Philip J Brooks

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. pmc Polyamines stimulate the formation of mutagenic 1,N2-propanodeoxyguanosine adducts from acetaldehyde
    Jacob A Theruvathu
    Section on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, NIH 5625 Fishers Lane, Room 3S32, MSC 9412, Bethesda, MD 20952 9412, USA
    Nucleic Acids Res 33:3513-20. 2005
  2. doi request reprint Blinded by the UV light: how the focus on transcription-coupled NER has distracted from understanding the mechanisms of Cockayne syndrome neurologic disease
    P J Brooks
    Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, NIH, 5625 Fishers Lane, 3S 32, Bethesda, MD 20892, USA
    DNA Repair (Amst) 12:656-71. 2013
  3. doi request reprint Moderate alcohol consumption and breast cancer in women: from epidemiology to mechanisms and interventions
    Philip J Brooks
    Division of Metabolism and Health Effects, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892 9304, USA
    Alcohol Clin Exp Res 37:23-30. 2013
  4. ncbi request reprint DNA adducts from acetaldehyde: implications for alcohol-related carcinogenesis
    Philip J Brooks
    Section on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, 5625 Fishers Lane, Room 3S32, MSC 9412, Bethesda, MD 20892 9412, USA
    Alcohol 35:187-93. 2005
  5. pmc Do all of the neurologic diseases in patients with DNA repair gene mutations result from the accumulation of DNA damage?
    P J Brooks
    Section on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, 5625 Fishers Lane, Room 3S32, Rockville, MD 20852, USA
    DNA Repair (Amst) 7:834-48. 2008
  6. pmc The 8,5'-cyclopurine-2'-deoxynucleosides: candidate neurodegenerative DNA lesions in xeroderma pigmentosum, and unique probes of transcription and nucleotide excision repair
    P J Brooks
    Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892 9412, USA
    DNA Repair (Amst) 7:1168-79. 2008
  7. ncbi request reprint DNA repair in neural cells: basic science and clinical implications
    P J Brooks
    Section on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, 12420 Parklawn Drive, MSC 8110, Bethesda, MD 20892 8110, USA
    Mutat Res 509:93-108. 2002
  8. pmc The case for 8,5'-cyclopurine-2'-deoxynucleosides as endogenous DNA lesions that cause neurodegeneration in xeroderma pigmentosum
    P J Brooks
    Section on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, 5625 Fishers Lane, Room 3S32, MSC 9412, Rockville, MD 20852, USA
    Neuroscience 145:1407-17. 2007
  9. doi request reprint Acetaldehyde and the genome: beyond nuclear DNA adducts and carcinogenesis
    Philip J Brooks
    Division of Metabolism and Health Effects, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland
    Environ Mol Mutagen 55:77-91. 2014
  10. ncbi request reprint A single 8,5'-cyclo-2'-deoxyadenosine lesion in a TATA box prevents binding of the TATA binding protein and strongly reduces transcription in vivo
    Cheryl Marietta
    Section on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD 20892 8110, USA
    DNA Repair (Amst) 1:967-75. 2002

