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1. Full Text TGF-β and BMP signaling in osteoblast differentiation and bone formation
by Chen, Guiqian and Deng, Chuxia and Li, Yi-Ping
International Journal of Biological Sciences, ISSN 1449-2288, 2012, Volume 8, Issue 2, pp. 272 - 288
Transforming growth factor-beta (TGF-beta)/bone morphogenic protein (BMP) signaling is involved in a vast majority of cellular processes and is fundamentally... 
BMP signaling | Smad | Bone | Osteoblasts | TGF signaling | Runx2 | BMP-9-INDUCED OSTEOGENIC DIFFERENTIATION | UBIQUITIN LIGASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | IA RECEPTOR BMPRIA | MESENCHYMAL STEM-CELLS | GROWTH-FACTOR-BETA | MORPHOGENETIC PROTEIN | P38 MAPK PATHWAYS | CHRONIC KIDNEY-DISEASE | CONDITIONAL DELETION | BRACHYDACTYLY TYPE A2 | Bone Morphogenetic Proteins - metabolism | Osteogenesis - physiology | Animals | Signal Transduction | Humans | Osteoblasts - physiology | Gene Expression Regulation - physiology | Cell Differentiation | Mice | Osteoblasts - cytology | Transforming Growth Factor beta - metabolism
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2. Full Text Efficient drug screening and gene correction for treating liver disease using patient‐specific stem cells
by Choi, Su Mi and Kim, Yonghak and Shim, Joong Sup and Park, Joon Tae and Wang, Rui‐Hong and Leach, Steven D and Liu, Jun O and Deng, Chuxia and Ye, Zhaohui and Jang, Yoon‐Young
Hepatology, ISSN 0270-9139, 06/2013, Volume 57, Issue 6, pp. 2458 - 2468
Patient‐specific induced pluripotent stem cells (iPSCs) represent a potential source for developing novel drug and cell therapies. Although increasing numbers... 
DISRUPTION | TALEN | IPSCS | IN-VIVO | MUTATION | GENERATION | AUTOPHAGY | GASTROENTEROLOGY & HEPATOLOGY | Targeted Gene Repair - methods | Hepatocytes - cytology | Liver Diseases - genetics | alpha 1-Antitrypsin Deficiency - therapy | Humans | Pluripotent Stem Cells - drug effects | Cells, Cultured | Liver Diseases - therapy | Cell Differentiation | Hepatocytes - drug effects | Disease | Efficiency | Hepatology | Stem cells
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3. Full Text BRCA1 controls homologous recombination at Tus/Ter-stalled mammalian replication forks
by Willis, Nicholas A and Chandramouly, Gurushankar and Huang, Bin and Kwok, Amy and Follonier, Cindy and Deng, Chuxia and Scully, Ralph
Nature, ISSN 0028-0836, 2014, Volume 510, Issue 7506, pp. 556 - 559
Replication fork stalling can promote genomic instability, predisposing to cancer and other diseases(1-3). Stalled replication forks may be processed by sister... 
CELLS | IN-VITRO | STRAND BREAK REPAIR | PROTEIN | SISTER-CHROMATID RECOMBINATION | DNA-DAMAGE RESPONSE | MULTIDISCIPLINARY SCIENCES | ESCHERICHIA-COLI | TRACT GENE CONVERSION | EPSTEIN-BARR-VIRUS | ORIP | Gene Conversion - genetics | Hereditary Breast and Ovarian Cancer Syndrome - genetics | DNA Replication | Escherichia coli Proteins - metabolism | Exons - genetics | Homologous Recombination | DNA Breaks, Double-Stranded | BRCA1 Protein - genetics | Animals | BRCA2 Protein - metabolism | Escherichia coli - genetics | BRCA1 Protein - metabolism | Escherichia coli Proteins - genetics | Mice | BRCA1 Protein - chemistry | BRCA2 Protein - genetics | Genomic Instability - genetics | DNA replication | Breast cancer | Genetic aspects | Genetic recombination | Health aspects | Ovarian cancer | Probability | Plasmids | Genes
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4. Full Text Redox-dependent Brca1 transcriptional regulation by an NADH-sensor CtBP1
by Deng, Y and Liu, J and Han, G and Lu, S.-L and Wang, S.-Y and Malkoski, S and Tan, A.C and Deng, C and Wang, X.-J and Zhang, Q
Oncogene, ISSN 0950-9232, 12/2010, Volume 29, Issue 50, pp. 6603 - 6608
C-terminal binding protein 1 (CtBP1) is a transcriptional co-repressor and metabolic sensory protein, which often represses tumor suppressor genes. Hence, we... 
