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1. Full Text Diverse epigenetic strategies interact to control epidermal differentiation
by Mulder, Klaas W and Wang, Xin and Escriu, Carles and Ito, Yoko and Schwarz, Roland F and Gillis, Jesse and Sirokmány, Gábor and Donati, Giacomo and Uribe-Lewis, Santiago and Pavlidis, Paul and Murrell, Adele and Markowetz, Florian and Watt, Fiona M
Nature Cell Biology, ISSN 1465-7392, 07/2012, Volume 14, Issue 7, pp. 753 - 763
It is becoming clear that interconnected functional gene networks, rather than individual genes, govern stem cell self-renewal and differentiation. To identify... 
STEM-CELLS | CHROMATIN | TISSUE | KERATINOCYTES | GENETIC INTERACTION | PHD FINGER | SKIN | P63 | EXPRESSION | MICE LACKING | CELL BIOLOGY | Antigens, Nuclear - metabolism | Epigenesis, Genetic | Humans | Multiprotein Complexes | Integrins - genetics | Gene Regulatory Networks | RNA, Messenger - metabolism | Stem Cells - metabolism | Integrins - metabolism | DNA-Binding Proteins - metabolism | Cell Differentiation - genetics | Transfection | RNA Interference | Tumor Suppressor Proteins - genetics | CCAAT-Enhancer-Binding Proteins - genetics | Stem Cell Niche - genetics | CCAAT-Enhancer-Binding Proteins - metabolism | Cell Adhesion - genetics | Tumor Suppressor Proteins - metabolism | Chromosomal Proteins, Non-Histone - metabolism | Cells, Cultured | Gene Expression Regulation | Adenosine Triphosphatases - metabolism | Chromatin Assembly and Disassembly | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Nerve Tissue Proteins - genetics | Enhancer of Zeste Homolog 2 Protein | Chromosomal Proteins, Non-Histone - genetics | Nerve Tissue Proteins - metabolism | Transcription Factors - metabolism | Polycomb Repressive Complex 2 | Antigens, Nuclear - genetics | Keratinocytes - metabolism | Bayes Theorem | Adenosine Triphosphatases - genetics | Models, Genetic | Cluster Analysis | Epidermis - cytology | Physiological aspects | Epigenetic inheritance | Genetic aspects | Research | Cell differentiation | Stem cells | Index Medicus
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2. Full Text BET Bromodomain Inhibition Suppresses the Function of Hematopoietic Transcription Factors in Acute Myeloid Leukemia
by Roe, Jae-Seok and Mercan, Fatih and Rivera, Keith and Pappin, Darryl J and Vakoc, Christopher R
Molecular Cell, ISSN 1097-2765, 06/2015, Volume 58, Issue 6, pp. 1028 - 1039
The bromodomain and extraterminal (BET) protein BRD4 is a validated drug target in leukemia, yet its regulatory function in this disease is not well... 
SELECTIVE-INHIBITION | RECRUITMENT | C/EBP-ALPHA | CREB-BINDING PROTEIN | CHROMATIN | ACETYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | IN-VIVO | C-MYC | P-TEFB | BRD4 | CELL BIOLOGY | Transcriptional Regulator ERG | NIH 3T3 Cells | Oncogene Proteins - genetics | Humans | Leukemia, Myeloid - genetics | Proto-Oncogene Proteins c-myb - genetics | Gene Expression Profiling | Leukemia, Myeloid - pathology | RNA Interference | Proto-Oncogene Protein c-fli-1 - metabolism | Protein Binding - drug effects | Trans-Activators - genetics | Nuclear Proteins - genetics | Proto-Oncogene Proteins - metabolism | Acute Disease | Proto-Oncogene Protein c-fli-1 - genetics | CCAAT-Enhancer-Binding Protein-beta - genetics | Oncogene Proteins - metabolism | Nuclear Proteins - metabolism | Proto-Oncogene Proteins - genetics | Transcription Factors - antagonists & inhibitors | Transcription Factors - genetics | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | CCAAT-Enhancer-Binding Protein-beta - metabolism | Proto-Oncogene Proteins c-myb - metabolism | Azepines - pharmacology | Transcription Factors - metabolism | Triazoles - pharmacology | Acetylation - drug effects | Animals | Hematopoietic System - metabolism | Leukemia, Myeloid - metabolism | Nuclear Proteins - antagonists & inhibitors | Cell Line, Tumor | Trans-Activators - metabolism | Mice | Histones - metabolism | DNA binding proteins | Medicine, Experimental | Medical research | Chromatin | Lysine | Index Medicus
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3. Full Text Novel susceptibility variants at 10p12.31-12.2 for childhood acute lymphoblastic leukemia in ethnically diverse populations
by Xu, Heng and Yang, Wenjian and Perez-Andreu, Virginia and Devidas, Meenakshi and Fan, Yiping and Cheng, Cheng and Pei, Deqing and Scheet, Paul and Burchard, Esteban González and Eng, Celeste and Huntsman, Scott and Torgerson, Dara G and Dean, Michael and Winick, Naomi J and Martin, Paul L and Camitta, Bruce M and Bowman, W. Paul and Willman, Cheryl L and Carroll, William L and Mullighan, Charles G and Bhojwani, Deepa and Hunger, Stephen P and Pui, Ching-Hon and Evans, William E and Relling, Mary V and Loh, Mignon L and Yang, Jun J
Journal of the National Cancer Institute, ISSN 0027-8874, 05/2013, Volume 105, Issue 10, pp. 733 - 742
Background Acute lymphoblastic leukemia (ALL) is the most common cancer in children and the incidence of ALL varies by ethnicity. Although accumulating... 
COMMON VARIANTS | COMPLEX | GENETIC POLYMORPHISMS | ONCOLOGY | CANCER INCIDENCE | DISEASE | MISSING HERITABILITY | RISK | LOCI | CONTRIBUTES | GENOME-WIDE ASSOCIATION | Humans | Child, Preschool | Male | Ikaros Transcription Factor - genetics | Female | CCAAT-Enhancer-Binding Proteins - genetics | Neoplasm Proteins - genetics | Child | European Continental Ancestry Group - genetics | Genetic Predisposition to Disease | Genome-Wide Association Study | Hispanic Americans - genetics | Risk Assessment | Risk Factors | African Americans - genetics | Logistic Models | Phosphotransferases (Alcohol Group Acceptor) - genetics | Mitogen-Activated Protein Kinase 7 - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics | Precursor Cell Lymphoblastic Leukemia-Lymphoma - ethnology | Adolescent | Polymorphism, Single Nucleotide | Chromosomes, Human, Pair 10 - genetics | Chromosomes, Human, Pair 7 - genetics | Chromosomes, Human, Pair 14 - genetics | Demographic aspects | Genetic susceptibility | Genetic variation | Analysis | Genetic aspects | Acute lymphocytic leukemia | Research | Risk factors | Ethnicity | Genomes | Multiculturalism & pluralism | Leukemia | Childrens health | Index Medicus
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4. Full Text CHOP potentially co-operates with FOXO3a in neuronal cells to regulate PUMA and BIM expression in response to ER stress
by Ghosh, Arindam P and Klocke, Barbara J and Ballestas, Mary E and Roth, Kevin A
PLoS ONE, ISSN 1932-6203, 06/2012, Volume 7, Issue 6, pp. e39586 - e39586
Endoplasmic reticulum (ER) stress-induced apoptosis has been implicated in various neurodegenerative diseases including Parkinson Disease, Alzheimer Disease... 
