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Journal Article
Nature Communications, ISSN 2041-1723, 12/2017, Volume 8, Issue 1, pp. 2078 - 12
.... Here we show that complement is activated in skeletal muscle injury and plays a key role during regeneration... 
CELLS | RECRUITMENT | ACTIVATION | IMMUNE-SYSTEM | PROTEIN | ALTERNATIVE PATHWAY | INFLAMMATION | MACROPHAGES | MULTIDISCIPLINARY SCIENCES | INJURY | EXPRESSION | Complement C3a - physiology | Cardiotoxins - toxicity | Humans | Receptors, Complement - deficiency | Chimera - physiology | Male | Muscle, Skeletal - injuries | Cell Movement - physiology | Complement C3a - antagonists & inhibitors | Muscle, Skeletal - drug effects | Bone Marrow Transplantation | Complement Pathway, Alternative - physiology | Chemokine CCL5 - metabolism | Monocytes - physiology | Disease Models, Animal | Macrophages - physiology | Cells, Cultured | Inflammation - immunology | Muscle, Skeletal - physiology | Elapid Venoms - pharmacology | Mice, Knockout | Regeneration - drug effects | Animals | Signal Transduction - physiology | Mice | Receptors, Complement - physiology | Wound Healing - physiology | Regeneration - immunology | Complement receptors | Complement component C3a | Antigen processing | Complement | Macrophages | Inactivation | Alternative pathway | Recruitment | Signal transduction | Cobra venom factor | Clonal deletion | Rodents | Injuries | Recombinant | Antigen presentation | Deactivation | Cytokines | Muscles | Inflammation | Ablation | Skeletal muscle | Regeneration | Musculoskeletal system | Signaling | Monocytes | Complement component C3 | Venom | Infiltration | Auditory defects
Journal Article
Journal of Cellular Biochemistry, ISSN 0730-2312, 09/2011, Volume 112, Issue 9, pp. 2594 - 2605
Journal Article
PLoS ONE, ISSN 1932-6203, 09/2016, Volume 11, Issue 9, p. e0162228
Journal Article
Blood, ISSN 0006-4971, 06/2012, Volume 119, Issue 26, pp. 6307 - 6316
Journal Article
Neuron, ISSN 0896-6273, 12/2018, Volume 100, Issue 6, pp. 1337 - 1353.e5
Strong evidence implicates the complement pathway as an important contributor to amyloid pathology in Alzheimer’s disease (AD... 
Alzheimer’s disease | neuroinflammation | STAT3 | tau | complement | microglia | C3aR | Alzheimer's disease | PROTEIN | INHIBITION | MICROGLIA | PATHWAY | PHOSPHORYLATION | SYNAPSE LOSS | PROLIFERATION | ASTROCYTE REACTIVITY | EXPRESSION | NEUROSCIENCES | INNATE IMMUNITY | Alzheimer Disease - complications | Humans | Middle Aged | tau Proteins - metabolism | Evoked Potentials - physiology | Male | Gene Regulatory Networks - physiology | Complement C3a - genetics | Alzheimer Disease - pathology | Receptors, Complement - metabolism | DNA-Binding Proteins - metabolism | tau Proteins - genetics | Cognition Disorders - etiology | Up-Regulation - physiology | Receptors, Complement - genetics | Aged, 80 and over | Tauopathies - complications | Adult | Female | Complement C3a - metabolism | Disease Models, Animal | Calcium-Binding Proteins | Cytokines - metabolism | Brain - physiopathology | Mice, Transgenic | Animals | Signal Transduction - drug effects | Microfilament Proteins | Alzheimer Disease - metabolism | Brain - pathology | Signal Transduction - physiology | Aged | Mice | Brain | Complement receptors | Animal models | Complement component C3a | Disease | Pathogenesis | Cognitive ability | Neuronal-glial interactions | Proteins | Neurotoxicity | Clonal deletion | Neurodegeneration | Transgenic animals | Rodents | Amyloid | Medical research | Data analysis | Immunoglobulins | Statistical analysis | Neurodegenerative diseases | Stat3 protein | Inflammation | Gene expression | Ribonucleic acid--RNA | Microglia | Pathology | Tau protein | Complement component C3 | Software | Neuroinflammation | Tau | Complement
Journal Article