Collaborators

Detail Information

Publications25

  1. pmc Polyamines stimulate the formation of mutagenic 1,N2-propanodeoxyguanosine adducts from acetaldehyde
    Jacob A Theruvathu
    Section on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, NIH 5625 Fishers Lane, Room 3S32, MSC 9412, Bethesda, MD 20952 9412, USA
    Nucleic Acids Res 33:3513-20. 2005
    ..We propose that AA derived from ethanol metabolism is converted to CrA by polyamines in dividing cells, forming Cr-PdG adducts, which may be responsible for the carcinogenicity of alcoholic beverage consumption...
  2. doi request reprint Blinded by the UV light: how the focus on transcription-coupled NER has distracted from understanding the mechanisms of Cockayne syndrome neurologic disease
    P J Brooks
    Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, NIH, 5625 Fishers Lane, 3S 32, Bethesda, MD 20892, USA
    DNA Repair (Amst) 12:656-71. 2013
    ..The implications of these ideas for interpreting results from mouse models of CS, and for the development of treatments and therapies for CS patients are discussed. ..
  3. doi request reprint Moderate alcohol consumption and breast cancer in women: from epidemiology to mechanisms and interventions
    Philip J Brooks
    Division of Metabolism and Health Effects, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892 9304, USA
    Alcohol Clin Exp Res 37:23-30. 2013
    ..Such mechanistic information is also important for the development of rational clinical interventions to reduce ethanol-related breast cancer mortality...
  4. ncbi request reprint DNA adducts from acetaldehyde: implications for alcohol-related carcinogenesis
    Philip J Brooks
    Section on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, 5625 Fishers Lane, Room 3S32, MSC 9412, Bethesda, MD 20892 9412, USA
    Alcohol 35:187-93. 2005
    ..Inherited variation in the genes encoding the proteins involved in the repair of PdG and its secondary adducts may contribute to susceptibility to alcoholic beverage-related carcinogenesis...
  5. pmc Do all of the neurologic diseases in patients with DNA repair gene mutations result from the accumulation of DNA damage?
    P J Brooks
    Section on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, 5625 Fishers Lane, Room 3S32, Rockville, MD 20852, USA
    DNA Repair (Amst) 7:834-48. 2008
    ..We discuss the implications of these different disease mechanisms for the rational development of treatments and therapies...
  6. pmc The 8,5'-cyclopurine-2'-deoxynucleosides: candidate neurodegenerative DNA lesions in xeroderma pigmentosum, and unique probes of transcription and nucleotide excision repair
    P J Brooks
    Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892 9412, USA
    DNA Repair (Amst) 7:1168-79. 2008
    ....
  7. ncbi request reprint DNA repair in neural cells: basic science and clinical implications
    P J Brooks
    Section on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, 12420 Parklawn Drive, MSC 8110, Bethesda, MD 20892 8110, USA
    Mutat Res 509:93-108. 2002
    ....
  8. pmc The case for 8,5'-cyclopurine-2'-deoxynucleosides as endogenous DNA lesions that cause neurodegeneration in xeroderma pigmentosum
    P J Brooks
    Section on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, 5625 Fishers Lane, Room 3S32, MSC 9412, Rockville, MD 20852, USA
    Neuroscience 145:1407-17. 2007
    ..A similar set of criteria might be used to evaluate other candidate DNA lesions responsible for neurological diseases resulting from defects in other DNA repair mechanisms as well...
  9. doi request reprint Acetaldehyde and the genome: beyond nuclear DNA adducts and carcinogenesis
    Philip J Brooks
    Division of Metabolism and Health Effects, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland
    Environ Mol Mutagen 55:77-91. 2014
    ..In summary, a comprehensive understanding of all of the mechanisms by which acetaldehyde impacts the function of the genome has implications not only for alcohol and cancer, but types of alcohol related pathologies as well...
  10. ncbi request reprint A single 8,5'-cyclo-2'-deoxyadenosine lesion in a TATA box prevents binding of the TATA binding protein and strongly reduces transcription in vivo
    Cheryl Marietta
    Section on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD 20892 8110, USA
    DNA Repair (Amst) 1:967-75. 2002
    ..In addition, the approach we used in this study represents a novel method for assessing the effects of DNA lesions in non-transcribed sequences on gene expression in living cells...
  11. pmc Transcriptional bypass of bulky DNA lesions causes new mutant RNA transcripts in human cells
    Cheryl Marietta
    Section on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, 5625 Fishers Lane, Room 3S 32, MSC 9412, Bethesda, Maryland 20892, USA
    EMBO Rep 8:388-93. 2007
    ..These results indicate that RNA pol II in living human cells can bypass helix-distorting DNA lesions that are substrates for nucleotide excision repair, resulting in transcriptional mutagenesis...
  12. pmc The oxidatively induced DNA lesions 8,5'-cyclo-2'-deoxyadenosine and 8-hydroxy-2'-deoxyadenosine are strongly resistant to acid-induced hydrolysis of the glycosidic bond
    Jacob A Theruvathu
    Section on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, 5625 Fishers Lane, Room 3S 32, MSC 9412, Bethesda, MD 20952 9412, USA
    Mech Ageing Dev 128:494-502. 2007
    ....