tumor suppressor | NADH | Brca1 | transcription | HNSCC | CtBP1 | RAT-LIVER | E1A PROTEIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | TERMINAL BINDING-PROTEIN | DOWN-REGULATION | FANCONI-ANEMIA | NECK-CANCER | CELL BIOLOGY | BREAST-CANCER | ONCOLOGY | GENETICS & HEREDITY | SQUAMOUS-CELL CARCINOMA | NEGATIVE MODULATION | ANTIOXIDANT TEMPOL | DNA Repair - drug effects | Oxidation-Reduction | Carcinoma, Squamous Cell - genetics | Down-Regulation | Humans | Gene Expression Regulation, Neoplastic | Alcohol Oxidoreductases - metabolism | Spin Labels | Promoter Regions, Genetic - drug effects | DNA-Binding Proteins - metabolism | BRCA1 Protein - genetics | Cyclic N-Oxides - pharmacology | Head and Neck Neoplasms - genetics | Transcription, Genetic | E2F4 Transcription Factor - metabolism | NAD - metabolism | Physiological aspects | NADH dehydrogenase | Research | Genetic transcription | Binding proteins | Proteins | Gene expression | Binding sites | Tumors | Index Medicus
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5. Full Text FGF signaling acts upstream of the NOTCH and WNT signaling pathways to control segmentation clock oscillations in mouse somitogenesis
by Matthias B. Wahl and Chuxia Deng and Mark Lewandoski and Olivier PourquiÃ
Development, ISSN 0950-1991, 11/2007, Volume 134, Issue 22, pp. 4033 - 4041
Fibroblast growth factor (FGF) signaling plays a crucial role in vertebrate segmentation. The FGF pathway establishes a posterior-to-anterior signaling... 
Somite | Vertebra | FGF | Segmentation | Clock | Oscillation | OPPOSING FGF | somite | vertebra | RETINOIC-ACID | DEVELOPMENTAL BIOLOGY | clock | INACTIVATION | TARGETED DISRUPTION | EMBRYO | PATTERN | BODY AXIS | oscillation | GENE-EXPRESSION | segmentation | PRESOMITIC MESODERM | PROSPECTIVE SOMITES | Somites - metabolism | Cleavage Stage, Ovum - physiology | Embryo, Mammalian | Receptors, Notch - metabolism | Mice, Inbred C57BL | Gene Expression Regulation, Developmental - drug effects | Receptors, Notch - physiology | Cleavage Stage, Ovum - metabolism | Male | Receptor, Fibroblast Growth Factor, Type 1 - genetics | Wnt Proteins - metabolism | Pregnancy | Somites - embryology | Animals | Models, Biological | Biological Clocks - genetics | Gene Deletion | Female | Signal Transduction - physiology | Mice | Wnt Proteins - physiology | Fibroblast Growth Factors - physiology | Tretinoin - pharmacology
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6. Full Text BMP signaling regulates sympathetic nervous system development through Smad4-dependent and -independent pathways
by Yuka Morikawa and Ahmet Zehir and Emily Maska and Chuxia Deng and Michael D. Schneider and Yuji Mishina and Peter Cserjesi
Development, ISSN 0950-1991, 11/2009, Volume 136, Issue 21, pp. 3575 - 3584
Induction of the sympathetic nervous system (SNS) from its neural crest (NC) precursors is dependent on BMP signaling from the dorsal aorta. To determine the... 
