Research Topics
Genomes and GenesSpecies | James CleaverSummaryAffiliation: University of California Country: USA Publications
Research Grants
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Detail Information
Publications
A novel role of DNA polymerase eta in modulating cellular sensitivity to chemotherapeutic agentsYih 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....
Photosensitivity syndrome brings to light a new transcription-coupled DNA repair cofactorJames E Cleaver
Department of Dermatology, University of California, San Francisco, California, USA
Nat Genet 44:477-8. 2012....
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...
Mechanisms by which human cells bypass damaged bases during DNA replication after ultraviolet irradiationJames 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...
Historical aspects of xeroderma pigmentosum and nucleotide excision repairJames E Cleaver
Auerback Melanoma Laboratory, UCSF Cancer Center, University of California, San Francisco, CA, USA
Adv Exp Med Biol 637:1-9. 2008....
DNA replication in the face of (In)surmountable oddsJ 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...
Clinical implications of the basic defects in Cockayne syndrome and xeroderma pigmentosum and the DNA lesions responsible for cancer, neurodegeneration and agingJ 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?..
Genome sequence and splice site analysis of low-fidelity DNA polymerases H and I involved in replication of damaged DNAJ 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...
Excision repair--its bacterial beginningsJames 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...
Splitting hairs--discovery of a new DNA repair and transcription factor for the human disease trichothiodystrophyJames 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....
Mending human genes: a job for a lifetimeJames 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...
Cockayne syndrome exhibits dysregulation of p21 and other gene products that may be independent of transcription-coupled repairJ 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....
Cancer in xeroderma pigmentosum and related disorders of DNA repairJames 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...
PhotoreactivationJames 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....
Ultraviolet photobiology: its early roots and insights into DNA repairJames 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...
Polymerase eta and p53 jointly regulate cell survival, apoptosis and Mre11 recombination during S phase checkpoint arrest after UV irradiationJ 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...
A summary of mutations in the UV-sensitive disorders: xeroderma pigmentosum, Cockayne syndrome, and trichothiodystrophyJ 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...
Disorders of nucleotide excision repair: the genetic and molecular basis of heterogeneityJames 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...
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...
Common pathways for ultraviolet skin carcinogenesis in the repair and replication defective groups of xeroderma pigmentosumJ 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...
Richard B. Setlow, a commentary on seminal contributions and scientific controversiesJ 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...
Pol eta is required for DNA replication during nucleotide deprivation by hydroxyureaS 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...
DNA polymerase eta undergoes alternative splicing, protects against UV sensitivity and apoptosis, and suppresses Mre11-dependent recombinationM 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...
DNA replication arrest in XP variant cells after UV exposure is diverted into an Mre11-dependent recombination pathway by the kinase inhibitor wortmanninC L Limoli
Department of Radiation Oncology, University of California, San Francisco, CA 94103-0806, USA
Mutat Res 510:121-9. 2002....
Defective repair replication of DNA in xeroderma pigmentosum. 1968J 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.
Increased ultraviolet sensitivity and chromosomal instability related to P53 function in the xeroderma pigmentosum variantJ 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...
Increased apoptosis, p53 up-regulation, and cerebellar neuronal degeneration in repair-deficient Cockayne syndrome miceR 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....
Quantification of XPA gene expression levels in human and mouse cell lines by competitive RT-PCRS 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...
Requirement for the Xrcc1 DNA base excision repair gene during early mouse developmentR S Tebbs
Department of Dermatology, University of California at San Francisco, San Francisco, California, 94143, USA
Dev Biol 208:513-29. 1999....
p53 suppression overwhelms DNA polymerase eta deficiency in determining the cellular UV DNA damage responseRebecca 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...
Cells have long experience of dealing with UVC lightJames E Cleaver
Nature 442:244. 2006
Adenovirus mediated transduction of the human DNA polymerase eta cDNAKeronninn Moreno Lima-Bessa
Department of Microbiology, Institute of Biomedical Sciences, , Av. Prof. Lineu Prestes, , 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...
H2AX phosphorylation within the G1 phase after UV irradiation depends on nucleotide excision repair and not DNA double-strand breaksThomas 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....
UV damage, DNA repair and skin carcinogenesisJames 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...
Relationship of neurologic degeneration to genotype in three xeroderma pigmentosum group G patientsSteffen 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...
Cambridge Laboratory of Molecular BiologyJames E Cleaver
Science 300:1875. 2003
Recapitulation of the cellular xeroderma pigmentosum-variant phenotypes using short interfering RNA for DNA polymerase HRebecca 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...
Rescue of Xrcc1 knockout mouse embryo lethality by transgene-complementationRobert 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...
Excision repair--the first steps into mammalian cells. 1968James E Cleaver
DNA Repair (Amst) 3:91-9. 2004
DNA-PKcs function regulated specifically by protein phosphatase 5Thomas 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...
UV-induced replication arrest in the xeroderma pigmentosum variant leads to DNA double-strand breaks, gamma -H2AX formation, and Mre11 relocalizationCharles 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...
Search for a prion-specific nucleic acidJiri G Safar
Institute for Neurodegenerative Diseases, University of California, San Francisco 94143-0518, USA
J Virol 79:10796-806. 2005....
Xeroderma pigmentosum group C in an isolated region of GuatemalaJames E Cleaver
J Invest Dermatol 127:493-6. 2007
Genes and pathways downstream of telomerase in melanoma metastasisSepideh 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...
Research Grants
- DNA Damage and Neurodegeneration in Cockayne SyndromeJames 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. ..
- The XP Variant: A Human Mutator Gene for UV DamageJames 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. ..
- XP VARIANT--A HUMAN MUTATOR GENE FOR UV DAMAGEJames Cleaver; Fiscal Year: 2000....
- DNA Damage and Neurodegeneration in Cockayne SyndromeJames 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. ..
