X
Search Filters
Format Format
Format Format
X
Sort by Item Count (A-Z)
Filter by Count
Journal Article (6476) 6476
Publication (747) 747
Book Review (109) 109
Book Chapter (20) 20
Dissertation (12) 12
Patent (11) 11
Conference Proceeding (10) 10
Data Set (1) 1
Paper (1) 1
Reference (1) 1
more...
Subjects Subjects
Subjects Subjects
X
Sort by Item Count (A-Z)
Filter by Count
index medicus (5877) 5877
transcription factor rela - metabolism (3778) 3778
humans (3649) 3649
animals (3467) 3467
mice (2205) 2205
nf-kappa b - metabolism (2005) 2005
male (1445) 1445
nf-kappa-b (1345) 1345
activation (1286) 1286
transcription factor rela - genetics (1280) 1280
inflammation (1223) 1223
signal transduction (1179) 1179
phosphorylation (1167) 1167
biochemistry & molecular biology (1071) 1071
cell line (1063) 1063
transcription factor rela (1061) 1061
expression (1048) 1048
apoptosis (1044) 1044
cell biology (1044) 1044
female (975) 975
cells, cultured (946) 946
cell line, tumor (936) 936
nf-κb (909) 909
rats (906) 906
nf-kappa b (775) 775
immunology (769) 769
gene expression (738) 738
signal transduction - drug effects (713) 713
cell nucleus - metabolism (710) 710
nf-kappab inhibitor alpha (682) 682
nf-kappa b - genetics (674) 674
i-kappa b proteins - metabolism (666) 666
proteins (650) 650
gene-expression (619) 619
tumor necrosis factor-alpha - metabolism (577) 577
apoptosis - drug effects (557) 557
cells (518) 518
mice, inbred c57bl (513) 513
oncology (509) 509
cytokines (495) 495
rna, messenger - metabolism (489) 489
tumor necrosis factor-alpha - pharmacology (472) 472
promoter regions, genetic (467) 467
transfection (462) 462
cancer (461) 461
transcription factors (460) 460
pharmacology & pharmacy (456) 456
gene expression regulation (442) 442
protein binding (442) 442
nf-kappa b - antagonists & inhibitors (440) 440
oxidative stress (440) 440
transcription (432) 432
research article (429) 429
nf-κb protein (418) 418
inhibition (417) 417
blotting, western (415) 415
phosphorylation - drug effects (410) 410
rela protein (406) 406
rats, sprague-dawley (403) 403
article (394) 394
disease models, animal (384) 384
lipopolysaccharides - pharmacology (381) 381
transcription, genetic (375) 375
multidisciplinary sciences (374) 374
abridged index medicus (366) 366
kinases (363) 363
rela (360) 360
i-kappa b kinase - metabolism (357) 357
transcription factor rela - antagonists & inhibitors (357) 357
transcriptional activation (352) 352
gene expression regulation - drug effects (347) 347
dna-binding proteins - metabolism (341) 341
mice, knockout (339) 339
time factors (338) 338
up-regulation (335) 335
dose-response relationship, drug (334) 334
research (333) 333
rodents (333) 333
medicine (332) 332
middle aged (330) 330
immunohistochemistry (327) 327
rna interference (326) 326
macrophages (324) 324
cytokines - metabolism (318) 318
down-regulation (317) 317
molecular sequence data (315) 315
cell proliferation (303) 303
base sequence (300) 300
adult (296) 296
binding sites (295) 295
cell proliferation - drug effects (290) 290
tumor-necrosis-factor (290) 290
analysis (286) 286
anti-inflammatory agents - pharmacology (285) 285
rna, messenger - genetics (281) 281
reverse transcriptase polymerase chain reaction (278) 278
biology (277) 277
macrophages - metabolism (277) 277
nf-kappa b - physiology (277) 277
nf-kappa b p50 subunit - metabolism (275) 275
more...
Language Language
Language Language
X
Sort by Item Count (A-Z)
Filter by Count
English (6276) 6276
Chinese (199) 199
Swedish (11) 11
Russian (7) 7
Portuguese (5) 5
French (3) 3
Japanese (3) 3
Korean (3) 3
Spanish (2) 2
German (1) 1
Polish (1) 1
more...