  13. pmc Differential blocking effects of the acetaldehyde-derived DNA lesion N2-ethyl-2'-deoxyguanosine on transcription by multisubunit and single subunit RNA polymerases
    Tsu Fan Cheng
    Section on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland 20892, USA
    J Biol Chem 283:27820-8. 2008
    ..We also include models of the N(2)-Et-dG within the active site of yeast RNAPII, which are compatible with our observations...
  14. ncbi request reprint Brain atrophy and neuronal loss in alcoholism: a role for DNA damage?
    P J Brooks
    Section on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, NIH, 12420 Parklawn Drive, MSC 8110, MD 20892 8110, Bethesda, USA
    Neurochem Int 37:403-12. 2000
    ..This results in neuronal death either by reduction in the levels of essential gene products or by apoptosis. The implications of this model for future studies are discussed...
  15. ncbi request reprint Detection of excision nuclease in cell-free extracts from the adult mammalian brain
    P J Brooks
    Section on Molecular Neurobiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20852, USA
    Mutat Res 408:37-46. 1998
    ..These results indicate that the NER pathway is functional in neuronal cells in the adult brain. The implications of this finding for XP and other neurodegenerative diseases is discussed...
  16. ncbi request reprint The oxidative DNA lesion 8,5'-(S)-cyclo-2'-deoxyadenosine is repaired by the nucleotide excision repair pathway and blocks gene expression in mammalian cells
    P J Brooks
    Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland 20892, USA
    J Biol Chem 275:22355-62. 2000
    ..Based on these findings, we propose that cyclo-dA is a candidate for an endogenous DNA lesion that might contribute to neurodegeneration in XP...
  17. doi request reprint Divergent effects of oxidatively induced modification to the C8 of 2'-deoxyadenosine on transcription factor binding: 8,5'(S)-cyclo-2'-deoxyadenosine inhibits the binding of multiple sequence specific transcription factors, while 8-oxo-2'-deoxyadenosine i
    Jessy Abraham
    Section on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20852, USA
    Environ Mol Mutagen 52:287-95. 2011
    ..The cyclo-dAdo lesion, in contrast, distorted the DNA structure, providing an explanation for the inhibition of NF-kappaB binding...
  18. ncbi request reprint Expression of long-patch and short-patch DNA mismatch repair proteins in the embryonic and adult mammalian brain
    C Marietta
    Section on Molecular Neurobiology, Laboratory of Neurogenetics, NIH DICBR NIAAA LNG, 12420 Parklawn Drive, Room 451 MSC 8110, Bethesda, MD 20892 8110, USA
    Brain Res Mol Brain Res 53:317-20. 1998
    ..These results suggest that adult brain cells have the capacity to carry out DNA mismatch repair, in spite of a lack of ongoing DNA replication...
  19. pmc ATM, the Mre11/Rad50/Nbs1 complex, and topoisomerase I are concentrated in the nucleus of Purkinje neurons in the juvenile human brain
    Elena Gorodetsky
    Section on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, 5625 Fishers Lane, Room 3S 32, MSC 9412, Bethesda, MD 20952 9412, USA
    DNA Repair (Amst) 6:1698-707. 2007
    ..Our results have direct implications for understanding the mechanisms of neurodegeneration in AT and AT-like disorder...
  20. ncbi request reprint DNA repair in human fibroblasts, as reflected by host-cell reactivation of a transfected UV-irradiated luciferase gene, is not related to donor age
    Thomas J Merkle
    Dermatology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Mutat Res 554:9-17. 2004
    ..44). Our study provides no indication that the higher incidence of skin cancer observed with increasing age is due to an age-related decrease in the ability to repair UV-induced DNA damage...
  21. pmc Acetaldehyde stimulates FANCD2 monoubiquitination, H2AX phosphorylation, and BRCA1 phosphorylation in human cells in vitro: implications for alcohol-related carcinogenesis
    Cheryl Marietta
    Section on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, 5625 Fishers Lane, Room 3S32, Rockville, MD 20852, United States
    Mutat Res 664:77-83. 2009
    ..We discuss the mechanistic implications of these results, as well as their possible relationship to alcohol-related carcinogenesis in different human tissues...
  22. ncbi request reprint Overexpression of an epitope-tagged serotonin transporter in serotonin neurons of the dorsal raphe nucleus using a defective HSV-1 vector
    Yajin Ni
    Section of Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20892 8110, USA
    Behav Brain Res 138:133-43. 2003
    ..These data demonstrate that the levels of the 5HTT in 5HT neurons can be manipulated in the adult rodent brain using an HSV-1 vector...
  23. pmc Enhancement of camptothecin-induced topoisomerase I cleavage complexes by the acetaldehyde adduct N2-ethyl-2'-deoxyguanosine
    Smitha Antony
    Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 4255, USA
    Nucleic Acids Res 32:5685-92. 2004
    ....
  24. pmc Complete release of (5'S)-8,5'-cyclo-2'-deoxyadenosine from dinucleotides, oligodeoxynucleotides and DNA, and direct comparison of its levels in cellular DNA with other oxidatively induced DNA lesions
    Pawel Jaruga
    Department of Chemical and Biochemical Engineering, University of Maryland Baltimore County, MD 22777, USA
    Nucleic Acids Res 32:e87. 2004
    ..We conclude that (5'S)-cdA can be completely released from DNA by enzymic hydrolysis, and the level of (5'S)-cdA in tissue DNA is comparable to those of other oxidatively induced DNA lesions...