TRANSCRIPTION FACTORS | CARDIAC OUTFLOW TRACT | ENTERIC NEURONS | BMP | MOUSE EMBRYOS | NEURONAL DIFFERENTIATION | DEVELOPMENTAL BIOLOGY | Neural crest | CONDITIONAL KNOCKOUT MICE | NEURAL CREST CELLS | TGF-BETA/BMP | Mouse | Smad4 independent | NORADRENERGIC DIFFERENTIATION | ADRENERGIC CELLS | Bone Morphogenetic Proteins - metabolism | Norepinephrine - metabolism | Signal Transduction | Cell Survival | Sympathetic Nervous System - embryology | Neurogenesis | Smad4 Protein - metabolism | Sympathetic Nervous System - metabolism | Embryo, Mammalian - metabolism
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7. Full Text The Steroid Receptor Coactivator SRC-3 (p/CIP/RAC3/AIB1/ACTR/TRAM-1) Is Required for Normal Growth, Puberty, Female Reproductive Function, and Mammary Gland Development
by Jianming Xu and Lan Liao and Guang Ning and Hiromi Yoshida-Komiya and Chuxia Deng and Bert W. O'Malley
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 6/2000, Volume 97, Issue 12, pp. 6379 - 6384
Steroid receptor coactivator-3 (SRC-3) is a coactivator of nuclear receptors in the SRC family as assayed in vitro. Here, we show that mouse SRC-3 is expressed... 
Biological Sciences | Mating behavior | Estrogens | Mammary development | Male animals | Mammary glands | Mice | Hormones | Female animals | Growth retardation | Oocytes | ACTIVATION | PROTEIN | GENE | THYROID-HORMONE | NUCLEAR RECEPTORS | TIF2 | MULTIDISCIPLINARY SCIENCES | TRANSCRIPTIONAL COACTIVATOR | HISTONE ACETYLTRANSFERASE | CANCER | ESTROGEN-RECEPTOR | Estradiol - blood | Histone Acetyltransferases | Growth | Organ Specificity | Trans-Activators - physiology | Reproduction | Animals | Trans-Activators - deficiency | Trans-Activators - genetics | Female | Nuclear Receptor Coactivator 3 | Sexual Maturation | Mammary Glands, Animal - physiology | Cell receptors | Analysis | Physiological aspects | Endocrine aspects | Steroids (Drugs)
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8. Full Text Adult Neurogenesis Requires Smad4-Mediated Bone Morphogenic Protein Signaling in Stem Cells
by Colak, Dilek and Mori, Tetsuji and Brill, Monika S and Pfeifer, Alexander and Falk, Sven and Deng, Chuxia and Monteiro, Rui and Mummery, Christine and Sommer, Lukas and Gotz, Magdalena
Journal of Neuroscience, ISSN 0270-6474, 01/2008, Volume 28, Issue 2, pp. 434 - 445
In the mammalian brain, neurogenesis continues only in few regions of the forebrain. The molecular signals governing neurogenesis in these unique neurogenic... 
