James Cleaver

Summary

Affiliation: University of California
Country: USA

Publications

  1. ncbi request reprint A novel role of DNA polymerase eta in modulating cellular sensitivity to chemotherapeutic agents
    Yih Wen Chen
    Department of Cell Biology and Neuroscience, University of South Alabama, 307 North University Boulevard, MSB 2350, Mobile, AL 36688, USA
    Mol Cancer Res 4:257-65. 2006
  2. doi request reprint Conceptual developments in the causes of Cockayne syndrome
    James E Cleaver
    Department of Dermatology, University of California San Francisco, 2340 Sutter Street, San Francisco, CA 94143, USA
    Mech Ageing Dev 134:284-90. 2013
  3. doi request reprint Photosensitivity syndrome brings to light a new transcription-coupled DNA repair cofactor
    James E Cleaver
    Department of Dermatology, University of California, San Francisco, California, USA
    Nat Genet 44:477-8. 2012
  4. ncbi request reprint Nucleotide excision repair "a legacy of creativity"
    J E Cleaver
    Department of Dermatology and UCSF Cancer Center, University of California, San Francisco, CA 94143 0808, USA
    Mutat Res 485:23-36. 2001
  5. ncbi request reprint Photoreactivation
    James E Cleaver
    Auerback Melanoma Laboratory, University of California, UCSF Cancer Center, Room N431, Box 0808, San Francisco, CA 94143 0808, USA
    DNA Repair (Amst) 2:629, 637-8. 2003
  6. ncbi request reprint Mechanisms by which human cells bypass damaged bases during DNA replication after ultraviolet irradiation
    James E Cleaver
    UCSF Cancer Center, University of California, San Francisco, USA
    ScientificWorldJournal 2:1296-305. 2002
  7. ncbi request reprint DNA replication in the face of (In)surmountable odds
    J E Cleaver
    Department of Dermatology and UCSF Cancer Center, University of California, San Francisco, California 94143 0808, USA
    Cell Cycle 2:310-5. 2003
  8. ncbi request reprint Genome sequence and splice site analysis of low-fidelity DNA polymerases H and I involved in replication of damaged DNA
    J E Cleaver
    UCSF Cancer Center, Box 0808, Room N431, University of California at San Francisco, San Francisco, CA 94143 0808, USA
    Genomics 82:561-70. 2003
  9. ncbi request reprint Excision repair--its bacterial beginnings
    James E Cleaver
    Auerbaok Melanoma Laboratory, UCSF Cancer Center, Room N431, University of California, PO Box 0808, San Francisco, CA 94143 0808, USA
    DNA Repair (Amst) 2:1273-4. 2003
  10. pmc Cockayne syndrome exhibits dysregulation of p21 and other gene products that may be independent of transcription-coupled repair
    J E Cleaver
    Auerback Melanoma Laboratory, Box 0808, Room N431, UCSF Cancer Center, University of California, San Francisco, CA 94143 0808, USA
    Neuroscience 145:1300-8. 2007

