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1. Full Text TGF-β signaling regulates neuronal C1q expression and developmental synaptic refinement
by Bialas, Allison R and Stevens, Beth
Nature Neuroscience, ISSN 1097-6256, 2013, Volume 16, Issue 12, pp. 1773 - 1782
Immune molecules, including complement proteins C1q and C3, have emerged as critical mediators of synaptic refinement and plasticity. Complement localizes to... 
Retina - drug effects | Protein-Serine-Threonine Kinases - deficiency | Retina - metabolism | Retina - growth & development | Age Factors | Cell Count | Green Fluorescent Proteins - genetics | Retinal Ganglion Cells - metabolism | Cerebral Cortex - cytology | Complement C1q - metabolism | Retina - cytology | Gene Expression Regulation, Developmental - physiology | Animals, Newborn | Neuroglia - chemistry | Green Fluorescent Proteins - metabolism | Synapses - drug effects | Synapses - physiology | Mice, Inbred C57BL | Cells, Cultured | Gene Expression Regulation, Developmental - drug effects | Neuroglia - physiology | Rats | Mice, Transgenic | Complement C1q - genetics | Transcription Factors - genetics | Rats, Sprague-Dawley | Homeodomain Proteins - genetics | Animals | Signal Transduction - drug effects | Signal Transduction - physiology | Mice | Transforming Growth Factor beta - metabolism | Retinal Ganglion Cells - drug effects | Receptors, Transforming Growth Factor beta - deficiency | Index Medicus
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2. Full Text C1q-induced LRP1B and GPR6 proteins expressed early in Alzheimer disease mouse models, are essential for the C1q-mediated protection against amyloid- β neurotoxicity
by Benoit, Marie E and Hernandez, Michael X and Dinh, Minhan L and Benavente, Francisca and Vasquez, Osvaldo and Tenner, Andrea J
Journal of Biological Chemistry, ISSN 0021-9258, 01/2013, Volume 288, Issue 1, pp. 654 - 665
Complement protein C1q is induced in the brain in response to a variety of neuronal injuries, including Alzheimer disease (AD), and blocks fibrillar... 
COMPLEMENT | C1Q | FIBRILLAR OLIGOMERS | BIOCHEMISTRY & MOLECULAR BIOLOGY | A-BETA | COUPLED RECEPTORS | COMMON MECHANISM | CELL-SURFACE | ELEMENT-BINDING PROTEIN | PRECURSOR PROTEIN | DENSITY-LIPOPROTEIN RECEPTOR | Up-Regulation | Tumor Suppressor Proteins - metabolism | Receptors, G-Protein-Coupled - metabolism | Humans | Gene Expression Regulation | Rats | Receptors, LDL - metabolism | Gene Expression Profiling | Neurodegenerative Diseases - metabolism | Complement C1q - metabolism | Tumor Suppressor Proteins - physiology | Animals | Models, Biological | Alzheimer Disease - metabolism | Amyloid beta-Peptides - metabolism | Mice | Receptors, LDL - physiology | Disease Models, Animal | Receptors, G-Protein-Coupled - physiology | Index Medicus | Neuroprotection | Gene Expression | C1q | Alzheimer disease | Neurodegeneration | Neurobiology | Amyloid | Complement | GPR6 | LRP1B
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3. Full Text Complement C1q-C3-associated synaptic changes in multiple sclerosis hippocampus
by Michailidou, Iliana and Willems, Janske G. P and Kooi, Evert-Jan and van Eden, Corbert and Gold, Stefan M and Geurts, Jeroen J. G and Baas, Frank and Huitinga, Inge and Ramaglia, Valeria
Annals of neurology, ISSN 0364-5134, 2015, Volume 77, Issue 6, pp. 1007 - 1026
Multiple sclerosis (MS) is a demyelinating disease of the central nervous system, leading to memory impairment in up to 65% of patients. Memory dysfunction in... 