Publication Date Publication Date
Click on a bar to filter by decade
Slide to change publication date range


Journal Article
Nature Immunology, ISSN 1529-2908, 02/2006, Volume 7, Issue 2, pp. 148 - 155
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2014, Volume 9, Issue 4, pp. e92408 - e92408
textabstractThe Copper Metabolism MURR1 domain protein 1 (COMMD1) is a protein involved in multiple cellular pathways, including copper homeostasis, NF-κB and... 
CU,ZN-SUPEROXIDE DISMUTASE | SUPEROXIDE-DISMUTASE SOD1 | MULTIDISCIPLINARY SCIENCES | IN-VIVO | MUTANT SOD1 | AMYOTROPHIC-LATERAL-SCLEROSIS | MOTOR-NEURON DISEASE | EPITHELIAL SODIUM-CHANNEL | HUNTINGTONS-DISEASE | FAMILIAL ALS | PARKINSONS-DISEASE | Adaptor Proteins, Signal Transducing - chemistry | Protein Aggregates | Molecular Weight | Peptides - chemistry | Humans | Protein Multimerization | Ubiquitin-Protein Ligases - metabolism | Mutant Proteins - metabolism | Ubiquitin-Protein Ligases - chemistry | Protein Folding | Animals | Peptides - metabolism | Amyotrophic Lateral Sclerosis - metabolism | HEK293 Cells | Protein Binding | Mice | HeLa Cells | Superoxide Dismutase-1 | Adaptor Proteins, Signal Transducing - metabolism | Superoxide Dismutase - metabolism | Copper in the body | Physiological aspects | Homeostasis | Nervous system | Development and progression | Genetic aspects | Degeneration | Research | Risk factors | Huntingtin | Disease | Superoxide dismutase | Biology | Agglomeration | Biochemistry | Inclusions | Sclerosis | Molecular weight | Protein turnover | Proteins | Signal transduction | Protein folding | Proteolysis | Copper | Trinucleotide repeat diseases | NF-κB protein | Neurodegenerative diseases | Neurons | Amyotrophic lateral sclerosis | Superoxide | Polyglutamine diseases | Metabolism | Substrates | Zinc | Signaling | Quality control | Hypoxia | Parkin protein | Mutation | RelA protein | Protein interaction | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 2011, Volume 6, Issue 7, pp. e21891 - e21891
Background: Microglial activation plays an important role in neurodegenerative diseases by producing several proinflammatory enzymes and proinflammatory... 
CELLS | SIGNALING PATHWAYS | ACTIVATED PROTEIN-KINASE | INFLAMMATION | BIOLOGY | NITRIC-OXIDE | P-HYDROXYBENZYL ALCOHOL | CENTRAL-NERVOUS-SYSTEM | NF-KAPPA-B | ADAPTIVE IMMUNE-RESPONSES | NEURODEGENERATIVE DISEASES | Tumor Necrosis Factor-alpha - metabolism | Transcription, Genetic - drug effects | Tumor Necrosis Factor-alpha - genetics | I-kappa B Proteins - metabolism | Interleukin-1beta - genetics | RNA, Messenger - metabolism | I-kappa B Proteins - genetics | Transcription Factor RelA - genetics | Cyclooxygenase 2 - genetics | Interleukin-1beta - metabolism | Benzyl Alcohols - pharmacology | Inflammation Mediators - metabolism | Glucosides - chemistry | Phosphorylation - drug effects | Cytokines - genetics | Benzyl Alcohols - chemistry | Cell Line | Glucosides - pharmacology | NF-KappaB Inhibitor alpha | Cytokines - metabolism | Microglia - drug effects | RNA, Messenger - genetics | Cells, Cultured | Microglia - enzymology | Animals | MAP Kinase Signaling System - drug effects | Nitric Oxide Synthase Type II - genetics | Transcription Factor RelA - metabolism | Cyclic AMP Response Element-Binding Protein - metabolism | Cyclooxygenase 2 - metabolism | Lipopolysaccharides - pharmacology | Protein Biosynthesis - drug effects | Mice | Mitogen-Activated Protein Kinases - metabolism | Nitric Oxide Synthase Type II - metabolism | COX-2 inhibitors | Nervous system diseases | Interleukins | RNA | Nitric oxide | Mitogens | Protein kinases | Protein binding | Transcription factors | Cytotoxicity | Nervous system | Lipopolysaccharides | Prostaglandin endoperoxide synthase | Proteins | Signal transduction | Neurodegeneration | Inhibition | Enzymes | NF-κB protein | Cytokines | AMP | Neurodegenerative diseases | Cyclic AMP | MAP kinase | IL-1β | Cyclic AMP response element-binding protein | Gene expression | Microglia | Neurological diseases | Studies | Inflammatory bowel disease | Polymerase chain reaction | Neurology | Hospitals | Engineering research | Phosphorylation | Interleukin | Activation | Kinases | Neurotoxicity | Rodents | Cascades | Microglial cells | Tumor necrosis factor-TNF | Pretreatment | Antiinflammatory agents | Extracellular signal-regulated kinase | c-Jun protein | Inflammation | Herbal medicine | Signaling | Brain research | Protein kinase | Phenols | Cyclooxygenase-2 | Alzheimers disease | Immunofluorescence | Chemokines | Index Medicus | phenolic compounds | Regulatory sequences | c-Jun amino-terminal kinase | Interleukin 1 | Herbal medicines | glucosides | Nitric-oxide synthase | NF- Kappa B protein | Tumor necrosis factor- alpha
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 07/2011, Volume 286, Issue 27, pp. 24113 - 24124
In LPS-treated macrophages, activation of STAT3 is considered to be crucial for terminating the production of inflammatory cytokines. By analyzing the role of... 