MITOCHONDRIAL APOPTOSIS | TRANSCRIPTION FACTOR CHOP | UNFOLDED PROTEIN RESPONSE | INDUCED APOPTOSIS | KINASE | BIOLOGY | GENE-EXPRESSION | SYMPATHETIC NEURONS | DEATH | ENDOPLASMIC-RETICULUM STRESS | BH3-ONLY PROTEINS | Transcription Factor CHOP - genetics | Apoptosis - drug effects | Neurons - cytology | Bcl-2-Like Protein 11 | Forkhead Transcription Factors - metabolism | Telencephalon - drug effects | Tumor Suppressor Proteins - genetics | Apoptosis Regulatory Proteins - genetics | Membrane Proteins - metabolism | Neurons - metabolism | Neurons - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Cell Survival - physiology | Proto-Oncogene Proteins - metabolism | Cell Survival - drug effects | Tumor Suppressor Proteins - metabolism | Telencephalon - metabolism | Telencephalon - cytology | Membrane Proteins - genetics | Proto-Oncogene Proteins - genetics | Forkhead Transcription Factors - genetics | Apoptosis Regulatory Proteins - metabolism | Animals | Signal Transduction - drug effects | Tunicamycin - pharmacology | Signal Transduction - physiology | Mice | Apoptosis - physiology | Forkhead Box Protein O3 | Transcription Factor CHOP - metabolism | Endoplasmic Reticulum Stress - physiology | Nervous system diseases | Parkinson's disease | Huntington's chorea | Neurons | Tumor proteins | Protein kinases | Apoptosis | Phosphorylation | Transcription factors | Transcription | p53 Protein | Tunicamycin | Homology | AKT protein | CCAAT/enhancer-binding protein | Kinases | Proteins | Signal transduction | Mitochondria | Cell activation | Cell growth | Cascades | Rodents | Forkhead protein | Alzheimer's disease | Movement disorders | Deoxyribonucleic acid--DNA | FOXO3 protein | Stresses | Neurodegenerative diseases | Mortality | Gene expression | Stress | Neurological diseases | Pathology | Signaling | Cell death | Endoplasmic reticulum | CHOP protein | BIM protein | Index Medicus | Deoxyribonucleic acid | DNA
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5. Full Text C/EBPα poises B cells for rapid reprogramming into induced pluripotent stem cells
by Di Stefano, Bruno and Sardina, Jose Luis and Van Oevelen, Chris and Collombet, Samuel and Kallin, Eric M and Vicent, Guillermo P and Lu, Jun and Thieffry, Denis and Beato, Miguel and Graf, Thomas
Nature, ISSN 0028-0836, 2014, Volume 506, Issue 7487, pp. 235 - 239
CCAAT/enhancer binding protein-alpha (C/EBP alpha) induces transdifferentiation of B cells into macrophages at high efficiencies and enhances reprogramming... 
NETWORK | MACROPHAGES | MULTIDISCIPLINARY SCIENCES | TET2 | TRANSDIFFERENTIATION | REQUIREMENT | REVEALS | Chromatin - metabolism | CCAAT-Enhancer-Binding Protein-alpha - metabolism | Epithelial-Mesenchymal Transition - genetics | SOXB1 Transcription Factors - metabolism | DNA-Binding Proteins - metabolism | Octamer Transcription Factor-3 - genetics | DNA Methylation | SOXB1 Transcription Factors - genetics | Cytosine - metabolism | Kruppel-Like Transcription Factors - metabolism | Cell Transdifferentiation | Induced Pluripotent Stem Cells - cytology | Cellular Reprogramming - genetics | B-Lymphocytes - metabolism | Induced Pluripotent Stem Cells - metabolism | Proto-Oncogene Proteins - metabolism | B-Lymphocytes - cytology | Cells, Cultured | Proto-Oncogene Proteins - genetics | Up-Regulation - genetics | DNA-Binding Proteins - genetics | Proto-Oncogene Proteins c-myc - metabolism | Deoxyribonuclease I - metabolism | Animals | Octamer Transcription Factor-3 - metabolism | CCAAT-Enhancer-Binding Protein-alpha - genetics | Mice | Proto-Oncogene Proteins c-myc - genetics | Chromatin - genetics | Kruppel-Like Transcription Factors - genetics | Index Medicus
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6. Full Text TRIB2 Acts Downstream of Wnt/TCF in Liver Cancer Cells to Regulate YAP and C/EBPα Function
by Wang, Jiayi and Park, Joo-Seop and Wei, Yingying and Rajurkar, Mihir and Cotton, Jennifer L and Fan, Qishi and Lewis, Brian C and Ji, Hongkai and Mao, Junhao
Molecular Cell, ISSN 1097-2765, 07/2013, Volume 51, Issue 2, pp. 211 - 225
Dysregulation of Wnt signaling is closely associated with human liver tumorigenesis. However, liver cancer-specific Wnt transcriptional programs and downstream... 