ACTIVATION | C1Q | MEMORY | MICROGLIA | ATROPHY | CNS | MECHANISMS | DYSFUNCTION | EXPRESSION | NEUROSCIENCES | DEMYELINATING LESIONS | CLINICAL NEUROLOGY | Tissue Banks | Complement C3 - metabolism | Cell Count | Humans | Middle Aged | Male | Hippocampus - pathology | Synapses - pathology | RNA, Messenger - metabolism | Complement C1q - metabolism | Alzheimer Disease - pathology | Hippocampus - metabolism | Synapses - metabolism | Alzheimer Disease - metabolism | Aged, 80 and over | Multiple Sclerosis - pathology | Adult | Female | Aged | Multiple Sclerosis - metabolism | Proteins | Medical research | Multiple sclerosis | Rodents | Index Medicus
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4. Full Text Complement C1q Activates Canonical Wnt Signaling and Promotes Aging-Related Phenotypes
by Naito, Atsuhiko T and Sumida, Tomokazu and Nomura, Seitaro and Liu, Mei-Lan and Higo, Tomoaki and Nakagawa, Akito and Okada, Katsuki and Sakai, Taku and Hashimoto, Akihito and Hara, Yurina and Shimizu, Ippei and Zhu, Weidong and Toko, Haruhiro and Katada, Akemi and Akazawa, Hiroshi and Oka, Toru and Lee, Jong-Kook and Minamino, Tohru and Nagai, Toshio and Walsh, Kenneth and Kikuchi, Akira and Matsumoto, Misako and Botto, Marina and Shiojima, Ichiro and Komuro, Issei
Cell, ISSN 0092-8674, 06/2012, Volume 149, Issue 6, pp. 1298 - 1313
Wnt signaling plays critical roles in development of various organs and pathogenesis of many diseases, and augmented Wnt signaling has recently been implicated... 
CELLS | IMMUNITY | 1ST COMPONENT | SUBCOMPONENT | INHIBITION | MECHANISM | PATHWAY | BIOCHEMISTRY & MOLECULAR BIOLOGY | RECEPTOR | BETA-CATENIN | PROTEINS | CELL BIOLOGY | Low Density Lipoprotein Receptor-Related Protein-6 - metabolism | Animals | Serum - metabolism | Humans | Mice | Complement C1s - metabolism | Complement C1q - metabolism | Wnt Signaling Pathway | Aging - metabolism | Medical colleges | Phenotype | Low density lipoproteins | Genes | Muscles | Genetic aspects | Universities and colleges | Index Medicus
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5. Full Text C1q Binding Activity of De Novo Donor-specific HLA Antibodies in Renal Transplant Recipients With and Without Antibody-mediated Rejection
by Yell, Maggie and Muth, Brenda L and Kaufman, Dixon B and Djamali, Arjang and Ellis, Thomas M
Transplantation, ISSN 0041-1337, 06/2015, Volume 99, Issue 6, pp. 1151 - 1155
BACKGROUNDComplement fixation by donor-specific HLA antibodies (DSA) is a primary mechanism for antibody-mediated damage of organ allografts. Using a recently... 
SURGERY | ASSAY | COMPLEMENT-BINDING | RISK | OUTCOMES | IMMUNOLOGY | TRANSPLANTATION | Isoantibodies - blood | Antibody Specificity | Complement Activation | Immunoglobulin G - blood | Humans | HLA Antigens - immunology | Graft Rejection - etiology | Graft Rejection - immunology | Tissue Donors | Complement C1q - metabolism | Transplant Recipients | Kidney Transplantation - adverse effects | Index Medicus
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6. Full Text Enhanced synaptic connectivity and epilepsy in C1q knockout mice
by Yunxiang Chu and Xiaoming Jin and Isabel Parada and Alexei Pesic and Beth Stevens and Ben Barres and David A. Prince and Edward G. Jones
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 4/2010, Volume 107, Issue 17, pp. 7975 - 7980
Excessive CNS synapses are eliminated during development to establish mature patterns of neuronal connectivity. A complement cascade protein, C1q, is involved... 
