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animals (152) 152
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multidisciplinary sciences (21) 21
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Nature, ISSN 0028-0836, 2013, Volume 495, Issue 7439, pp. 103 - 106
Post-transcriptional switches are flexible effectors of dynamic changes in gene expression(1). Here we report a new post-transcriptional switch that dictates... 
DIABETIC FOOT ULCERS | KERATINOCYTES | PATHWAY | CELL-MIGRATION | MULTIDISCIPLINARY SCIENCES | RNA-Binding Proteins - genetics | Urokinase-Type Plasminogen Activator - antagonists & inhibitors | Skin - cytology | Skin - metabolism | Humans | Transforming Growth Factor beta1 - metabolism | Laminin - antagonists & inhibitors | Skin - injuries | Time Factors | Adaptor Proteins, Signal Transducing - antagonists & inhibitors | Trans-Activators - genetics | Wound Healing - genetics | Skin - pathology | Follistatin-Related Proteins - genetics | Gene Expression Regulation - genetics | RNA, Messenger - genetics | Diabetic Foot - pathology | Exons - genetics | Keratinocytes - cytology | Open Reading Frames - genetics | Follistatin-Related Proteins - biosynthesis | Diabetic Foot - genetics | Diabetic Foot - metabolism | Urokinase-Type Plasminogen Activator - metabolism | Keratinocytes - metabolism | Trans-Activators - metabolism | MicroRNAs - genetics | Laminin - metabolism | Transcription, Genetic - genetics | Adaptor Proteins, Signal Transducing - metabolism | In Vitro Techniques | RNA-Binding Proteins - metabolism | Cell Movement | Wound healing | MicroRNA | Messenger RNA | Research | Genetic transcription | Properties | Binding proteins | Gene expression | Proteins | Skin | Diabetes | Binding sites | Cell adhesion & migration
Journal Article
Oncogene, ISSN 0950-9232, 2018, Volume 38, Issue 15, pp. 2706 - 2721
Temozolomide was recognized as the first-line therapy for glioblastoma to prolong the survival of patients noticeably, while recent clinical studies found that... 
FOLLISTATIN-LIKE 1 | HDAC2 | PROMOTER METHYLATION | MGMT | BIOCHEMISTRY & MOLECULAR BIOLOGY | BINDING-PROTEIN | FSTL1 | CELL BIOLOGY | HISTONE DEACETYLATION | REPAIR | ONCOLOGY | GENE O-6-METHYLGUANINE-DNA METHYLTRANSFERASE | GENETICS & HEREDITY | EXPRESSION | Follistatin-Related Proteins - genetics | Humans | DNA Repair Enzymes - genetics | Repressor Proteins - genetics | Histone Deacetylase 2 | Up-Regulation - genetics | Signal Transduction - genetics | Promoter Regions, Genetic - genetics | Temozolomide - pharmacology | Carrier Proteins - genetics | DNA Modification Methylases - genetics | Drug Resistance, Neoplasm - genetics | Glioblastoma - genetics | Tumor Suppressor Proteins - genetics | Cell Line, Tumor | Acetylation | Transcription, Genetic - genetics | Glioblastoma - drug therapy | Nuclear Proteins - genetics | Gene Expression Regulation, Neoplastic - genetics | Care and treatment | Dosage and administration | Research | Temozolomide | Drug resistance | Drug therapy | Glioblastoma multiforme | Cancer | Histone deacetylase | Transcription | Methylguanine | Glioblastoma | Poly(ADP-ribose) polymerase | DNA repair | Patients | Nuclear transport | O6-methylguanine-DNA methyltransferase | Signal transduction | Deacetylation | Mismatch repair | DNA methyltransferase | HDAC2 protein | Transcriptomics | CNS cancer
Journal Article
Nature, ISSN 0028-0836, 09/2016, Volume 538, Issue 7623, pp. 114 - 117
The common participation of oncogenic KRAS proteins in many of the most lethal human cancers, together with the ease of detecting somatic KRAS mutant alleles... 
