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PLoS ONE, ISSN 1932-6203, 08/2013, Volume 8, Issue 8, p. e72278
Background: Opioidergic SLP (sustained ligand-activated preconditioning) induced by 3-5 days of opioid receptor (OR) agonism induces persistent protection... 
NATRIURETIC-PEPTIDE | ISCHEMIA/REPERFUSION INJURY | INFARCTION | OPIOID RECEPTOR | MULTIDISCIPLINARY SCIENCES | CARDIOPROTECTIVE PHENOTYPE | MICE | MECHANISMS | ISCHEMIA-REPERFUSION | MOUSE HEARTS | MYOSIN HEAVY-CHAIN | Myocardial Ischemia - genetics | Animals | Polymerase Chain Reaction | Ischemic Preconditioning | Myocardial Ischemia - physiopathology | Ligands | Male | Transcription, Genetic | Gene Expression Profiling | Mice | Mice, Inbred BALB C | Heart | Genes | HLA histocompatibility antigens | Heat shock proteins | Genetic transcription | Proteins | Histocompatibility antigens | DNA microarrays | Ischemia | Analysis | Genetic research | Genetic aspects | Natriuretic peptides | Heart attacks | Peptides | Morphine | Immunity | Interrogation | Egr-3 protein | Cytokines | Contractility | GSTM1 protein | Gene expression | CD83 antigen | Gene silencing | Injury prevention | Myocardium | Preconditioning | Monocyte chemoattractant protein 1 | Health sciences | Oxidative stress | CD86 antigen | Carbon tetrachloride | Kinases | Interleukin 6 | Reperfusion | Fos protein | Rodents | Interleukin 1 | Drb1 protein | Egr-2 protein | Heart diseases | Hypertension | Opioid receptors | CCL4 protein | Muscle contraction | Signaling | Protein expression | Infarction | Histocompatibility antigen HLA | Diabetes | Stress proteins | Chemokines | Cellular stress response | Apoptosis | Questioning
Journal Article
PLoS ONE, ISSN 1932-6203, 03/2016, Volume 11, Issue 3, p. e0150893
Serum amyloid A (SAA) is an evolutionary highly conserved acute phase protein that is predominantly secreted by hepatocytes. However, its role in liver injury... 
APOPTOSIS | HUMAN NEUTROPHILS | ACUTE-PHASE REACTANT | RAT-LIVER FIBROSIS | MULTIDISCIPLINARY SCIENCES | SECRETION | MONOCYTE CHEMOTACTIC PROTEIN-1 | A SAA PROTEIN | NF-KAPPA-B | EXPRESSION | INTESTINAL EPITHELIAL-CELLS | Cholestasis - genetics | Cholestasis - metabolism | Serum Amyloid A Protein - pharmacology | Carbon Tetrachloride | Humans | Hepatic Stellate Cells - metabolism | Male | NF-kappa B - metabolism | Liver Cirrhosis - chemically induced | Proto-Oncogene Proteins c-akt - genetics | Matrix Metalloproteinase 9 - metabolism | Ligation | MAP Kinase Kinase 4 - metabolism | I-kappa B Kinase - metabolism | Matrix Metalloproteinase 9 - genetics | Mitogen-Activated Protein Kinase 1 - genetics | Liver Cirrhosis - metabolism | Chemokine CCL2 - metabolism | Chemokine CCL5 - metabolism | Cell Death - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Liver Cirrhosis - genetics | Hepatic Stellate Cells - pathology | Disease Models, Animal | Hepatic Stellate Cells - drug effects | Mitogen-Activated Protein Kinase 3 - genetics | Signal Transduction | Gene Expression Regulation | Rats | Chemokine CCL2 - genetics | Inflammation | I-kappa B Kinase - genetics | Rats, Sprague-Dawley | Cholestasis - pathology | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | NF-kappa B - genetics | Chemokine CCL5 - genetics | Liver Cirrhosis - pathology | MAP Kinase Kinase 4 - genetics | Cell Proliferation - drug effects | Mice, Inbred BALB C | Primary Cell Culture | Mitogen-Activated Protein Kinase 1 - metabolism | Biochemistry | RNA | Cell death | Luciferase | Cell proliferation | Animal models | Transcription factors | Transcription | RANTES | Liver | Carbon tetrachloride | Cytotoxicity | AKT protein | Kinases | Caspase-3 | Proteins | Signal transduction | Immunology | Rodents | Hepatology | Gastroenterology | Fibroblasts | Amyloid | NF-κB protein | Stellate cells | Cytokines | Mortality | Neutrophils | Extracellular signal-regulated kinase | c-Jun protein | Caspase | Poly(ADP-ribose) polymerase | CCL4 protein | Bile duct | Gelatinase B | Medicine | Antibiotics | Hepatocytes | Surgeons | Skin | Annexin V | Monocyte chemoattractant protein 1 | Apoptosis | Bile
Journal Article
Journal of Leukocyte Biology, ISSN 0741-5400, 03/2015, Volume 97, Issue 3, pp. 557 - 571
Journal Article
Clinical Cancer Research, ISSN 1078-0432, 05/2017, Volume 23, Issue 9, pp. 2313 - 2324
Purpose: B-cell receptor (BCR)-associated kinase inhibitors, such as ibrutinib, have revolutionized the treatment of chronic lymphocytic leukemia (CLL).... 