Neural stem cells | Dlx2 | Transplantation | Olig2 | Neurogenesis | Oligodendrocytes | PROGENITOR CELLS | MOUSE SUBVENTRICULAR ZONE | neural stem cells | oligodendrocytes | NEUROSCIENCES | LINEAGE COMMITMENT | OLFACTORY-BULB | transplantation | IN-VIVO | neurogenesis | CENTRAL-NERVOUS-SYSTEM | SPINAL-CORD-INJURY | PRECURSOR CELLS | EXPRESSION | BRAIN | Adult Stem Cells - physiology | Homeodomain Proteins - metabolism | Estrogen Antagonists - pharmacology | Glial Fibrillary Acidic Protein - metabolism | Bone Morphogenetic Proteins - metabolism | Amino Acid Transport System X-AG - metabolism | Basic Helix-Loop-Helix Transcription Factors - metabolism | Carrier Proteins - pharmacology | Bromodeoxyuridine - metabolism | Cell Differentiation - physiology | Mice, Inbred C57BL | Smad4 Protein - physiology | Oligodendrocyte Transcription Factor 2 | Gene Expression Regulation - drug effects | Nerve Tissue Proteins - metabolism | Transcription Factors - metabolism | Cell Movement - drug effects | Animals | Signal Transduction - drug effects | Cell Differentiation - drug effects | Tamoxifen - pharmacology | Signal Transduction - physiology | Cell Proliferation - drug effects | Mice | Smad4 Protein - deficiency | Cell Transplantation - methods
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9. Full Text Olfactomedin 4 down-regulates innate immunity against Helicobacter pylori infection
by Wenli Liu and Ming Yan and Yueqin Liu and Ruihong Wang and Cuiling Li and Chuxia Deng and Aparna Singh and William G. Coleman and Griffin P. Rodgers and Harvey J. Alter
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 6/2010, Volume 107, Issue 24, pp. 11056 - 11061
Olfactomedin 4 (OLFM4) is a glycoprotein that has been found to be up-regulated in inflammatory bowel diseases and Helicobacter pylori infected patients.... 
Immune response | Cytokines | Helicobacter pylori | HEK293 cells | Epithelial cells | Gastric mucosa | Antibodies | Infections | Inflammation | Mice | NF-κB | Nucleotide oligomerization domain-1 and -2 | ACTIVATION | MULTIDISCIPLINARY SCIENCES | nucleotide oligomerization domain-1 and-2 | IDENTIFICATION | MUCOSA | OPEN-ANGLE GLAUCOMA | NF-kappa B | EPITHELIAL-CELLS | PROTEINS | NF-KAPPA-B | TRANSCRIPTION FACTOR | EXPRESSION | HGC-1 | Up-Regulation | Gastric Mucosa - microbiology | Extracellular Matrix Proteins - deficiency | NF-kappa B - metabolism | Gastric Mucosa - metabolism | RNA, Messenger - metabolism | Nod1 Signaling Adaptor Protein - metabolism | Glycoproteins - deficiency | Helicobacter Infections - metabolism | Cytokines - genetics | Glycoproteins - genetics | Chemokines - biosynthesis | Signal Transduction | Down-Regulation | Extracellular Matrix Proteins - genetics | Mice, Inbred C57BL | RNA, Messenger - genetics | Helicobacter Infections - immunology | Helicobacter Infections - genetics | Immunity, Innate | Chemokines - genetics | Mice, Knockout | Gastric Mucosa - immunology | Glycoproteins - immunology | Animals | Nod2 Signaling Adaptor Protein - metabolism | Extracellular Matrix Proteins - immunology | In Vitro Techniques | Cytokines - biosynthesis | Helicobacter Infections - microbiology | Oligomers | Autoimmunity | Gastrointestinal diseases | Helicobacter infections | Research | Health aspects | Risk factors | Inflammatory bowel diseases | Oligomerization | macrophage inflammatory protein 1 | Interleukin 12 | Glycoproteins | Nucleotides | Immunity | Infection | Interleukin 5 | Olfactomedin | Feedback | Interleukin 1 | Nod1 protein | Chemokines | Colonization | NOD2 protein | Biological Sciences | nucleotide oligomerization domain-1 and -2
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10. Full Text Smad4 loss in mice causes spontaneous head and neck cancer with increased genomic instability and inflammation
by Bornstein, Sophia and White, Ruth and Malkoski, Stephen and Oka, Masako and Han, Gangwen and Cleaver, Timothy and Reh, Douglas and Andersen, Peter and Gross, Neil and Olson, Susan and Deng, Chuxia and Lu, Shi-Long and Wang, Xiao-Jing
Journal of Clinical Investigation, ISSN 0021-9738, 11/2009, Volume 119, Issue 11, pp. 3408 - 3419
Smad4 is a central mediator of TGF-beta signaling, and its expression is downregulated or lost at the malignant stage in several cancer types. In this study,... 
