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by Amps, Katherine and Andrews, Peter W and Anyfantis, George and Armstrong, Lyle and Avery, Stuart and Baharvand, Hossein and Baker, Julie and Baker, Duncan and Munoz, Maria B and Beil, Stephen and Benvenisty, Nissim and Ben-Yosef, Dalit and Biancotti, Juan-Carlos and Bosman, Alexis and Brena, Romulo Martin and Brison, Daniel and Caisander, Gunilla and Camarasa, Marãa V and Chen, Jieming and Chiao, Eric and Choi, Young Min and Choo, Andre B. H and Collins, Daniel and Colman, Alan and Crook, Jeremy M and Daley, George Q and Dalton, Anne and De Sousa, Paul A and Denning, Chris and Downie, Janet and Dvorak, Petr and Montgomery, Karen D and Feki, Anis and Ford, Angela and Fox, Victoria and Fraga, Ana M and Frumkin, Tzvia and Ge, Lin and Gokhale, Paul J and Golan-Lev, Tamar and Gourabi, Hamid and Gropp, Michal and Guangxiu, Lu and Hampl, Ales and Harron, Katie and Healy, Lyn and Herath, Wishva and Holm, Frida and Hovatta, Outi and Hyllner, Johan and Inamdar, Maneesha S and Irwanto, Astrid Kresentia and Ishii, Tetsuya and Jaconi, Marisa and Jin, Ying and Kimber, Susan and Kiselev, Sergey and Knowles, Barbara B and Kopper, Oded and Kukharenko, Valeri and Kuliev, Anver and Lagarkova, Maria A and Laird, Peter W and Lako, Majlinda and Laslett, Andrew L and Lavon, Neta and Lee, Dong Ryul and Lee, Jeoung Eun and Li, Chunliang and Lim, Linda S and Ludwig, Tenneille E and Ma, Yu and Maltby, Edna and Mateizel, Ileana and Mayshar, Yoav and Mileikovsky, Maria and Minger, Stephen L and Miyazaki, Takamichi and Moon, Shin Yong and Moore, Harry and Mummery, Christine and Nagy, Andras and Nakatsuji, Norio and Narwani, Kavita and Oh, Steve K. W and Oh, Sun Kyung and Olson, Cia and Otonkoski, Timo and Pan, Fei and Park, In-Hyun and Pells, Steve and Pera, Martin F and Pereira, Lygia V and Qi, Ouyang and Raj, Grace Selva and Reubinoff, Benjamin and Robins, Alan and Robson, Paul and Rossant, Janet and Salekdeh, Ghasem H and ... and Int Stem Cell Initiative and International Stem Cell Initiative and The International Stem Cell Initiative
Nature Biotechnology, ISSN 1087-0156, 12/2011, Volume 29, Issue 12, pp. 1132 - 1144
Journal Article
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 08/2013, Volume 123, Issue 8, pp. 3600 - 3613
Dysfunctional bone morphogenetic protein receptor-2 (BMPR2) signaling is implicated in the pathogenesis of pulmonary arterial hypertension (PAH). We used a... 
MEDICINE, RESEARCH & EXPERIMENTAL | GENE | BONE MORPHOGENETIC PROTEIN | ARTERIAL-HYPERTENSION | HEART-FAILURE | IN-VIVO | APELIN | SMOOTH-MUSCLE-CELLS | TGF-BETA RECEPTOR | EXPRESSION | T-CELLS | Cell Proliferation | Humans | Microvessels - pathology | Male | Cell Hypoxia | Tacrolimus - pharmacology | Hypertension, Pulmonary - drug therapy | Endothelial Cells - physiology | Bone Morphogenetic Protein Receptors, Type II - genetics | Signal Transduction | Bone Morphogenetic Protein 4 - physiology | Endothelium, Vascular - physiopathology | Rats | Hypertension, Pulmonary - metabolism | Inhibitor of Differentiation Protein 1 - metabolism | Neointima - metabolism | Rats, Sprague-Dawley | Bone Morphogenetic Protein Receptors, Type II - metabolism | Mice, Knockout | Animals | High-Throughput Screening Assays | Neointima - drug therapy | Neointima - pathology | Tacrolimus Binding Protein 1A - metabolism | Cell Line, Tumor | Inhibitor of Differentiation Protein 1 - genetics | Endothelium, Vascular - pathology | Mice | Hypertension, Pulmonary - pathology | Smad Proteins - metabolism | Pulmonary Artery - pathology | Apoptosis | Endothelial Cells - drug effects | Hypertension | Cell receptors | Physiological aspects | Cellular signal transduction | Research | Properties | Endothelium | Proteins | Medical research | Scholarships & fellowships | Research & development--R&D | Pulmonary arteries | Rodents | Hypoxia | Ligands | Mutation | Drug dosages
Journal Article
Nature Genetics, ISSN 1061-4036, 2014, Volume 46, Issue 5, pp. 451 - 456
Journal Article
Cancer Cell, ISSN 1535-6108, 06/2012, Volume 21, Issue 6, pp. 777 - 792
There is increasing evidence that some cancers are hierarchically organized, sustained by a relatively rare population of cancer-initiating cells (C-ICs).... 