SURFACE IGM | APOPTOSIS | CLL | ACTIVATION | TREATMENT-NAIVE | ONCOLOGY | IDELALISIB | RESISTANCE | IBRUTINIB | TYROSINE KINASE INHIBITOR | EXPRESSION | Receptors, Antigen, B-Cell - drug effects | Tumor Microenvironment - drug effects | Antineoplastic Combined Chemotherapy Protocols - administration & dosage | Leukocytes, Mononuclear - drug effects | Apoptosis - drug effects | Pyrimidines - administration & dosage | Humans | Bridged Bicyclo Compounds, Heterocyclic - administration & dosage | Leukemia, Lymphocytic, Chronic, B-Cell - genetics | Syk Kinase - antagonists & inhibitors | Leukemia, Lymphocytic, Chronic, B-Cell - pathology | Janus Kinases - antagonists & inhibitors | B-Lymphocytes - drug effects | Pyrazoles - administration & dosage | Flow Cytometry | Janus Kinase Inhibitors - administration & dosage | Signal Transduction - drug effects | Proto-Oncogene Proteins c-bcr - genetics | Gene Expression Regulation, Neoplastic - drug effects | Leukemia, Lymphocytic, Chronic, B-Cell - drug therapy | Proto-Oncogene Proteins c-bcr - antagonists & inhibitors | Neoplasm Proteins - genetics | Sulfonamides - administration & dosage | Sulfones - administration & dosage | BCR protein | Immunoglobulin M | Flow cytometry | Bcl-2 protein | Leukemia | Carbon tetrachloride | Medical services | Clinical trials | Immunoblotting | ZAP-70 protein | B-cell receptor | CD40L protein | Lymph nodes | Signal transduction | Interleukin 4 | Bcl-x protein | Pathways | Enzyme-linked immunosorbent assay | Medical research | Chronic lymphatic leukemia | CD49d antigen | CCL3 protein | Lymphatic leukemia | CCL4 protein | Patients | Mcl-1 protein | Cytometry | Signaling | Inhibitors | Lymphocytes B | Experimental design | Cell death | Syk protein | Cancer | Apoptosis | Cerdulatinib | STAT6 | JAK3
Journal Article
PLoS ONE, ISSN 1932-6203, 12/2013, Volume 8, Issue 12, p. e81065
Background and Aims: C/EBP homologous protein (CHOP) plays pro-apoptotic roles in the integrated stress response. Recently, a tumor suppressive role for CHOP... 
INDUCED APOPTOSIS | ROLES | MULTIDISCIPLINARY SCIENCES | GENE-EXPRESSION | ENDOPLASMIC-RETICULUM STRESS | PROTEOLYSIS | ATF6 | CONTRIBUTES | TUMORS | PROGRESSION | HEPATOCARCINOGENESIS | Diethylnitrosamine - toxicity | Transcription Factor CHOP - genetics | Carcinoma, Hepatocellular - chemically induced | Humans | Liver Neoplasms - chemically induced | Inflammation - metabolism | Cell Nucleus - metabolism | Liver Neoplasms - pathology | Carcinoma, Hepatocellular - immunology | Macrophages - immunology | Unfolded Protein Response - drug effects | Liver Neoplasms - immunology | Transcription Factor CHOP - deficiency | Gene Knockout Techniques | Disease Progression | Carcinogenesis - drug effects | Animals | Active Transport, Cell Nucleus - drug effects | Carcinoma, Hepatocellular - pathology | Liver Neoplasms - metabolism | Macrophages - drug effects | Mice | Cell Nucleus - drug effects | Transcription Factor CHOP - metabolism | Carcinoma, Hepatocellular - metabolism | RNA | Lung cancer | Analysis | Physiological aspects | Hepatoma | Protein binding | Apoptosis | Crosstalk | Carbon tetrachloride | Parenchyma | Hepatocellular carcinoma | Homology | mRNA | CCAAT/enhancer-binding protein | Kinases | Macrophages | Machinery | Carcinogenesis | Recruitment | Liver cancer | Signal transduction | Carcinogens | Pathways | Diethylnitrosamine | Rodents | Immune system | Stresses | Metabolism | CCL4 protein | Stress | Nodules | Signaling | γ-Interferon | Human pathology | Endoplasmic reticulum | Tumors | Cancer
Journal Article
Journal Article
Journal of Immunology, ISSN 0022-1767, 02/2004, Volume 172, Issue 4, pp. 2332 - 2340
Macrophages produce an array of proinflammatory mediators at sites of inflammation and contribute to the development of inflammatory responses. Important roles... 