Research Grants

Collaborators

Detail Information

Publications45

  1. ncbi request reprint A novel role of DNA polymerase eta in modulating cellular sensitivity to chemotherapeutic agents
    Yih Wen Chen
    Department of Cell Biology and Neuroscience, University of South Alabama, 307 North University Boulevard, MSB 2350, Mobile, AL 36688, USA
    Mol Cancer Res 4:257-65. 2006
    ....
  2. doi request reprint Conceptual developments in the causes of Cockayne syndrome
    James E Cleaver
    Department of Dermatology, University of California San Francisco, 2340 Sutter Street, San Francisco, CA 94143, USA
    Mech Ageing Dev 134:284-90. 2013
    ..The source of nuclear DNA damage to central nervous system tissue most likely occurs from extrinsic neurotransmitter signaling...
  3. doi request reprint Photosensitivity syndrome brings to light a new transcription-coupled DNA repair cofactor
    James E Cleaver
    Department of Dermatology, University of California, San Francisco, California, USA
    Nat Genet 44:477-8. 2012
    ....
  4. ncbi request reprint Nucleotide excision repair "a legacy of creativity"
    J E Cleaver
    Department of Dermatology and UCSF Cancer Center, University of California, San Francisco, CA 94143 0808, USA
    Mutat Res 485:23-36. 2001
    ..With these fascinating problems to investigate, the field of DNA repair will surely not disappoint the next generation...
  5. ncbi request reprint Photoreactivation
    James E Cleaver
    Auerback Melanoma Laboratory, University of California, UCSF Cancer Center, Room N431, Box 0808, San Francisco, CA 94143 0808, USA
    DNA Repair (Amst) 2:629, 637-8. 2003
    ....
  6. ncbi request reprint Mechanisms by which human cells bypass damaged bases during DNA replication after ultraviolet irradiation
    James E Cleaver
    UCSF Cancer Center, University of California, San Francisco, USA
    ScientificWorldJournal 2:1296-305. 2002
    ..The resulting chromosomal instability in surviving cells will contribute to malignant transformation...
  7. ncbi request reprint DNA replication in the face of (In)surmountable odds
    J E Cleaver
    Department of Dermatology and UCSF Cancer Center, University of California, San Francisco, California 94143 0808, USA
    Cell Cycle 2:310-5. 2003
    ..A network of signaling kinases modulates the efficiency of many damage responsive proteins to tailor their activities and subcellular localizations by phosphorylation and dephosphorylation...
  8. ncbi request reprint Genome sequence and splice site analysis of low-fidelity DNA polymerases H and I involved in replication of damaged DNA
    J E Cleaver
    UCSF Cancer Center, Box 0808, Room N431, University of California at San Francisco, San Francisco, CA 94143 0808, USA
    Genomics 82:561-70. 2003
    ..This analysis explains previous observations of tissue-specific skipping during mRNA processing, resulting in the loss of the transcription start site in exon II, in human tissues...
  9. ncbi request reprint Excision repair--its bacterial beginnings
    James E Cleaver
    Auerbaok Melanoma Laboratory, UCSF Cancer Center, Room N431, University of California, PO Box 0808, San Francisco, CA 94143 0808, USA
    DNA Repair (Amst) 2:1273-4. 2003
    ..These reports were the starting point for subsequent development of the whole field of DNA excision point...
  10. pmc Cockayne syndrome exhibits dysregulation of p21 and other gene products that may be independent of transcription-coupled repair
    J E Cleaver
    Auerback Melanoma Laboratory, Box 0808, Room N431, UCSF Cancer Center, University of California, San Francisco, CA 94143 0808, USA
    Neuroscience 145:1300-8. 2007
    ....
  11. ncbi request reprint Cancer in xeroderma pigmentosum and related disorders of DNA repair
    James E Cleaver
    Auerback Melanoma Laboratory, Room N431, UCSF Cancer Center, University of California, 94143 0808, USA
    Nat Rev Cancer 5:564-73. 2005
    ..Complex clinical phenotypes might therefore result from unanticipated effects on other genes and proteins...
  12. ncbi request reprint Splitting hairs--discovery of a new DNA repair and transcription factor for the human disease trichothiodystrophy
    James E Cleaver
    Auerback Melanoma Laboratory, Room N431, UCSF Cancer Center, University of California, Box 0808, San Francisco, CA 94143 0808, USA
    DNA Repair (Amst) 4:285-7. 2005
    ....
  13. ncbi request reprint Ultraviolet photobiology: its early roots and insights into DNA repair
    James E Cleaver
    Auerback Melanoma Laboratory, UCSF Cancer Center, Room N431, Box 0808, University of California at San Francisco, 94143, USA