BETA-CATENIN GENE | TRANSCRIPTION FACTORS | ORGAN SIZE CONTROL | WNT/BETA-CATENIN | APC LOSS | BIOCHEMISTRY & MOLECULAR BIOLOGY | HIPPO PATHWAY | SMALL-INTESTINE | SELF-RENEWAL | HEPATOCELLULAR CARCINOMAS | MYC DELETION | CELL BIOLOGY | CCAAT-Enhancer-Binding Protein-alpha - metabolism | Cell Proliferation | Immunoprecipitation | Oligonucleotide Array Sequence Analysis | Humans | Gene Expression Profiling | Intracellular Signaling Peptides and Proteins - metabolism | Wnt Proteins - metabolism | Immunoenzyme Techniques | Wnt Proteins - genetics | Carcinoma, Hepatocellular - genetics | Biomarkers, Tumor - metabolism | Liver Neoplasms - pathology | Cell Differentiation | Nuclear Proteins - genetics | T Cell Transcription Factor 1 - metabolism | Intracellular Signaling Peptides and Proteins - genetics | Real-Time Polymerase Chain Reaction | Liver Neoplasms - genetics | RNA, Messenger - genetics | Nuclear Proteins - metabolism | Transcription Factors - genetics | Calcium-Calmodulin-Dependent Protein Kinases | Reverse Transcriptase Polymerase Chain Reaction | beta Catenin - metabolism | Blotting, Western | beta Catenin - genetics | T Cell Transcription Factor 1 - genetics | Transcription Factors - metabolism | Carcinoma, Hepatocellular - pathology | Fluorescent Antibody Technique | Liver Neoplasms - metabolism | CCAAT-Enhancer-Binding Protein-alpha - genetics | Biomarkers, Tumor - genetics | Carcinoma, Hepatocellular - metabolism | Index Medicus
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7. Full Text Critical role of Trib1 in differentiation of tissue-resident M2-like macrophages
by Satoh, Takashi and Kidoya, Hiroyasu and Naito, Hisamichi and Yamamoto, Masahiro and Takemura, Naoki and Nakagawa, Katsuhiro and Yoshioka, Yoshichika and Morii, Eiichi and Takakura, Nobuyuki and Takeuchi, Osamu and Akira, Shizuo
Nature, ISSN 0028-0836, 03/2013, Volume 495, Issue 7442, pp. 524 - 528
Macrophages consist of at least two subgroups, M1 and M2 (refs 1-3). Whereas M1 macrophages are proinflammatory and have a central role in host defence against... 
GLUCOSE-HOMEOSTASIS | OBESITY | TRIBBLES HOMOLOG | INSULIN-RESISTANCE | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | MYELOID LEUKEMOGENESIS | POLARIZATION | ASSOCIATION | ALTERNATIVE ACTIVATION | ADIPOSE-TISSUE | Neutrophils - cytology | Protein-Serine-Threonine Kinases - deficiency | CCAAT-Enhancer-Binding Protein-alpha - metabolism | Eosinophils - metabolism | Hypertriglyceridemia - genetics | Cell Count | Ubiquitin - metabolism | Adipose Tissue - cytology | Diet, High-Fat - adverse effects | Male | Intracellular Signaling Peptides and Proteins - metabolism | Lung - cytology | Intracellular Signaling Peptides and Proteins - deficiency | Adipose Tissue - metabolism | Inflammation Mediators - metabolism | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Cycle Proteins - genetics | Female | Cell Differentiation | Cytokines - genetics | Intracellular Signaling Peptides and Proteins - genetics | Neutrophils - metabolism | Protein-Serine-Threonine Kinases - metabolism | Protein Structure, Tertiary | Macrophages - classification | Bone Marrow Cells - cytology | Adipose Tissue - pathology | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Cell Cycle Proteins - deficiency | Lipodystrophy - metabolism | Spleen - cytology | Macrophages - cytology | Organ Specificity | Lipolysis | Hypertriglyceridemia - chemically induced | Macrophages - metabolism | Animals | Intracellular Signaling Peptides and Proteins - chemistry | Insulin Resistance - genetics | Lipodystrophy - pathology | Lipodystrophy - chemically induced | Mice | Protein-Serine-Threonine Kinases - chemistry | Eosinophils - cytology | Bone Marrow Cells - metabolism | Proteins | Care and treatment | Metabolic diseases | Cellular signal transduction | Research | Macrophages | Properties | Identification and classification | Testing | Studies | Spleen | Heart attacks | Transplants & implants | Bone marrow | Binding sites | Metabolic disorders | Defects | Index Medicus
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8. Full Text Identification of Common Transcriptional Regulatory Elements in Interleukin-17 Target Genes
by Fang Shen and Zihua Hu and Jaya Goswami and Sarah L. Gaffen
Journal of Biological Chemistry, ISSN 0021-9258, 08/2006, Volume 281, Issue 34, pp. 24138 - 24148
Interleukin (IL)-17 is the founding member of a novel family of inflammatory cytokines. Although produced by T cells, IL-17 activates genes and signals typical... 