SIGNAL-TRANSDUCTION | CELLS | TUMOR-NECROSIS-FACTOR | MESSENGER-RNA | TAK1 | PATHWAY | MONOCYTE-CHEMOATTRACTANT PROTEIN-1 | TYROSINE KINASE | GENE-EXPRESSION | P38-ALPHA | IMMUNOLOGY | Tetradecanoylphorbol Acetate - pharmacology | Humans | Receptor Protein-Tyrosine Kinases - physiology | I-kappa B Proteins - metabolism | Receptors, Mitogen - physiology | Interleukin-1 - biosynthesis | Trans-Activators - physiology | Discoidin Domain Receptors | Protein Isoforms - metabolism | Cattle | I-kappa B Proteins - antagonists & inhibitors | Trans-Activators - biosynthesis | Interleukin-8 - metabolism | p38 Mitogen-Activated Protein Kinases | Macrophages - immunology | Shc Signaling Adaptor Proteins | Carrier Proteins - physiology | Proteins - physiology | Tumor Necrosis Factor Receptor-Associated Peptides and Proteins | Chemokine CCL4 | Chemokines - biosynthesis | Adaptor Proteins, Vesicular Transport - physiology | Interleukin-8 - biosynthesis | Macrophage Activation - immunology | Macrophage Inflammatory Proteins - metabolism | Receptors, Mitogen - metabolism | Receptor Protein-Tyrosine Kinases - metabolism | src Homology Domains - physiology | Protein Isoforms - physiology | Macrophages - enzymology | Cell Differentiation - immunology | Collagen Type I - physiology | Adaptor Proteins, Signal Transducing | Macrophages - metabolism | TNF Receptor-Associated Factor 6 | Animals | Src Homology 2 Domain-Containing, Transforming Protein 1 | Mitogen-Activated Protein Kinases - physiology | Up-Regulation - immunology | NF-kappa B - biosynthesis | NF-kappa B - physiology | Cell Line, Tumor | Chemokine CCL2 - biosynthesis | Macrophage Inflammatory Proteins - biosynthesis | Protein Structure, Tertiary - physiology
Journal Article
Blood, ISSN 0006-4971, 05/2003, Volume 101, Issue 9, pp. 3568 - 3573
Recently, it has been demonstrated that macrophage inflammatory protein 1-alpha (MIP-1alpha) is crucially involved in the development of osteolytic bone... 
APOPTOSIS | KINASE PATHWAY | INHIBITION | PROTEIN-1-ALPHA | MECHANISM | GROWTH | INTERLEUKIN-6 | HEMATOLOGY | LESIONS | CYTOKINE-DEPENDENT SURVIVAL | MAP Kinase Signaling System - physiology | Phosphorylation | Humans | Macrophage Inflammatory Proteins - physiology | Neoplasm Proteins - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | MAP Kinase Kinase 1 | Mitogen-Activated Protein Kinase Kinases - metabolism | Cell Division | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Tumor Cells, Cultured - secretion | Flavonoids - pharmacology | Protein-Serine-Threonine Kinases - metabolism | Proto-Oncogene Proteins - antagonists & inhibitors | Chemokine CCL4 | Chemokine CCL3 | Cell Survival | Receptors, Chemokine - metabolism | Cytokines - secretion | Enzyme Inhibitors - pharmacology | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Multiple Myeloma - metabolism | Osteolysis - metabolism | Proto-Oncogene Proteins c-akt | Multiple Myeloma - pathology | Androstadienes - pharmacology | Proto-Oncogene Proteins - physiology | Phosphatidylinositol 3-Kinases - physiology | Signal Transduction - physiology | Protein Processing, Post-Translational | Enzyme Activation | Mitogen-Activated Protein Kinase 3 | Tumor Cells, Cultured - cytology | Mitogen-Activated Protein Kinase 1 - metabolism | Mitogen-Activated Protein Kinases - metabolism
Journal Article
PLoS ONE, ISSN 1932-6203, 12/2012, Volume 7, Issue 12, p. e51355
Background: The anaphylatoxin C3a binds to the G protein coupled receptor (GPCR, C3aR) and activates divergent signaling pathways to induce degranulation and... 