    DNA Repair (Amst) 1:977-9. 2002
    ..Most remarkably, a discovery of DNA repair by the use of split doses of UV light was reported in 1919. Later commentaries will take us sequentially through the early years of DNA repair...
  14. ncbi request reprint Polymerase eta and p53 jointly regulate cell survival, apoptosis and Mre11 recombination during S phase checkpoint arrest after UV irradiation
    J E Cleaver
    UCSF Comprehensive Cancer Center, University of California, 2340 Sutter Street, Box 0808, Room N 424, San Francisco, CA 94143, USA
    DNA Repair (Amst) 1:41-57. 2002
    ..The S phase checkpoints are therefore, a complex set of different checkpoints that are coordinated by p53 with the capacity to differentially modulate cell survival, apoptosis, bypass replication and hMre11 recombination...
  15. ncbi request reprint Mending human genes: a job for a lifetime
    James E Cleaver
    Auerback Melanoma Laboratory, UCSF Cancer Center, Box 0808, Room N431, University of California, San Francisco, CA 94143 0808, USA
    DNA Repair (Amst) 4:635-8. 2005
    ..This ushered in a new field of research involving numerous investigators and which continues to expand and amaze...
  16. ncbi request reprint Historical aspects of xeroderma pigmentosum and nucleotide excision repair
    James E Cleaver
    Auerback Melanoma Laboratory, UCSF Cancer Center, University of California, San Francisco, CA, USA
    Adv Exp Med Biol 637:1-9. 2008
    ....
  17. doi request reprint Disorders of nucleotide excision repair: the genetic and molecular basis of heterogeneity
    James E Cleaver
    Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California 94143 0981, USA
    Nat Rev Genet 10:756-68. 2009
    ..The mapping of mutations in recently solved protein structures has begun to clarify the links between the molecular defects and phenotypes, but the identification of additional sources of clinical variability is still necessary...
  18. doi request reprint γH2Ax: biomarker of damage or functional participant in DNA repair "all that glitters is not gold!"
    James E Cleaver
    Department of Dermatology, University of California, San Francisco, CA, USA
    Photochem Photobiol 87:1230-9. 2011
    ..Despite the prominence of S139 phosphorylation following UV damage, mutation of this site has no influence on the UV damage response indicating that γH2Ax is a biomarker but not a participant in the UV-DNA damage response...
  19. ncbi request reprint A summary of mutations in the UV-sensitive disorders: xeroderma pigmentosum, Cockayne syndrome, and trichothiodystrophy
    J E Cleaver
    UCSF Cancer Center and Department of Dermatology, University of California, San Francisco 94143 0808, USA
    Hum Mutat 14:9-22. 1999
    ..XP-E by this definition contains only those cell lines and patients that have mutations in the small subunit, DDB2, of a damage-specific DNA binding protein...
  20. ncbi request reprint Richard B. Setlow, a commentary on seminal contributions and scientific controversies
    J E Cleaver
    UCSF Cancer Center and Department of Dermatology, University of California, San Francisco, California 94143 0808, USA
    Environ Mol Mutagen 38:122-31. 2001
    ..Small reductions in the efficiency of repair, especially transcription-coupled repair, may overemphasize carcinogenesis in mice, while minimizing neurodegeneration, as compared to human patients...
  21. ncbi request reprint Common pathways for ultraviolet skin carcinogenesis in the repair and replication defective groups of xeroderma pigmentosum
    J E Cleaver
    Box 0808, UCSF Cancer Center, University of California San Francisco, San Francisco, CA 94143 0808, USA
    J Dermatol Sci 23:1-11. 2000
    ..The absence of pol eta would require cells to use the error-prone pol zeta pathway, also increasing mutation rates from UV damage. A common pathway for increased mutagenesis therefore underlies both forms of XP...
  22. pmc Clinical implications of the basic defects in Cockayne syndrome and xeroderma pigmentosum and the DNA lesions responsible for cancer, neurodegeneration and aging
    J E Cleaver
    Department of Dermatology and UCSF Cancer Center, University of California San Francisco, CA 94143 0808, USA
    Mech Ageing Dev 129:492-7. 2008
    ..specific pathways of DNA damage relevant to clinical outcomes; if naturally occurring reactive oxygen species are pathological in human repair deficient disease, would anti-oxidants or anti-apoptotic agents be feasible therapeutic agent?..
  23. ncbi request reprint Pol eta is required for DNA replication during nucleotide deprivation by hydroxyurea
    S de Feraudy
