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Scientific Reports, ISSN 2045-2322, 04/2016, Volume 6, Issue 1, p. 23820
Journal Article
Molecular and Cellular Biology, ISSN 0270-7306, 06/2017, Volume 37, Issue 11
Journal Article
Science, ISSN 0036-8075, 02/2019, Volume 363, Issue 6427, pp. 639 - 639
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 2/2016, Volume 113, Issue 5, pp. 1387 - 1392
Journal Article
Proceedings of the National Academy of Sciences of the United States, ISSN 0027-8424, 02/2017, Volume 114, Issue 7, p. 1148
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 02/2017, Volume 114, Issue 7, p. E1148
  Wnt signaling, named after the secreted proteins that bind to cell surface receptors to activate the pathway, plays critical roles both in embryonic... 
Proteins | Enzymes | Signal transduction | Homeostasis | Mutation | Binding sites
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 02/2017, Volume 114, Issue 7, pp. E1148 - E1157
Journal Article
PLoS ONE, ISSN 1932-6203, 2011, Volume 6, Issue 3, p. e14789
Protein tyrosine kinase 6 (PTK6), also called breast tumor kinase (BRK), is expressed in epithelial cells of various tissues including the prostate. Previously... 
ANDROGEN RECEPTOR | BREAST-TUMOR KINASE | OXIDATIVE STRESS | CELL FACTOR | PROSTATE-CANCER | GASTROINTESTINAL-TRACT | BIOLOGY | SMALL-INTESTINE | DISTINCT FAMILY | BRK | EXPRESSION | Colonic Neoplasms - genetics | Phosphorylation | Cell Proliferation | Protein-Tyrosine Kinases - metabolism | Humans | Gene Expression Regulation, Neoplastic | Male | Neoplasm Proteins - metabolism | RNA, Messenger - metabolism | Cell Nucleus - enzymology | TCF Transcription Factors - metabolism | Protein-Tyrosine Kinases - genetics | Prostatic Neoplasms - genetics | Transcription, Genetic | Neoplasm Proteins - genetics | Repressor Proteins - metabolism | Prostatic Neoplasms - pathology | Tumor Stem Cell Assay | Alternative Splicing - genetics | RNA, Messenger - genetics | beta Catenin - metabolism | beta Catenin - antagonists & inhibitors | Colonic Neoplasms - pathology | Cell Line, Tumor | Prostatic Neoplasms - enzymology | Colonic Neoplasms - enzymology | TCF Transcription Factors - genetics | Adenocarcinoma | Cell proliferation | Biotechnology | Alternative splicing | Cell culture | Transcription | Epithelial cells | c-Myc protein | Insulin-like growth factors | Biochemistry | Myc protein | Kinases | Cyclin D1 | Tissues | Nuclei | Proteins | β-catenin | Hepatitis | Site selection | Rodents | Cell cycle | Inhibition | Colon | Localization | Vascular endothelial growth factor | Protein-tyrosine kinase | Hepatitis delta virus | Tyrosine | Breast cancer | Substrates | Medicine | Polymerase chain reaction | Signaling | Acids | Cell lines | Nuclei (cytology) | Mutation | Prostate cancer | Prostate | Tumors | Cancer
Journal Article
Genes and Development, ISSN 0890-9369, 05/2013, Volume 27, Issue 10, pp. 1101 - 1114
Tumorigenesis results from dysregulation of oncogenes and tumor suppressors that influence cellular proliferation, differentiation, apoptosis, and/or... 
Huwe1 | c-Myc | Mule | Ras | p21 | Miz1 | DNA-DAMAGE | KERATINOCYTE GROWTH | DEVELOPMENTAL BIOLOGY | CELL BIOLOGY | BASE EXCISION-REPAIR | HUWE1 UBIQUITIN LIGASE | NEGATIVE REGULATION | GENETICS & HEREDITY | ARF TUMOR-SUPPRESSOR | DIFFERENTIATION | MIZ-1 | HUMAN CANCER | Protein Inhibitors of Activated STAT - deficiency | Tetradecanoylphorbol Acetate - pharmacology | 9,10-Dimethyl-1,2-benzanthracene - pharmacology | Male | Protein Inhibitors of Activated STAT - metabolism | Cyclin-Dependent Kinase Inhibitor p15 - biosynthesis | Oncogene Protein p21(ras) - metabolism | Cyclin-Dependent Kinase Inhibitor p16 | Oncogene Protein p21(ras) - antagonists & inhibitors | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Cell Transformation, Neoplastic - genetics | Cyclin-Dependent Kinase Inhibitor p15 - genetics | Nuclear Proteins - deficiency | Protein Inhibitors of Activated STAT - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Female | Nuclear Proteins - genetics | Protein Inhibitors of Activated STAT - antagonists & inhibitors | Skin Neoplasms - pathology | Cyclin-Dependent Kinase Inhibitor p21 - biosynthesis | Signal Transduction | Down-Regulation | Cells, Cultured | Ubiquitin-Protein Ligases - metabolism | Nuclear Proteins - metabolism | Skin Neoplasms - chemically induced | Proto-Oncogene Proteins c-myc - metabolism | Mice, Knockout | Skin Neoplasms - metabolism | Keratinocytes - pathology | Animals | Tumor Suppressor Protein p53 | Keratinocytes - drug effects | Keratinocytes - metabolism | Nuclear Proteins - antagonists & inhibitors | Proto-Oncogene Proteins c-myc - deficiency | Skin Neoplasms - genetics | Proto-Oncogene Proteins c-myc - antagonists & inhibitors | Ubiquitin-Protein Ligases - deficiency | Mice | Proto-Oncogene Proteins c-myc - genetics | Cyclin-Dependent Kinase Inhibitor p15 - metabolism | Genes, ras | Ubiquitin-Protein Ligases - genetics | Oncogene Protein p21(ras) - genetics | Carcinogenesis | Ras genes | Analysis | Research Paper
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 02/2016, Volume 113, Issue 5, p. 1387
  Gain-of-function mutations in isocitrate dehydrogenase 1 (IDH1) are key drivers of hematopoietic malignancies. Although these mutations are most commonly... 
Lymphocytes | Rodents | Genetic engineering | Mutation | Gene expression | Cancer
Journal Article
Proceedings of the National Academy of Sciences, ISSN 0027-8424, 02/2016, Volume 113, Issue 5, pp. 1387 - 1392
Journal Article
Proceedings of the National Academy of Sciences, USA, ISSN 0027-8424, 02/2016, Volume 113, Issue 5, pp. 1387 - 1387
Gain-of-function mutations in isocitrate dehydrogenase 1 (IDH1) are key drivers of hematopoietic malignancies. Although these mutations are most commonly... 
Journal Article
Molecular and cellular biology, 06/2017, Volume 37, Issue 11
Journal Article