TARGET | CRM1/XPO1 | ACTIVATION | MODELS | MULTIDISCIPLINARY SCIENCES | KINASE | YAP | MUTATIONS | INHIBITORS | IDENTIFICATION | Lung Neoplasms - drug therapy | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Lung Neoplasms - metabolism | Cell Survival - genetics | Lung Neoplasms - pathology | NF-kappa B - metabolism | Phosphoproteins - antagonists & inhibitors | Phosphoproteins - metabolism | DNA-Binding Proteins - metabolism | Cell Nucleus - metabolism | RNA Interference | Adaptor Proteins, Signal Transducing - antagonists & inhibitors | Female | Verteporfin | Protein-Serine-Threonine Kinases - metabolism | Carcinoma, Non-Small-Cell Lung - pathology | Follistatin-Related Proteins - genetics | Lung Neoplasms - genetics | Cell Survival - drug effects | NF-kappa B - antagonists & inhibitors | DNA-Binding Proteins - antagonists & inhibitors | Signal Transduction | Carcinoma, Non-Small-Cell Lung - genetics | Carcinoma, Non-Small-Cell Lung - metabolism | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Porphyrins - pharmacology | Transcription Factors - metabolism | Xenograft Model Antitumor Assays | Animals | Karyopherins - metabolism | Active Transport, Cell Nucleus - drug effects | Genes, Lethal - genetics | NF-KappaB Inhibitor alpha - metabolism | Nuclear Proteins - antagonists & inhibitors | Receptors, Cytoplasmic and Nuclear - antagonists & inhibitors | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | RNA, Small Interfering | Carcinoma, Non-Small-Cell Lung - drug therapy | Mutation | Adaptor Proteins, Signal Transducing - metabolism | Cell Nucleus - drug effects | Karyopherins - antagonists & inhibitors | Receptors, Cytoplasmic and Nuclear - metabolism | Care and treatment | Genetic aspects | Gene mutations | Health aspects | Guanosine triphosphatase | Lung cancer | Genomics | Genomes | Kinases | Drug resistance | Gene expression | Drug dosages
Journal Article
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 4/2011, Volume 108, Issue 17, pp. 7058 - 7063
Journal Article
The Journal of Clinical Endocrinology & Metabolism, ISSN 0021-972X, 08/2017, Volume 102, Issue 8, pp. 2751 - 2761
Context: Although calorie restriction has proven beneficial for weight loss, long-term weight control is variable between individuals. Objective: To identify... 
SKELETAL-MUSCLE | TGF-BETA | MACROPHAGES | GLUCOSE | TISSUE GENE-EXPRESSION | ENDOCRINOLOGY & METABOLISM | FAT | RESTRICTION | FOLLISTATIN | ADIPOSE-TISSUE | ADIPOCYTE | Insulin-Like Growth Factor Binding Protein 3 - genetics | Obesity - diet therapy | alpha-Crystallin B Chain - genetics | Ubiquitin-Specific Proteases - genetics | Membrane Glycoproteins - metabolism | Caloric Restriction | Humans | Middle Aged | Transforming Growth Factor beta1 - metabolism | Male | alpha-Crystallin B Chain - metabolism | Gene Expression Profiling | Gene Regulatory Networks | RNA, Messenger - metabolism | Obesity - genetics | Subcutaneous Fat - metabolism | Osteonectin - genetics | Insulin-Like Growth Factor Binding Protein 3 - metabolism | Microarray Analysis | Adult | Female | Membrane Proteins - metabolism | Ubiquitin-Specific Proteases - metabolism | Real-Time Polymerase Chain Reaction | Extracellular Matrix Proteins - metabolism | Biomarkers - metabolism | Follistatin-Related Proteins - genetics | Follistatin-Related Proteins - metabolism | Enzyme-Linked Immunosorbent Assay | Membrane Proteins - genetics | Down-Regulation | Extracellular Matrix Proteins - genetics | Osteonectin - metabolism | Membrane Glycoproteins - genetics | Obesity - metabolism | Polymorphism, Genetic | Quantitative Trait Loci | Adipose tissues | Intervention | Controllers | Nutrient deficiency | Adipose tissue | Transforming growth factor | Genes | Weight loss | Reverse transcription | Gene expression | Quantitative trait loci | Polymerase chain reaction | Proteins | Weight control | Diet | Ribonucleic acids | Osteonectin | Biomarkers | Insulin-like growth factor-binding protein 3 | Bioindicators | Enzyme-linked immunosorbent assay | Life Sciences
Journal Article
Nature, ISSN 0028-0836, 09/2015, Volume 525, Issue 7570, pp. 479 - 485
Journal Article
Journal of Experimental Medicine, ISSN 0022-1007, 2015, Volume 212, Issue 2, pp. 235 - 252
Progressive tissue fibrosis is a cause of major morbidity and mortality. Pulmonary fibrosis is an epithelial-mesenchymal disorder in which TGF-beta 1 plays a... 