    Auerback Melanoma Laboratory, UCSF Cancer Center, University of California, San Francisco, CA, USA
    Oncogene 26:5713-21. 2007
    ..Our results suggest that hydroxyurea-induced apoptosis occurs at the G1/S boundary and that initiation of the S-phase requires greater nucleotide concentrations than does S-phase progression...
  24. ncbi request reprint DNA polymerase eta undergoes alternative splicing, protects against UV sensitivity and apoptosis, and suppresses Mre11-dependent recombination
    M Thakur
    UCSF Comprehensive Cancer Center, University of California, San Francisco, California 94115, USA
    Genes Chromosomes Cancer 32:222-35. 2001
    ..In normal cells, the predominant mechanism of replication of UV damage involves pol eta-dependent bypass, and Mre11-dependent recombination that acts is a secondary, backup mechanism when cells are severely depleted of pol eta...
  25. ncbi request reprint DNA replication arrest in XP variant cells after UV exposure is diverted into an Mre11-dependent recombination pathway by the kinase inhibitor wortmannin
    C L Limoli
    Department of Radiation Oncology, University of California, San Francisco, CA 94103 0806, USA
    Mutat Res 510:121-9. 2002
    ....
  26. ncbi request reprint Defective repair replication of DNA in xeroderma pigmentosum. 1968
    J E Cleaver
    Laboratory of Radiobiology, University of California Medical Center, San Francisco, California, USA
    DNA Repair (Amst) 3:183-87. 2004
    ..This discovery by James Cleaver had an important impact on our understanding of nucleotide excision repair in mammals.
  27. ncbi request reprint Increased ultraviolet sensitivity and chromosomal instability related to P53 function in the xeroderma pigmentosum variant
    J E Cleaver
    Department of Dermatology, University of California at San Francisco, 94143 0750, USA
    Cancer Res 59:1102-8. 1999
    ..The symptoms of elevated solar carcinogenesis in XPV patients may, therefore, be associated with increased genomic instability in cells of the skin in which p53 is inactivated by UV-induced mutations...
  28. pmc Increased apoptosis, p53 up-regulation, and cerebellar neuronal degeneration in repair-deficient Cockayne syndrome mice
    R R Laposa
    Department of Dermatology and Cancer Center, University of California, San Francisco, CA 94143 0808, USA
    Proc Natl Acad Sci U S A 104:1389-94. 2007
    ....
  29. ncbi request reprint Quantification of XPA gene expression levels in human and mouse cell lines by competitive RT-PCR
    S K Layher
    Laboratory of Radiobiology and Environmental Health, University of California, San Francisco 94143 0750, USA
    Mutat Res 383:9-19. 1997
    ..The similarity of results in human and mouse cells shows that a difference in XPA expression cannot account for the greater repair of nontranscribed DNA in human cells...
  30. ncbi request reprint Requirement for the Xrcc1 DNA base excision repair gene during early mouse development
    R S Tebbs
    Department of Dermatology, University of California at San Francisco, San Francisco, California, 94143, USA
    Dev Biol 208:513-29. 1999
    ....
  31. ncbi request reprint Relationship of neurologic degeneration to genotype in three xeroderma pigmentosum group G patients
    Steffen Emmert
    Basic Research Laboratory, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland 20892, USA
    J Invest Dermatol 118:972-82. 2002
    ..Retaining residual functional activity in one allele was associated with mild clinical features without neurologic abnormalities...
  32. ncbi request reprint Excision repair--the first steps into mammalian cells. 1968
    James E Cleaver
    DNA Repair (Amst) 3:91-9. 2004
  33. pmc p53 suppression overwhelms DNA polymerase eta deficiency in determining the cellular UV DNA damage response
    Rebecca R Laposa
    UCSF Comprehensive Cancer Center, Auerback Melanoma Laboratory, Room N461, Box 0808, University of California San Francisco, CA 94143 0808, United States
    DNA Repair (Amst) 6:1794-804. 2007
    ..Inhibition of p53 expression dominated the DNA damage response. Comparison with earlier results indicates that in virally transformed cells cellular targets other than p53 play important roles in the UV DNA damage response...
  34. ncbi request reprint Cambridge Laboratory of Molecular Biology
    James E Cleaver
    Science 300:1875. 2003
  35. pmc UV-induced replication arrest in the xeroderma pigmentosum variant leads to DNA double-strand breaks, gamma -H2AX formation, and Mre11 relocalization
    Charles L Limoli
    Department of Radiation Oncology, University of California, San Francisco, CA 94103 0806, USA