TUMOR-NECROSIS-FACTOR | SOCS3 MESSENGER-RNA | CYTOKINE SIGNALING-3 | HUMAN MACROPHAGES | BIOCHEMISTRY & MOLECULAR BIOLOGY | GENE-EXPRESSION | TNF-ALPHA | NF-KAPPA-B | IL-10 | CUTTING EDGE | BETA | Active Transport, Cell Nucleus - physiology | Humans | Intracellular Signaling Peptides and Proteins - metabolism | I-kappa B Proteins - metabolism | I-kappa B Proteins - genetics | Interferon Regulatory Factor-3 - genetics | Transcription Factor RelA - genetics | Cell Nucleus - metabolism | Interferon-beta - genetics | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Gene Expression Regulation - physiology | Interferon-beta - biosynthesis | Macrophages - cytology | Mice, Knockout | Gene Expression Regulation - drug effects | Macrophages - metabolism | Animals | Cell Nucleus - genetics | Signal Transduction - drug effects | Transcription Factor RelA - metabolism | Active Transport, Cell Nucleus - drug effects | Interleukin-10 - genetics | Lipopolysaccharides - pharmacology | Interferon Regulatory Factor-3 - metabolism | Interleukin-10 - biosynthesis | Signal Transduction - physiology | Mice | Index Medicus | NF-κB | STAT Transcription Factor | Signal Transduction | Interleukin | Interferon | Lipopolysaccharide (LPS) | Macrophage
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 9/2011, Volume 108, Issue 36, pp. 14902 - 14907
Epstein-Barr virus nuclear antigen 2 (EBNA2) regulation of transcription through the cell transcription factor RBPJ is essential for resting B-lymphocyte (RBL)... 
T lymphocytes | Up regulation | Chromatin | B lymphocytes | DNA | Nucleosomes | Gene expression regulation | Epstein Barr virus infections | Human herpesvirus 4 | Binding sites | Development | Lymphoma | Leukemia | Notch | leukemia | development | SIGNAL-BINDING-PROTEIN | CIS-ELEMENT | MULTIDISCIPLINARY SCIENCES | lymphoma | C-MYC | NUCLEAR ANTIGEN-2 | FATE | GENOME | LONG-RANGE INTERACTION | GENE | PROMOTER | J-KAPPA | Cell Proliferation | Herpesvirus 4, Human - genetics | Proto-Oncogene Proteins c-ets - genetics | Genome, Viral - genetics | Humans | Transcription Factor RelA - genetics | Viral Proteins - metabolism | Trans-Activators - genetics | B-Lymphocytes - virology | Epstein-Barr Virus Infections - genetics | Core Binding Factor alpha Subunits - metabolism | Transcription, Genetic | Proto-Oncogene Proteins c-ets - metabolism | Epstein-Barr Virus Nuclear Antigens - metabolism | Immunoglobulin J Recombination Signal Sequence-Binding Protein - genetics | B-Lymphocytes - metabolism | Proto-Oncogene Proteins - metabolism | Immunoglobulin J Recombination Signal Sequence-Binding Protein - metabolism | Epstein-Barr Virus Nuclear Antigens - genetics | Response Elements | Nucleosomes - metabolism | Viral Proteins - genetics | Nucleosomes - genetics | Proto-Oncogene Proteins - genetics | Proto-Oncogene Proteins c-myc - metabolism | Core Binding Factor alpha Subunits - genetics | Transcription Factor RelA - metabolism | Cell Line, Tumor | Trans-Activators - metabolism | Proto-Oncogene Proteins c-myc - genetics | Herpesvirus 4, Human - metabolism | Epstein-Barr Virus Infections - metabolism | Physiological aspects | Transcription factors | Epstein-Barr virus | Genetic aspects | Lymphocytes | Health aspects | Cell growth | Deoxyribonucleic acid--DNA | Index Medicus | ETS protein | Lymphoblasts | Introns | Data processing | Genomes | Myc protein | Promoters | Early B-cell factor | Infection | Enhancers | PU.1 protein | Lymphocytes B | Fluorescence in situ hybridization | RelA protein | Conformation | Biological Sciences
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 2016, Volume 311, Issue 4, pp. H871 - H880
We previously reported that endoplasmic reticulum (ER) stress is induced in the subfornical organ (SFO) and the hypothalamic paraventricular nucleus (PVN) of... 