PATHOGENESIS | MEDICINE, RESEARCH & EXPERIMENTAL | CELLS | TGF-BETA | GREMLIN | DISEASE | MYOFIBROBLAST | LUNG DEVELOPMENT | MECHANISMS | GROWTH-FACTOR | IMMUNOLOGY | EPITHELIAL-MESENCHYMAL INTERACTIONS | Inflammation - pathology | Lung Injury - pathology | Myofibroblasts - immunology | Humans | Middle Aged | Transforming Growth Factor beta1 - metabolism | Antibiotics, Antineoplastic - adverse effects | Follistatin-Related Proteins - antagonists & inhibitors | Male | Pulmonary Fibrosis - genetics | Bone Morphogenetic Protein 4 - metabolism | Myofibroblasts - metabolism | Respiratory Mucosa - pathology | Inflammation - metabolism | Respiratory Mucosa - immunology | Lung Injury - metabolism | Female | Pulmonary Fibrosis - metabolism | Disease Models, Animal | Follistatin-Related Proteins - genetics | Follistatin-Related Proteins - metabolism | Cell Line | Gene Expression | Signal Transduction | Antibodies, Monoclonal - pharmacology | Cell Communication | Mesenchymal Stromal Cells - metabolism | Antibodies, Neutralizing - pharmacology | Inflammation - immunology | Bleomycin - adverse effects | Follistatin-Related Proteins - deficiency | Mice, Knockout | Lung Injury - genetics | Phenotype | Animals | Inflammation - genetics | Protein Binding | Pulmonary Fibrosis - chemically induced | Aged | Mice | Pulmonary Fibrosis - drug therapy | Respiratory Mucosa - metabolism | Lung Injury - chemically induced | Smad Proteins - metabolism
Journal Article
PLoS ONE, ISSN 1932-6203, 08/2016, Volume 11, Issue 8, p. e0161682
Wnt/beta-catenin signaling is relatively understudied in immunity and autoimmunity. beta-catenin blocks inflammatory mediators and favors tolerogenic dendritic... 
ADHESION | DENDRITIC CELLS | GENE | PATHWAY | COLORECTAL-CANCER | MULTIDISCIPLINARY SCIENCES | MICE | E-CADHERIN | MUTATIONS | WNT | NF-KAPPA-B | Leukocytes - pathology | Spleen - immunology | Axin Protein - genetics | Dendritic Cells - immunology | Humans | Dendritic Cells - pathology | Male | Wnt Proteins - metabolism | Axin Protein - metabolism | Intercellular Signaling Peptides and Proteins - blood | Leukocytes - immunology | beta Catenin - immunology | Wnt Proteins - genetics | Axin Protein - immunology | Gene Deletion | Lupus Erythematosus, Systemic - immunology | Female | Spleen - pathology | Macrophages - immunology | Wnt Signaling Pathway | Disease Models, Animal | Follistatin-Related Proteins - genetics | Follistatin-Related Proteins - metabolism | Macrophages - pathology | Mice, Inbred C57BL | beta Catenin - deficiency | Gene Expression Regulation | Intercellular Signaling Peptides and Proteins - genetics | Mice, Transgenic | beta Catenin - genetics | Wnt Proteins - immunology | Animals | Follistatin-Related Proteins - immunology | Lupus Erythematosus, Systemic - genetics | Mice | Lupus Erythematosus, Systemic - pathology | Intercellular Signaling Peptides and Proteins - immunology | Autoimmunity | Care and treatment | Systemic lupus erythematosus | Dendritic cells | Analysis | Hepatoma | Diagnosis | Research | Macrophages | Wnt protein | Disease | Leukocytes | Immunity | Cell adhesion & migration | β-catenin | Engineering | Immunology | Clonal deletion | Rodents | Deletion | Biomedical engineering | Lupus | Myeloid cells | Kidneys | Internal medicine | Rheumatic diseases | Inflammation | Preempting | Patients | Human subjects | White blood cells | Medicine | Serum levels | Signaling | Chronic conditions | Insects | Mutation | Autoimmune diseases | Dkk1 protein
Journal Article
PLoS ONE, ISSN 1932-6203, 08/2007, Volume 2, Issue 8, p. e789
Myostatin is a transforming growth factor-beta family member that normally acts to limit skeletal muscle growth. Mice genetically engineered to lack myostatin... 
BIOLOGY | Proteins - genetics | Animals | Proteins - metabolism | Signal Transduction | Follistatin-Related Proteins | Myostatin - genetics | Mice, Transgenic | Muscle, Skeletal - metabolism | Mice | Mutation | Myostatin - metabolism
Journal Article
Scientific Reports, ISSN 2045-2322, 12/2017, Volume 7, Issue 1, pp. 9830 - 11
Journal Article