    Proc Natl Acad Sci U S A 99:233-8. 2002
    ..These UV-induced foci occur in cells that are unable to carry out efficient bypass replication of UV damage and may contribute to further genetic variation...
  36. ncbi request reprint Rescue of Xrcc1 knockout mouse embryo lethality by transgene-complementation
    Robert S Tebbs
    Biology and Biotechnology Research Program, L441, Lawrence Livermore National Laboratory, P O Box 808, Livermore, CA 94551 0808, USA
    DNA Repair (Amst) 2:1405-17. 2003
    ..The presence of XRCC1, even at reduced levels of expression, is therefore capable of supporting mouse development and DNA repair...
  37. ncbi request reprint Recapitulation of the cellular xeroderma pigmentosum-variant phenotypes using short interfering RNA for DNA polymerase H
    Rebecca R Laposa
    Department of Dermatology, University of California, San Francisco, California 94143 0808, USA
    Cancer Res 63:3909-12. 2003
    ..Therefore, suppression of POLH expression levels by siRNA recapitulates most of the phenotypes seen in cells from XP-V patients with inactivating mutations in POLH...
  38. ncbi request reprint Cells have long experience of dealing with UVC light
    James E Cleaver
    Nature 442:244. 2006
  39. ncbi request reprint Adenovirus mediated transduction of the human DNA polymerase eta cDNA
    Keronninn Moreno Lima-Bessa
    Department of Microbiology, Institute of Biomedical Sciences, University of Sao Paulo, Av Prof Lineu Prestes, 1374 São Paulo, SP 05508 900, Brazil
    DNA Repair (Amst) 5:925-34. 2006
    ..These results suggest that TLS by DNA polymerase eta is not a limiting factor for recovery from cellular responses induced by UV in excision-repair deficient fibroblasts...
  40. pmc H2AX phosphorylation within the G1 phase after UV irradiation depends on nucleotide excision repair and not DNA double-strand breaks
    Thomas M Marti
    Auerback Melanoma Laboratory, Room N461, Box 0808, UCSF Cancer Center, University of California San Francisco, San Francisco, CA 94143 0808, USA
    Proc Natl Acad Sci U S A 103:9891-6. 2006
    ....
  41. pmc DNA-PKcs function regulated specifically by protein phosphatase 5
    Thomas Wechsler
    Department of Microbiology and Immunology and UCSF Cancer Center, University of California, San Francisco, CA 94143, USA
    Proc Natl Acad Sci U S A 101:1247-52. 2004
    ..Cells with either hypo- or hyperphosphorylation of DNA-PKcs at these sites show increased radiation sensitivity...
  42. ncbi request reprint UV damage, DNA repair and skin carcinogenesis
    James E Cleaver
    UCSF Cancer Center and Department of Dermatology, Box 0808, University of California, San Francisco, CA 94143 0808, USA
    Front Biosci 7:d1024-43. 2002
    ..The subsequent development of malignant tumors involves many additional genomic changes that have yet to be fully cataloged...
  43. pmc Search for a prion-specific nucleic acid
    Jiri G Safar
    Institute for Neurodegenerative Diseases, University of California, San Francisco 94143 0518, USA
    J Virol 79:10796-806. 2005
    ....
  44. pmc Genes and pathways downstream of telomerase in melanoma metastasis
    Sepideh Bagheri
    Auerback Melanoma Research Laboratory, Cutaneous Oncology Program, Comprehensive Cancer Center, University of California, San Francisco, CA 94115, USA
    Proc Natl Acad Sci U S A 103:11306-11. 2006
    ..These studies have important implications for understanding the mechanisms by which telomerase promotes tumor invasion and metastasis...
  45. pmc Xeroderma pigmentosum group C in an isolated region of Guatemala
    James E Cleaver
    J Invest Dermatol 127:493-6. 2007

Research Grants12

  1. DNA Damage and Neurodegeneration in Cockayne Syndrome
    James Cleaver; Fiscal Year: 2007
    ..Successful conclusion of these studies will expand our knowledge of mechanisms of neurodegeneration and lay groundwork for development of therapeutic approaches for CS patients. ..
  2. The XP Variant: A Human Mutator Gene for UV Damage
    James Cleaver; Fiscal Year: 2005
    ..We will express hRad3O on the keratin 14 promoter for over-expression in the skin, and make targeted knockout of mRad3O in vivo to identify roles for hRad3O in promoting and preventing carcinogenesis. ..
  3. XP VARIANT--A HUMAN MUTATOR GENE FOR UV DAMAGE
    James Cleaver; Fiscal Year: 2000
    ....
  4. DNA Damage and Neurodegeneration in Cockayne Syndrome
    James Cleaver; Fiscal Year: 2009
    ..Successful conclusion of these studies will expand our knowledge of mechanisms of neurodegeneration and lay groundwork for development of therapeutic approaches for CS patients. ..