ISCHEMIA-REPERFUSION INJURY | ACTIVATED PROTEIN-KINASE | CXC CHEMOKINE | MESSENGER-RNA | T-CELL INTERLEUKIN-17 | BIOCHEMISTRY & MOLECULAR BIOLOGY | NECROSIS-FACTOR-ALPHA | AIRWAY SMOOTH-MUSCLE | TNF-ALPHA | KAPPA-B-ZETA | NEUTROPHIL RECRUITMENT | Tumor Necrosis Factor-alpha - metabolism | Oncogene Proteins - genetics | Transcriptional Activation - genetics | Humans | Transcriptional Activation - drug effects | Tumor Necrosis Factor-alpha - genetics | Acute-Phase Proteins - genetics | Interleukin-17 - pharmacology | Promoter Regions, Genetic - drug effects | Lipocalins | Transcription, Genetic | CCAAT-Enhancer-Binding Proteins - genetics | Proto-Oncogene Proteins - metabolism | Recombinant Proteins - metabolism | Cell Line | Gene Targeting | Acute-Phase Proteins - metabolism | Oncogene Proteins - metabolism | Interleukin-17 - genetics | Proto-Oncogene Proteins - genetics | Recombinant Proteins - genetics | Signal Transduction - genetics | Binding Sites - genetics | Recombinant Proteins - pharmacology | Drug Synergism | Interleukin-17 - metabolism | Tumor Necrosis Factor-alpha - pharmacology | Animals | NF-kappa B - genetics | Signal Transduction - drug effects | Lipocalin-2 | Protein Binding | Mice | Index Medicus
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9. Full Text C/EBP Transcription Factors Mediate Epicardial Activation During Heart Development and Injury
by Guo N. Huang and Jeffrey E. Thatcher and John McAnally and Yongli Kong and Xiaoxia Qi and Wei Tan and J. Michael DiMaio and James F. Amatruda and Robert D. Gerard and Joseph A. Hill and Rhonda Bassel-Duby and Eric N. Olson
Science, ISSN 0036-8075, 12/2012, Volume 338, Issue 6114, pp. 1599 - 1603
The epicardium encapsulates the heart and functions as a source of multipotent progenitor cells and paracrine factors essential for cardiac development and... 
Heart | Transcription factors | HEK293 cells | Transgenic animals | RESEARCH ARTICLES | Neutrophils | Epicardium | Physical trauma | Gene expression | Embryos | Transgenic plants | CELLS | IMMUNITY | RETINOIC ACID | ZEBRAFISH | GRAINY-HEAD | MOUSE HEART | INTEGRITY | REGENERATION | MULTIDISCIPLINARY SCIENCES | BINDING PROTEIN | DROSOPHILA | Myocardial Infarction - genetics | WT1 Proteins - metabolism | Oligonucleotide Array Sequence Analysis | Heart - embryology | Male | Pericardium - metabolism | Neutrophil Infiltration | Ventricular Remodeling | Gene Expression Regulation, Developmental | Uroplakin III - genetics | Pericardium - embryology | Female | CCAAT-Enhancer-Binding Protein-delta - metabolism | CCAAT-Enhancer-Binding Proteins - genetics | Binding Sites | Myocardial Reperfusion Injury - genetics | WT1 Proteins - genetics | Organ Culture Techniques | CCAAT-Enhancer-Binding Proteins - metabolism | Heart - physiopathology | Myocardial Contraction | Signal Transduction | CCAAT-Enhancer-Binding Protein-beta - genetics | Gene Expression Regulation | Mice, Transgenic | Aldehyde Oxidoreductases - genetics | Myocardial Infarction - metabolism | CCAAT-Enhancer-Binding Protein-beta - metabolism | Pericardium - cytology | Aldehyde Oxidoreductases - metabolism | Myocardial Reperfusion Injury - metabolism | Animals | Enhancer Elements, Genetic | CCAAT-Enhancer-Binding Protein-delta - genetics | Mice | Models, Genetic | Uroplakin III - metabolism | Cellular signal transduction | Genetic aspects | Research | Genetic transcription | Regeneration (Biology) | Properties | Observations | Proteins | Signal transduction | Cardiovascular disease | Embryology | Rodents | Index Medicus | Injury prevention | Activation | Mathematical models | Adults | Heart function | Protective | Injuries
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10. Full Text DNMT1-interacting RNAs block gene-specific DNA methylation
by Di Ruscio, Annalisa and Ebralidze, Alexander K and Benoukraf, Touati and Amabile, Giovanni and Goff, Loyal A and Terragni, Jolyon and Figueroa, Maria Eugenia and De Figueiredo Pontes, Lorena Lobo and Alberich-Jorda, Meritxell and Zhang, Pu and Wu, Mengchu and D'Alò, Francesco and Melnick, Ari and Leone, Giuseppe and Ebralidze, Konstantin K and Pradhan, Sriharsa and Rinn, John L and Tenen, Daniel G
Nature, ISSN 0028-0836, 2013, Volume 503, Issue 7476, pp. 371 - 376
DNA methylation was first described almost a century ago; however, the rules governing its establishment and maintenance remain elusive. Here we present data... 
