic polypeptide-like (APOBEC) cytidine deaminases cause genetic instability during cancer…”
    Get full text
    Journal Article
  16. 16
  17. 17

    DNA polymerase [zeta]-dependent lesion bypass in Saccharomyces cerevisiae is accompanied by error-prone copying of long stretches of adjacent DNA by Kochenova, Olga V, Daee, Danielle L, Mertz, Tony M, Shcherbakova, Polina V

    Published in PLoS genetics (01-03-2015)
    “…Translesion synthesis (TLS) helps cells to accomplish chromosomal replication in the presence of unrepaired DNA lesions. In eukaryotes, the bypass of most…”
    Get full text
    Journal Article
  18. 18

    Postreplication Repair Inhibits CAG · CTG Repeat Expansions in Saccharomyces cerevisiae by Daee, Danielle L., Mertz, Tony, Lahue, Robert S.

    Published in Molecular and Cellular Biology (01-01-2007)
    “…Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley…”
    Get full text
    Journal Article
  19. 19

    Colon cancer-associated mutator DNA polymerase d variant causes expansion of dNTP pools increasing its own infidelity by Mertz, Tony M, Sharma, Sushma, Chabes, Andrei, Shcherbakova, Polina V

    “…Defects in DNA polymerases ... (Pol...) and ... (Pol...) cause hereditary colorectal cancer and have been implicated in the etiology of some sporadic…”
    Get full text
    Journal Article
  20. 20

    Nucleotide selectivity defect and mutator phenotype conferred by a colon cancer-associated DNA polymerase δ mutation in human cells by Mertz, T M, Baranovskiy, A G, Wang, J, Tahirov, T H, Shcherbakova, P V

    Published in Oncogene (01-08-2017)
    “…Mutations in the POLD1 and POLE genes encoding DNA polymerases δ (Polδ) and ɛ (Polɛ) cause hereditary colorectal cancer (CRC) and have been found in many…”
    Get full text
    Journal Article