PROTEIN-COUPLED RECEPTOR | PDZ DOMAINS | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | CHEMOKINE PRODUCTION | KINASE | PARATHYROID-HORMONE | FACTOR-I | NA+/H+-EXCHANGER | PLASMA-MEMBRANE | RENAL PHOSPHATE-TRANSPORT | RNA, Small Interfering - genetics | Chemokine CCL4 - biosynthesis | Antigens, CD34 - metabolism | Cell Degranulation | Signal Transduction | Humans | Receptors, Complement - deficiency | Gene Expression Regulation | Gene Silencing | NF-kappa B - metabolism | Phosphoproteins - genetics | Phosphoproteins - metabolism | Gene Knockdown Techniques | Receptors, Complement - metabolism | Sodium-Hydrogen Exchangers - metabolism | HEK293 Cells | Mast Cells - metabolism | Receptors, Complement - genetics | Mast Cells - cytology | Sodium-Hydrogen Exchangers - genetics | Proteins | G proteins | Cytokines | Protein binding | Complement receptors | Phosphorylation | G protein-coupled receptors | Complement component C3a | Reverse transcription | AKT protein | Activation | Western blotting | Cell activation | Rodents | Tumor necrosis factor-TNF | Adaptor proteins | CD34 antigen | NF-κB protein | Desensitization | Na+/H+-exchanging ATPase | Adapters | Extracellular signal-regulated kinase | Dentistry | Chemotaxis | Histamine | Pathology | Signaling | Internalization | Cell lines | Degranulation | Mast cells | Regulation | Postsynaptic density proteins | Adapter proteins | Chemokines
Journal Article
Journal of Investigative Dermatology, ISSN 0022-202X, 07/2006, Volume 126, Issue 7, pp. 1574 - 1581
Toll-like receptor (TLR)3 is a receptor for virus-associated double-stranded RNA, and triggers antiviral immune responses during viral infection. Epidermal... 
TOLL-LIKE RECEPTOR-3 | TRANSCRIPTION FACTORS | DOUBLE-STRANDED-RNA | ANTIVIRAL RESPONSES | EPITHELIAL-CELLS | IRF FAMILY | FACTOR-KAPPA-B | EPIDERMAL-KERATINOCYTES | INTERFERON REGULATORY FACTOR-7 | VIRAL-INFECTION | DERMATOLOGY | Humans | Interferon Regulatory Factor-3 - drug effects | STAT1 Transcription Factor - analysis | STAT1 Transcription Factor - drug effects | Suppressor of Cytokine Signaling 1 Protein | Interferon Regulatory Factor-7 - genetics | Keratinocytes - chemistry | Repressor Proteins - analysis | Toll-Like Receptor 3 - analysis | Interferon Regulatory Factor-7 - physiology | Repressor Proteins - physiology | STAT3 Transcription Factor - physiology | Phosphorylation - drug effects | Interferon Regulatory Factor-7 - analysis | Intracellular Signaling Peptides and Proteins - genetics | STAT3 Transcription Factor - genetics | STAT1 Transcription Factor - physiology | Chemokine CCL4 | Interferon Regulatory Factor-3 - analysis | Poly I-C - pharmacology | Chemokine CCL3 | Immunity, Innate - drug effects | Macrophage Inflammatory Proteins - metabolism | Cells, Cultured | Intracellular Signaling Peptides and Proteins - analysis | Repressor Proteins - genetics | Suppressor of Cytokine Signaling Proteins - genetics | STAT3 Transcription Factor - analysis | STAT1 Transcription Factor - genetics | Genetic Vectors - genetics | Keratinocytes - immunology | Interferon Regulatory Factor-3 - physiology | Gene Expression Regulation - drug effects | Immunity, Innate - immunology | Toll-Like Receptor 3 - physiology | Signal Transduction - drug effects | Homeostasis - physiology | STAT3 Transcription Factor - drug effects | NF-kappa B - physiology | RNA, Double-Stranded - pharmacology | Signal Transduction - physiology | Suppressor of Cytokine Signaling Proteins - physiology | Adenoviruses, Human - genetics | Feedback, Physiological - physiology | Intracellular Signaling Peptides and Proteins - physiology | Suppressor of Cytokine Signaling Proteins - analysis | Keratinocytes - physiology | Phosphorylation | Immune response | Transcription | macrophage inflammatory protein 1 | Dermatology | Double-stranded RNA | Stat3 protein | Keratinocytes | Intracellular signalling | Poly (I:C) | Nuclear transport | TLR3 protein | Infection | Interferon regulatory factor 7 | Signal transduction | NF- Kappa B protein | Feedback | Toll-like receptors | Interferon | Internet | Stat1 protein | Macrophage inflammatory protein | Expression vectors
Journal Article