Heart failure | Brain | Sympathetic activity | Hypothalamic paraventricular nucleus | Mitogen-activated protein kinase | Subfornical organ | Endoplasmic reticulum stress | heart failure | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | INDUCED PHOSPHORYLATION | MYOCARDIAL-INFARCTION | ER STRESS | subfornical organ | KINASE | RATS | sympathetic activity | KAPPA-B | brain | endoplasmic reticulum stress | hypothalamic paraventricular nucleus | mitogen-activated protein kinase | UNFOLDED PROTEIN RESPONSE | PERIPHERAL VASCULAR DISEASE | UP-REGULATION | Cholagogues and Choleretics - pharmacology | Tumor Necrosis Factor-alpha - genetics | Heart Failure - physiopathology | Male | NF-KappaB Inhibitor alpha - genetics | Peptidyl-Dipeptidase A - drug effects | Interleukin-1beta - genetics | Sympathetic Nervous System - physiopathology | RNA, Messenger - metabolism | Activating Transcription Factor 6 - genetics | Subfornical Organ - drug effects | Brain - metabolism | Heat-Shock Proteins - genetics | Inflammation - metabolism | Receptor, Angiotensin, Type 1 - genetics | Cyclooxygenase 2 - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | Real-Time Polymerase Chain Reaction | Echocardiography | Signal Transduction | Rats | Cyclooxygenase 2 - drug effects | Heart Failure - metabolism | Rats, Sprague-Dawley | Blotting, Western | Brain - drug effects | Tumor Necrosis Factor-alpha - drug effects | Mitogen-Activated Protein Kinase 3 - metabolism | Endoplasmic Reticulum Stress | Paraventricular Hypothalamic Nucleus - metabolism | Infusions, Intraventricular | Mitogen-Activated Protein Kinases - drug effects | Mitogen-Activated Protein Kinase 1 - metabolism | Interleukin-1beta - drug effects | Sympathetic Nervous System - drug effects | Mitogen-Activated Protein Kinase 1 - drug effects | X-Box Binding Protein 1 - drug effects | Sympathetic Nervous System - metabolism | Transcription Factor RelA - genetics | Activating Transcription Factor 6 - drug effects | Mitogen-Activated Protein Kinase 3 - drug effects | Taurochenodeoxycholic Acid - pharmacology | Peptidyl-Dipeptidase A - genetics | Renin-Angiotensin System | Receptor, Angiotensin, Type 1 - drug effects | RNA, Messenger - drug effects | Subfornical Organ - metabolism | Heat-Shock Proteins - drug effects | Activating Transcription Factor 4 - genetics | Activating Transcription Factor 4 - drug effects | NF-KappaB Inhibitor alpha - drug effects | Paraventricular Hypothalamic Nucleus - drug effects | p38 Mitogen-Activated Protein Kinases - drug effects | Animals | Transcription Factor RelA - drug effects | X-Box Binding Protein 1 - genetics | Mitogen-Activated Protein Kinases - metabolism | Physiological aspects | Cellular signal transduction | Endoplasmic reticulum | Health aspects | Mitogen-activated protein kinases | Signal transduction | Inflammation | Kinases | Index Medicus | Cardiovascular Neurohormonal Regulation
Journal Article
Science, ISSN 0036-8075, 3/2009, Volume 323, Issue 5922, pp. 1722 - 1725
Patten recognition receptors, which recognize pathogens or components of injured cells (danger), trigger activation of the innate immune system. Whether and... 
