Richard B. Pearson focuses on Molecular biology, Cancer research, PI3K/AKT/mTOR pathway, Cell biology and Protein kinase B. His studies deal with areas such as HMGA2, Gene knockdown, Ribosome biogenesis, Phosphorylation and Transcription as well as Molecular biology. Richard B. Pearson has researched Ribosome biogenesis in several fields, including RNA polymerase I, Transcription factor and P70-S6 Kinase 1.
His study in Phosphorylation is interdisciplinary in nature, drawing from both Cell and Peptide sequence. His Cancer research research incorporates themes from Cancer and Mutant. He interconnects Angiogenesis and PTEN in the investigation of issues within Protein kinase B.
The scientist’s investigation covers issues in Cancer research, Cell biology, PI3K/AKT/mTOR pathway, Protein kinase B and Biochemistry. Richard B. Pearson has researched Cancer research in several fields, including Ribosome biogenesis, Cancer, Ovarian cancer and Transcription. While the research belongs to areas of Ribosome biogenesis, Richard B. Pearson spends his time largely on the problem of Molecular biology, intersecting his research to questions surrounding RNA polymerase I, Ribosomal protein, Cell and Mutant.
Regulation of gene expression is closely connected to Transcription factor in his research, which is encompassed under the umbrella topic of Cell biology. His study in PI3K/AKT/mTOR pathway is interdisciplinary in nature, drawing from both Carcinogenesis and Cell growth. His Phosphorylation study combines topics from a wide range of disciplines, such as P-type ATPase, Kinase and ATP7A.
Cancer research, Gene, Cancer, Transcription and Melanoma are his primary areas of study. His studies deal with areas such as Translation, Ribosome biogenesis, Ovarian cancer and DNA damage as well as Cancer research. His Translation research integrates issues from mTORC1, Protein kinase B and PI3K/AKT/mTOR pathway.
His biological study spans a wide range of topics, including Computational biology and Cell biology. In general Transcription study, his work on RNA polymerase I often relates to the realm of Nucleolus, thereby connecting several areas of interest. His research integrates issues of Oncogene, Cyclin-dependent kinase 6, Kinase and Cyclin-dependent kinase 4 in his study of Melanoma.
His primary areas of investigation include Cancer research, Gene, RNA polymerase I, Transcription and Cyclin-dependent kinase 4. His studies in Cancer research integrate themes in fields like PARP inhibitor, DNA methylation, Cancer cell, Ovarian cancer and In vivo. His Gene research includes themes of Network medicine, Systems biology and Cell type.
The RNA polymerase I study combines topics in areas such as Heterochromatin, Molecular biology, Genome instability and ATRX. His Transcription research is multidisciplinary, incorporating elements of Toxicity, Anaplastic large-cell lymphoma, Adverse effect and Ribosome biogenesis. The study incorporates disciplines such as Melanoma, Oncogene and Cyclin-dependent kinase 6 in addition to Cyclin-dependent kinase 4.
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Protein kinase recognition sequence motifs
Bruce E. Kemp;Richard B. Pearson.
Trends in Biochemical Sciences (1990)
Protein kinase phosphorylation site sequences and consensus specificity motifs: tabulations.
Richard B. Pearson;Bruce E. Kemp.
Methods in Enzymology (1991)
Rapamycin suppresses 5′TOP mRNA translation through inhibition of p70s6k
Harold B.J. Jefferies;Stefano Fumagalli;Patrick B. Dennis;Christoph Reinhard.
The EMBO Journal (1997)
Mutation of the PIK3CA gene in ovarian and breast cancer.
Ian G. Campbell;Sarah E. Russell;David Y. H. Choong;Karen G. Montgomery.
Cancer Research (2004)
A potent synthetic peptide inhibitor of the cAMP-dependent protein kinase.
Heung-Chin Cheng;B. E. Kemp;R. B. Pearson;A. J. Smith.
Journal of Biological Chemistry (1986)
The Akt kinase signals directly to endothelial nitric oxide synthase.
B.J. Michell;J.E. Griffiths;K.I. Mitchelhill;I. Rodriguez-Crespo.
Current Biology (1999)
mTOR-dependent regulation of ribosomal gene transcription requires S6K1 and is mediated by phosphorylation of the carboxy-terminal activation domain of the nucleolar transcription factor UBF.
Katherine M. Hannan;Yves Brandenburger;Anna Jenkins;Kerith Sharkey.
Molecular and Cellular Biology (2003)
The principal target of rapamycin-induced p70s6k inactivation is a novel phosphorylation site within a conserved hydrophobic domain.
R. B. Pearson;P. B. Dennis;J.-W. Han;N. A. Williamson.
The EMBO Journal (1995)
Inhibition of RNA polymerase I as a therapeutic strategy to promote cancer-specific activation of p53.
Megan J Bywater;Gretchen Poortinga;Gretchen Poortinga;Elaine Sanij;Elaine Sanij;Nadine Hein.
Cancer Cell (2012)
Genomic Dissection of Bipolar Disorder and Schizophrenia, Including 28 Subphenotypes
Douglas M. Ruderfer;Stephan Ripke;Stephan Ripke;Stephan Ripke;Andrew McQuillin;James Boocock.
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