HUMAN COLORECTAL-CARCINOMA | STEM-CELLS | ONCOLOGY | INDUCED APOPTOSIS | PROTECTIVE ROLE | PROSTATE-CANCER | DNA-DAMAGE | ACUTE MYELOID-LEUKEMIA | ID-1 PROTEIN | EXPRESSION | HUMAN PANCREATIC-CANCER | CELL BIOLOGY | Cell Cycle - genetics | Colonic Neoplasms - genetics | Neoplastic Stem Cells - drug effects | Colonic Neoplasms - drug therapy | Humans | Gene Expression Regulation, Neoplastic | Spheroids, Cellular - pathology | Inhibitor of Differentiation Proteins - genetics | Neoplasm Proteins - metabolism | Organoplatinum Compounds - pharmacology | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Neoplastic Stem Cells - metabolism | RNA Interference | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Neoplastic Stem Cells - pathology | Antineoplastic Agents - pharmacology | Spheroids, Cellular - drug effects | Tumor Cells, Cultured | Neoplasm Proteins - genetics | Spheroids, Cellular - metabolism | Inhibitor of Differentiation Proteins - metabolism | Inhibitor of Differentiation Protein 1 - metabolism | Mice, SCID | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Xenograft Model Antitumor Assays | Microscopy, Confocal | Animals | Colonic Neoplasms - pathology | Inhibitor of Differentiation Protein 1 - genetics | Mice, Inbred NOD | Cell Proliferation - drug effects | Mice | Cell Cycle - drug effects | Chemotherapy | Genes | Cancer | Tumors
Journal Article
Biochimie, ISSN 0300-9084, 05/2015, Volume 112, pp. 139 - 150
The four known ID proteins (ID1-4, Inhibitor of Differentiation) share a homologous helix loop helix (HLH) domain and act as dominant negative regulators of... 
ID4 | DNA-Protein interaction | Protein–protein interaction | Tumor suppressor gene | Cancer | Protein-protein interaction | DOXORUBICIN-INDUCED APOPTOSIS | UNFAVORABLE PROGNOSIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | TUMOR-SUPPRESSOR GENES | POOR DIFFERENTIATION | CELLULAR SENESCENCE | NEGATIVE REGULATOR | BREAST-CANCER | EPIGENETIC INACTIVATION | PROSTATE-CANCER CELLS | EXPRESSION PATTERN | Prostatic Neoplasms - metabolism | Prostatic Neoplasms - pathology | Basic Helix-Loop-Helix Transcription Factors - genetics | Humans | Inhibitor of Differentiation Proteins - genetics | Inhibitor of Differentiation Protein 1 - antagonists & inhibitors | Male | Neoplasm Proteins - antagonists & inhibitors | Inhibitor of Differentiation Proteins - metabolism | Inhibitor of Differentiation Protein 1 - metabolism | Neoplasm Proteins - metabolism | Inhibitor of Differentiation Protein 2 - metabolism | Inhibitor of Differentiation Proteins - antagonists & inhibitors | Prostatic Neoplasms - genetics | Basic Helix-Loop-Helix Transcription Factors - metabolism | Inhibitor of Differentiation Protein 2 - genetics | Cell Line, Tumor | Inhibitor of Differentiation Protein 1 - genetics | Inhibitor of Differentiation Protein 2 - antagonists & inhibitors | Transcription, Genetic | Neoplasm Proteins - genetics | Proteins | DNA | Genetic research | Genetic aspects | Genetic transcription | Prostate cancer | DNA-ligand interactions | protein-protein interaction | cancer | DNA-protein interaction | tumor suppressor gene
Journal Article