Electrodes | Axons | Neurons | Pyramidal cells | Epilepsy | Pruning | Connectivity | Mice | Synapses | Seizures | Synaptic pruning | Development | Complement cascade | Seizure | Axonal boutons | development | seizure | TEMPORAL-LOBE EPILEPSY | axonal boutons | COMPLEMENT ACTIVATION | MULTIDISCIPLINARY SCIENCES | RATS | MATURATION | complement cascade | IN-VITRO | V PYRAMIDAL NEURONS | VISUAL-CORTEX | synaptic pruning | MUTATIONS | EXPRESSION | BRAIN | Synapses - physiology | Mice, Inbred C57BL | Evoked Potentials | Glutamates - metabolism | Electroencephalography | Microscopy, Video | Complement C1q - genetics | Epilepsy - physiopathology | Complement C1q - metabolism | Mice, Knockout | Patch-Clamp Techniques | Animals | Synapses - metabolism | Analysis of Variance | Neocortex - physiopathology | Complement C1q - deficiency | Photic Stimulation | Cellular proteins | Central nervous system | Research | Properties | Health aspects | Proteins | Brain | Biochemistry | Rodents | Index Medicus | Biological Sciences
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7. Full Text Classical Pathway of Complement Activation: Longitudinal Associations of C1q and C1-INH With Cardiovascular Outcomes: The CODAM Study (Cohort on Diabetes and Atherosclerosis Maastricht)—Brief Report
by Hertle, Elisabeth and Arts, Ilja C.W and van der Kallen, Carla J.H and Feskens, Edith J.M and Schalkwijk, Casper G and Stehouwer, Coen D.A and van Greevenbroek, Marleen M.J
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 05/2018, Volume 38, Issue 5, pp. 1242 - 1244
OBJECTIVE—The classical complement pathway has been assigned both protective and pathological effects in cardiovascular disease (CVD), but human data are... 
SYSTEMIC-LUPUS-ERYTHEMATOSUS | C1Q-ADIPONECTIN/TOTAL ADIPONECTIN RATIO | EVENTS | RISK | JAPANESE TYPE-2 DIABETICS | SERUM | cardiovascular diseases | carotid intima-media thickness | follow-up studies | INSULIN-RESISTANCE | MBL | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | humans | incidence | Prognosis | Prospective Studies | Complement C1q - immunology | Humans | Middle Aged | Netherlands - epidemiology | Complement C1 Inhibitor Protein - immunology | Male | Complement C1q - metabolism | Incidence | Time Factors | Cardiovascular Diseases - diagnostic imaging | Cardiovascular Diseases - epidemiology | Adult | Female | Complement C1 Inhibitor Protein - metabolism | Complement Pathway, Classical | Cell Adhesion Molecules - blood | Risk Assessment | Carotid Intima-Media Thickness | Risk Factors | Inflammation Mediators - blood | Biomarkers - blood | Cardiovascular Diseases - immunology | Aged | Longitudinal Studies | Index Medicus
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8. Full Text C1q acts in the tumour microenvironment as a cancer-promoting factor independently of complement activation
by Bulla, Roberta and Tripodo, Claudio and Rami, Damiano and Ling, Guang Sheng and Agostinis, Chiara and Guarnotta, Carla and Zorzet, Sonia and Durigutto, Paolo and Botto, Marina and Tedesco, Francesco
Nature Communications, ISSN 2041-1723, 02/2016, Volume 7, Issue 1, pp. 10346 - 10346
Complement C1q is the activator of the classical pathway. However, it is now recognized that C1q can exert functions unrelated to complement activation. Here... 
IMMUNE-RESPONSE | MELANOMA | PROTEIN | TROPHOBLAST INVASION | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | DISEASE | MECHANISMS | EFFECTOR SYSTEM | ANTIBODY THERAPY | DEFICIENCY | Complement C5 - genetics | Neoplasms - metabolism | Cell Proliferation | Complement C5 - metabolism | Complement C3 - metabolism | Humans | Mice, Inbred C57BL | Complement C1q - genetics | Complement C1q - metabolism | Mice, Knockout | Animals | Cell Line, Tumor | Mice | Complement C3 - genetics | Apoptosis | Cell Movement | Complement Activation - physiology | Index Medicus
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9. Full Text Progranulin Deficiency Promotes Circuit-Specific Synaptic Pruning by Microglia via Complement Activation
by Lui, Hansen and Zhang, Jiasheng and Makinson, Stefanie R and Cahill, Michelle K and Kelley, Kevin W and Huang, Hsin-Yi and Huang, Eric J and Shang, Yulei and Oldham, Michael C and Martens, Lauren Herl and Gao, Fuying and Coppola, Giovanni and Sloan, Steven A and Hsieh, Christine L and Kim, Charles C and Bigio, Eileen H and Weintraub, Sandra and Mesulam, Marek-Marsel and Rademakers, Rosa and Mackenzie, Ian R and Seeley, William W and Karydas, Anna and Miller, Bruce L and Borroni, Barbara and Ghidoni, Roberta and Farese, Robert V and Paz, Jeanne T and Barres, Ben A
Cell, ISSN 0092-8674, 05/2016, Volume 165, Issue 4, pp. 921 - 935
Microglia maintain homeostasis in the brain, but whether aberrant microglial activation can cause neurodegeneration remains controversial. Here, we use... 