MEDICINE, RESEARCH & EXPERIMENTAL | TGF-BETA | EPITHELIAL-CELLS | SIGNALING PATHWAY | SQUAMOUS-CELL CARCINOMA | TUMOR-SUPPRESSOR GENE | SKIN | FANCONI ANEMIA/BRCA PATHWAY | KNOCKOUT MICE | EXPRESSION | T-CELLS | Rad51 Recombinase - metabolism | Carcinoma, Squamous Cell - genetics | Carcinoma, Squamous Cell - pathology | Down-Regulation | Humans | Mice, Inbred C57BL | Head and Neck Neoplasms - physiopathology | DNA Repair - genetics | Carcinoma, Squamous Cell - physiopathology | Smad4 Protein - metabolism | Head and Neck Neoplasms - pathology | Mice, Knockout | Fanconi Anemia Complementation Group Proteins - metabolism | Animals | Smad4 Protein - genetics | Gene Deletion | Inflammation - genetics | Head and Neck Neoplasms - genetics | Mice | Genes, BRCA1 | Genomic Instability - genetics | Inflammation - physiopathology | Usage | Care and treatment | Animal models in research | Physiological aspects | Head and neck cancer | Genetic aspects | Inflammation | Research | Transforming growth factors | Risk factors
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11. Full Text Partitioning Circadian Transcription by SIRT6 Leads to Segregated Control of Cellular Metabolism
by Masri, Selma and Rigor, Paul and Cervantes, Marlene and Ceglia, Nicholas and Sebastian, Carlos and Xiao, Cuiying and Roqueta-Rivera, Manuel and Deng, Chuxia and Osborne, Timothy F and Mostoslavsky, Raul and Baldi, Pierre and Sassone-Corsi, Paolo
Cell, ISSN 0092-8674, 07/2014, Volume 158, Issue 3, pp. 659 - 672
Circadian rhythms are intimately linked to cellular metabolism. Specifically, the NAD -dependent deacetylase SIRT1, the founding member of the sirtuin family,... 
GENOMIC INSTABILITY | ACTIVATION | CLOCK-BMAL1 | ACETYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | DEACETYLASE SIRT6 | GENE-EXPRESSION | REGULATORS | PROMOTER | IDENTIFICATION | CLOCK | CELL BIOLOGY | Sirtuin 1 - metabolism | Chromatin | Liver - metabolism | ARNTL Transcription Factors - metabolism | Gene Expression Profiling | Circadian Rhythm | Sirtuin 1 - genetics | Mice, Knockout | CLOCK Proteins - metabolism | Animals | Transcription, Genetic | Mice | Sirtuins - genetics | Sirtuins - metabolism | Computer science | Epigenetic inheritance | Metabolites | Analysis | Physiological aspects | Genetic research | Genetic transcription | Fatty acids
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12. Full Text Smad4 signalling in T cells is required for suppression of gastrointestinal cancer
by Anver, Miriam and Fu, Xin-Yuan and Li, Cuiling and Letterio, John J and Qiao, Wenhui and Wolfraim, Lawrence and Kim, Seong-Jin and Hong, Suntaek and Deng, Chuxia and Mamura, Mizuko and Kim, Byung-Gyu and Mushinski, Elizabeth and Potter, Michael and Kasperczak, Barbara
Nature, ISSN 0028-0836, 06/2006, Volume 441, Issue 7096, pp. 1015 - 1019
SMAD4 (MAD homologue 4 (Drosophila)), also known as DPC4 (deleted in pancreatic cancer), is a tumour suppressor gene that encodes a central mediator of... 
