His primary scientific interests are in Molecular biology, Cell biology, Histone, DNA damage and Chromatin. His research in Molecular biology intersects with topics in Processivity, STIM1 and Genome instability. The various areas that Michael J. Kruhlak examines in his Cell biology study include CTLA-4, Cell membrane and Antigen.
In general Histone study, his work on Histone methyltransferase and Histone H2A often relates to the realm of Histone code, thereby connecting several areas of interest. His DNA damage research entails a greater understanding of DNA. His Chromatin research is multidisciplinary, relying on both Cell cycle and MDC1.
Michael J. Kruhlak spends much of his time researching Cell biology, Molecular biology, Chromatin, Cancer research and Immunology. His work carried out in the field of Cell biology brings together such families of science as DNA, DNA damage, Ezrin, Radixin and Chromatin remodeling. His Molecular biology research is multidisciplinary, incorporating elements of RNA, Ataxia-telangiectasia, Lytic cycle and Viral replication.
Michael J. Kruhlak has researched Chromatin in several fields, including Histone, Transcription factor and Microscopy. His Cancer research study deals with Immunotherapy intersecting with Induced pluripotent stem cell. In his study, Macrophage is inextricably linked to Microbiology, which falls within the broad field of Immunology.
Michael J. Kruhlak mainly focuses on Cell biology, Cancer research, Organelle, Transcription factor and Chromatin. His Cell biology research includes elements of Sarcomere organization, RAD51, Homologous recombination, Mutation and Gene silencing. Michael J. Kruhlak combines subjects such as DNA damage, Ubiquitin, Synthetic lethality and Effector with his study of Homologous recombination.
The study incorporates disciplines such as Tumor necrosis factor alpha, Chromophobe cell, Clear cell, PD-L1 and Adenocarcinoma in addition to Cancer research. His Organelle research includes themes of Golgi apparatus, Endoplasmic reticulum and Cell cycle, CEP63, Centrosome. His Transcription factor study integrates concerns from other disciplines, such as Promoter, Transcription and Activator.
The scientist’s investigation covers issues in Cell biology, Chromatin, Transcription, Activator and Gene. He has included themes like RAD51 and Homologous recombination in his Cell biology study. The concepts of his RAD51 study are interwoven with issues in Ubiquitin, Ubiquitin ligase, Synthetic lethality, PARP inhibitor and Haploinsufficiency.
His studies in Homologous recombination integrate themes in fields like Mutation and DNA damage, Genome instability. His Transcription study incorporates themes from Promoter, Regulation of gene expression, Transcription factor and Genome.
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Histone H2AX phosphorylation is dispensable for the initial recognition of DNA breaks
Arkady Celeste;Oscar Fernandez-Capetillo;Michael J. Kruhlak;Duane R. Pilch.
Nature Cell Biology (2003)
Changes in chromatin structure and mobility in living cells at sites of DNA double-strand breaks
Michael J. Kruhlak;Arkady Celeste;Graham Dellaire;Oscar Fernandez-Capetillo.
Journal of Cell Biology (2006)
Inhibition of the intestinal glucose transporter GLUT2 by flavonoids
Oran Kwon;Peter Eck;Shenglin Chen;Christopher P. Corpe.
The FASEB Journal (2007)
TLR9 Is Localized in the Endoplasmic Reticulum Prior to Stimulation
Cynthia A. Leifer;Margaret N. Kennedy;Alessandra Mazzoni;ChangWoo Lee.
Journal of Immunology (2004)
53BP1 facilitates long-range DNA end-joining during V(D)J recombination
Simone Difilippantonio;Eric Gapud;Nancy Wong;Ching Yu Huang.
Heterochromatin is refractory to gamma-H2AX modification in yeast and mammals.
Jung-Ae Kim;Michael Kruhlak;Farokh Dotiwala;André Nussenzweig.
Journal of Cell Biology (2007)
Regulation of Histone Deacetylase 4 by Binding of 14-3-3 Proteins
Audrey H. Wang;Michael J. Kruhlak;Jiong Wu;Nicholas R. Bertos.
Molecular and Cellular Biology (2000)
53BP1 mediates productive and mutagenic DNA repair through distinct phosphoprotein interactions
Elsa Callen;Michela Di Virgilio;Michael J. Kruhlak;Maria Nieto-Soler.
Cooperative Epigenetic Modulation by Cancer Amplicon Genes
Lixin Rui;N. C.Tolga Emre;Michael J. Kruhlak;Hye Jung Chung.
Cancer Cell (2010)
The ATM repair pathway inhibits RNA polymerase I transcription in response to chromosome breaks.
Michael Kruhlak;Elizabeth E. Crouch;Marika Orlov;Carolina Montaño.
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