TRANSCRIPTION FACTORS | MESSENGER-RNAS | MAINTENANCE | NONCODING RNAS | MULTIDISCIPLINARY SCIENCES | POLYMERASE | GENOME-WIDE IDENTIFICATION | EXPRESSION | CANCER | CIS-REGULATORY ELEMENT | SEQ | Cell Line | RNA, Untranslated - metabolism | DNA (Cytosine-5-)-Methyltransferase 1 | Gene Expression Regulation - genetics | Humans | RNA, Messenger - genetics | Substrate Specificity | DNA Methylation - genetics | Gene Expression Profiling | DNA - metabolism | RNA, Messenger - metabolism | RNA, Untranslated - genetics | Genome, Human - genetics | DNA - genetics | DNA (Cytosine-5-)-Methyltransferases - metabolism | Base Sequence | CCAAT-Enhancer-Binding Proteins - genetics | Transcription, Genetic - genetics | RNA-Binding Proteins - metabolism | RNA sequencing | Methyltransferases | Research | Properties | Methylation | Gene expression | Methods | DNA methylation | Epigenetics | Gene loci | Genomes | Deoxyribonucleic acid--DNA | Index Medicus
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11. Full Text TSC1 controls macrophage polarization to prevent inflammatory disease
by Zhu, Linnan and Yang, Tao and Li, Longjie and Sun, Lina and Hou, Yuzhu and Hu, Xuelian and Zhang, Lianjun and Tian, Hongling and Zhao, Qingjie and Peng, Jianxia and Zhang, Hongbing and Wang, Ruoyu and Yang, Zhongzhou and Zhang, Lianfeng and Zhao, Yong
Nature Communications, ISSN 2041-1723, 09/2014, Volume 5, Issue 1, pp. 4696 - 4696
Macrophages acquire distinct phenotypes during tissue stress and inflammatory responses, but the mechanisms that regulate the macrophage polarization are... 
MAMMALIAN TARGET | MTOR COMPLEX-2 | ALTERNATIVELY ACTIVATED MACROPHAGES | SIGNALING PATHWAYS | TUBEROUS SCLEROSIS COMPLEX | DENDRITIC CELLS | C/EBP-BETA | MULTIDISCIPLINARY SCIENCES | GENE-EXPRESSION | AUTOIMMUNE-DISEASE | INNATE IMMUNITY | Male | MAP Kinase Signaling System | TOR Serine-Threonine Kinases - antagonists & inhibitors | Tuberous Sclerosis - pathology | ras GTPase-Activating Proteins - genetics | TOR Serine-Threonine Kinases - genetics | Tumor Suppressor Proteins - deficiency | Tumor Suppressor Proteins - genetics | Asthma - immunology | Female | Cell Differentiation | Macrophages - immunology | Tuberous Sclerosis - immunology | Macrophages - pathology | Proto-Oncogene Proteins c-raf - genetics | CCAAT-Enhancer-Binding Protein-beta - genetics | Gene Expression Regulation | Proto-Oncogene Proteins c-raf - immunology | Tumor Suppressor Proteins - immunology | Asthma - genetics | Mice, Knockout | Tuberous Sclerosis - genetics | TOR Serine-Threonine Kinases - immunology | Animals | CCAAT-Enhancer-Binding Protein-beta - immunology | Mice | ras GTPase-Activating Proteins - immunology | Asthma - pathology | Cell Lineage - immunology | Index Medicus
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