Stanford University
United States
Katrin F. Chua mainly focuses on Chromatin, Cell biology, DNA damage, Histone H3 and DNA repair. The Chromatin study combines topics in areas such as Histone, Sirtuin and Cancer research. Her Cell biology research integrates issues from Histone deacetylase, SIRT7, SIRT6 and FOXO Family.
Her DNA damage study integrates concerns from other disciplines, such as Molecular biology and Mutant. Her Histone H3 study incorporates themes from Regulation of gene expression and Haploinsufficiency. Her DNA repair study deals with Genome instability intersecting with Base excision repair, MDC1, Stem cell and Histone H2AX.
Her main research concerns Chromatin, Cell biology, Histone, Genetics and Biochemistry. Her Chromatin research incorporates themes from SIRT7, SIRT6 and Sirtuin. Her SIRT7 research is multidisciplinary, incorporating perspectives in Transcription factor and Epigenetics.
Her study in Cell biology is interdisciplinary in nature, drawing from both Genome instability, Histone deacetylase, Chromatin silencing, DNA repair and Heterochromatin. Katrin F. Chua regularly ties together related areas like Molecular biology in her Histone studies. Her Histone H3 research is multidisciplinary, relying on both Carcinogenesis, H3K4me3 and SIRT3.
Katrin F. Chua mostly deals with Chromatin, Cell biology, Acetylation, Biochemistry and Histone. Her research on Chromatin focuses in particular on Histone H3. Her SIRT7 research extends to the thematically linked field of Cell biology.
The various areas that she examines in her SIRT7 study include DNA, SIRT6, Genome maintenance, Nucleosome and Heterochromatin. Her Acetylation research is multidisciplinary, incorporating elements of Peptide sequence, Subcellular localization, Peptide and Transactivation. Her work on SIRT2, Active site and Structure–activity relationship as part of general Biochemistry study is frequently connected to Isoquercetin and Allosteric regulation, therefore bridging the gap between diverse disciplines of science and establishing a new relationship between them.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
Stress-Dependent Regulation of FOXO Transcription Factors by the SIRT1 Deacetylase
Anne Brunet;Lora B. Sweeney;J. Fitzhugh Sturgill;Katrin F. Chua.
Science (2004)
Genomic Instability and Aging-like Phenotype in the Absence of Mammalian SIRT6
Raul Mostoslavsky;Katrin F. Chua;Katrin F. Chua;David B. Lombard;Wendy W. Pang.
Cell (2006)
Developmental defects and p53 hyperacetylation in Sir2 homolog (SIRT1)-deficient mice
Hwei-Ling Cheng;Raul Mostoslavsky;Shin'ichi Saito;John P. Manis.
Proceedings of the National Academy of Sciences of the United States of America (2003)
SIRT6 is a histone H3 lysine 9 deacetylase that modulates telomeric chromatin
Eriko Michishita;Ronald A. McCord;Elisabeth Berber;Mitomu Kioi.
Nature (2008)
ING2 PHD domain links histone H3 lysine 4 methylation to active gene repression
Xiaobing Shi;Tao Hong;Kay L. Walter;Mark Ewalt.
Nature (2006)
DNA Repair, Genome Stability, and Aging
David B. Lombard;Katrin F. Chua;Raul Mostoslavsky;Sonia Franco.
Cell (2005)
SIRT6 Links Histone H3 Lysine 9 Deacetylation to NF-κB-Dependent Gene Expression and Organismal Life Span
Tiara L.A. Kawahara;Eriko Michishita;Eriko Michishita;Adam S. Adler;Mara Damian;Mara Damian.
Cell (2009)
Transcription-targeted DNA deamination by the AID antibody diversification enzyme
Jayanta Chaudhuri;Ming Tian;Chan Khuong;Katrin Chua.
Nature (2003)
Increased ionizing radiation sensitivity and genomic instability in the absence of histone H2AX
Craig H. Bassing;Katrin F. Chua;Jo Ann Sekiguchi;Heikyung Suh.
Proceedings of the National Academy of Sciences of the United States of America (2002)
Histone H2AX: a dosage-dependent suppressor of oncogenic translocations and tumors.
Craig H. Bassing;Heikyung Suh;David O. Ferguson;David O. Ferguson;Katrin F. Chua.
Cell (2003)
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