COLON-CANCER | INACTIVATION | TGF-BETA | GENE | MULTIDISCIPLINARY SCIENCES | STAT3 | JUVENILE POLYPOSIS | TUMOR-GROWTH | CONDITIONAL KNOCKOUT MICE | IL-6 | TRANSGENIC MICE | Adenomatous Polyposis Coli - etiology | Gene Targeting | Neoplasms, Glandular and Epithelial - pathology | Signal Transduction | Mice, Inbred C57BL | Cell Communication | Neoplasms, Glandular and Epithelial - metabolism | Adenomatous Polyposis Coli - pathology | Neoplasms, Glandular and Epithelial - immunology | Smad4 Protein - metabolism | Gastrointestinal Neoplasms - immunology | Gastrointestinal Neoplasms - pathology | Animals | Smad4 Protein - genetics | T-Lymphocytes - metabolism | Gene Deletion | Mice | Adenomatous Polyposis Coli - genetics | Cytokines - biosynthesis | Disease Models, Animal | Gastrointestinal Neoplasms - metabolism | Signal transduction | Mutation | Gene expression | Rodents | Cancer
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13. Full Text Alternative Gnas Gene Products Have Opposite Effects on Glucose and Lipid Metabolism
by Min Chen and Oksana Gavrilova and Jie Liu and Tao Xie and Chuxia Deng and Annie T. Nguyen and Lisa M. Nackers and Javier Lorenzo and Laura Shen and Lee S. Weinstein and Lutz Birnbaumer
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 5/2005, Volume 102, Issue 20, pp. 7386 - 7391
Gnas is an imprinted gene with multiple gene products resulting from alternative splicing of different first exons onto a common exon 2. These products include... 
Obesity | Edema | Biological Sciences | Phenotypes | Exons | Alleles | Insulin resistance | Mice | Lipid metabolism | Insulin | Genetic mutation | Pseudohypoparathyroidism | G protein | Genomic imprinting | pseudohypoparathyroidism | PROTEIN ALPHA-SUBUNIT | G(S)ALPHA KNOCKOUT MICE | MULTIDISCIPLINARY SCIENCES | TISSUE | genomic imprinting | IDENTIFICATION | CONTROL REGION | TRANSCRIPTS | NESP55 | MOUSE-CHROMOSOME 2 | MUTATIONS | INCREASED INSULIN SENSITIVITY | Body Composition | GTP-Binding Protein alpha Subunits, Gs - metabolism | Alternative Splicing - genetics | Blood Glucose | Lipid Metabolism | DNA Primers | Mutation - genetics | Mice, Knockout | GTP-Binding Protein alpha Subunits, Gs - genetics | Genomic Imprinting - genetics | Blotting, Northern | Chromogranins | Phenotype | Animals | Protein Isoforms - metabolism | Analysis of Variance | Radioimmunoassay | Insulin Resistance - genetics | Triglycerides - blood | Glucose - metabolism | Energy Metabolism - genetics | Genetic Vectors | Protein Isoforms - genetics | Research | G proteins
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14. Full Text A Vital Role for Glycosphingolipid Synthesis during Development and Differentiation
by Tadashi Yamashita and Ryuichi Wada and Teiji Sasaki and Chuxia Deng and Uwe Bierfreund and Konrad Sandhoff and Richard L. Proia
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 8/1999, Volume 96, Issue 16, pp. 9142 - 9147
Glycosphingolipids (GSLs) are believed to be integral for the dynamics of many cell membrane events, including cellular interactions, signaling, and... 
Glucosylceramides | Neurons | Stem cells | Cell lines | Ceramides | Erythroid cells | Embryonic stem cells | Embryos | Cellular differentiation | Tumors | GASTRULATION | ADHESION | GLUCOSYLCERAMIDE | VISCERAL ENDODERM | GENE | MEMBRANE | MULTIDISCIPLINARY SCIENCES | EMBRYONIC STEM-CELLS | SURFACE | NEURONAL DIFFERENTIATION | EXPRESSION | In Situ Nick-End Labeling | Embryo, Mammalian - pathology | Embryonic and Fetal Development - genetics | Glycosphingolipids - biosynthesis | Genomic Library | Genotype | Gastrula - cytology | Embryonic and Fetal Development - physiology | Gastrula - physiology | Mice, Knockout | Cell Differentiation - genetics | Embryo, Mammalian - physiology | Glucosyltransferases - metabolism | Teratoma - pathology | Animals | In Situ Hybridization |