Receptors | Immune response | Cytokines | Hepatocytes | Splenocytes | Liver | Antibodies | Heat shock proteins | Ligands | Reports | Physiological regulation | SYSTEM | ACTIVATION | PROTEIN | AUTOIMMUNITY | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | MOBILITY GROUP BOX-1 | HMGB1 | HEAT-STABLE ANTIGEN | T-CELL GROWTH | ISCHEMIA-REPERFUSION | Liver - pathology | Immunoprecipitation | Receptors, Pattern Recognition - immunology | CD24 Antigen - metabolism | Dendritic Cells - immunology | Humans | HMGB1 Protein - immunology | Receptors, Antigen, B-Cell - metabolism | Necrosis - immunology | Lectins - metabolism | Receptors, Pattern Recognition - metabolism | Liver - immunology | HMGB1 Protein - chemistry | HMGB1 Protein - metabolism | CD24 Antigen - genetics | Protein Structure, Tertiary | Lipopolysaccharides - toxicity | Cytokines - metabolism | Signal Transduction | Acetaminophen - toxicity | Receptors, Cell Surface - metabolism | Mutant Proteins - metabolism | Inflammation - immunology | Immunity, Innate | HSP70 Heat-Shock Proteins - metabolism | Necrosis - chemically induced | Animals | Protein Tyrosine Phosphatase, Non-Receptor Type 6 - metabolism | Transcription Factor RelA - metabolism | Mutant Proteins - chemistry | HSP90 Heat-Shock Proteins - metabolism | Mice | Research | Properties | Cell adhesion molecules | Proteins | Immunology | Cellular biology | Molecular biology | Rodents | Index Medicus
Journal Article
Journal Article
Science, ISSN 0036-8075, 9/2002, Volume 297, Issue 5589, pp. 2048 - 2051
The bacterium Bacillus anthracis causes the death of macrophages, which may allow it to avoid detection by the innate immune system. We found that B. anthracis... 
Bacteriophages | Myeloid cells | Anthrax | Cell death | Genes | Innate immunity | Reports | Infections | Macrophages | Apoptosis | Necrosis | CELLS | ACTIVATED PROTEIN-KINASE | TOXIN | MULTIDISCIPLINARY SCIENCES | SUSCEPTIBILITY | TRANSCRIPTION | BACILLUS-ANTHRACIS | MICE | Mitogen-Activated Protein Kinase Kinases - genetics | Protein-Tyrosine Kinases - metabolism | Bacterial Toxins - toxicity | Transcription Factor RelA | NF-kappa B - metabolism | MAP Kinase Kinase 3 | MAP Kinase Signaling System | MAP Kinase Kinase 6 | Mitogen-Activated Protein Kinase Kinases - metabolism | Protein-Tyrosine Kinases - genetics | Teichoic Acids - pharmacology | p38 Mitogen-Activated Protein Kinases | Macrophages - immunology | Protein-Serine-Threonine Kinases - metabolism | Macrophages - physiology | Carrier Proteins - toxicity | Cell Line | Gene Expression | Calcium-Calmodulin-Dependent Protein Kinases - genetics | Mice, Inbred C57BL | Enzyme Inhibitors - pharmacology | Protein-Serine-Threonine Kinases - genetics | Antigens, Bacterial | Imidazoles - pharmacology | I-kappa B Kinase | Macrophage Activation | Macrophages - enzymology | Animals | Mitogen-Activated Protein Kinases - antagonists & inhibitors | NF-kappa B - genetics | Lipopolysaccharides - pharmacology | Mice | Pyridines - pharmacology | Enzyme Activation | Calcium-Calmodulin-Dependent Protein Kinases - metabolism | Mitogen-Activated Protein Kinases - metabolism | Bacillus anthracis | Research | Proteins | Enzymes | Pharmacology | Bacteriology | Index Medicus
Journal Article
Journal of Cellular Physiology, ISSN 0021-9541, 03/2017, Volume 232, Issue 3, pp. 517 - 525
Journal Article