NETWORK ANALYSIS | ORGANIZATION | CELLS | C1Q | DEMENTIA | TRANSCRIPTOME | BIOCHEMISTRY & MOLECULAR BIOLOGY | MUTATION | FRONTOTEMPORAL LOBAR DEGENERATION | NEURONAL CEROID-LIPOFUSCINOSIS | OBSESSIVE-COMPULSIVE DISORDER | CELL BIOLOGY | Frontotemporal Dementia - genetics | Microglia - metabolism | Thalamus - metabolism | Complement Activation | Cerebrospinal Fluid | Humans | Intercellular Signaling Peptides and Proteins - genetics | Obsessive-Compulsive Disorder - metabolism | Complement C1q - genetics | Immunity, Innate | Complement C1q - metabolism | Brain - metabolism | Frontotemporal Dementia - metabolism | Intercellular Signaling Peptides and Proteins - metabolism | Obsessive-Compulsive Disorder - genetics | Aging - immunology | Animals | Lysosomes - metabolism | Synapses - metabolism | Metabolic Networks and Pathways | Mice | Intercellular Signaling Peptides and Proteins - deficiency | Aging - metabolism | Nervous system diseases | Neurosciences | Human acts | Mortality | Obsessive-compulsive disorder | Human behavior | Health aspects | Dementia | Index Medicus
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10. Full Text Sustained Systemic Glucocerebrosidase Inhibition Induces Brain α-Synuclein Aggregation, Microglia and Complement C1q Activation in Mice
by Rocha, Emily M and Smith, Gaynor A and Park, Eric and Cao, Hongmei and Graham, Anne-Renee and Brown, Eilish and McLean, Jesse R and Hayes, Melissa A and Beagan, Jonathan and Izen, Sarah C and Perez-Torres, Eduardo and Hallett, Penelope J and Isacson, Ole
Antioxidants & Redox Signaling, ISSN 1523-0864, 08/2015, Volume 23, Issue 6, pp. 55 - 564
Aims: Loss-of-function mutations in GBA1 , which cause the autosomal recessive lysosomal storage disease, Gaucher disease (GD), are also a key genetic risk... 
Forum Original Research Communications | PERRY SYNDROME | CHAPERONE-MEDIATED AUTOPHAGY | BIOCHEMISTRY & MOLECULAR BIOLOGY | MOUSE MODEL | IN-VIVO | ENDOCRINOLOGY & METABOLISM | DEGRADATION | ACID BETA-GLUCOSIDASE | MUTATIONS | SUBSTANTIA-NIGRA | NEURONOPATHIC GAUCHER-DISEASE | PARKINSONS-DISEASE | Axonal Transport | Inositol - pharmacology | Protein Aggregation, Pathological - chemically induced | Protein Aggregation, Pathological - enzymology | Complement Activation | Cerebral Cortex - pathology | Male | Glucosylceramidase - metabolism | Inositol - analogs & derivatives | Autophagy | Complement C1q - metabolism | Cerebral Cortex - metabolism | Synaptic Transmission | Glucosylceramidase - antagonists & inhibitors | Parkinson Disease, Secondary - enzymology | Animals | Microglia - physiology | Proteins - metabolism | Mice | Parkinson Disease, Secondary - chemically induced | alpha-Synuclein - metabolism | Index Medicus
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11. Full Text Structures of C1q-like Proteins Reveal Unique Features among the C1q/TNF Superfamily
by Ressl, Susanne and Vu, Brandon K and Vivona, Sandro and Martinelli, David C and Südhof, Thomas C and Brunger, Axel T
Structure, ISSN 0969-2126, 04/2015, Volume 23, Issue 4, pp. 688 - 699
C1q-like (C1QL) -1, -2, and -3 proteins are encoded by homologous genes that are highly expressed in brain. C1QLs bind to brain-specific angiogenesis inhibitor... 
COMPLEMENT | C1Q | CRYSTAL-STRUCTURE | BIOCHEMISTRY & MOLECULAR BIOLOGY | RECEPTOR | MYOBLAST FUSION | FAMILY | CELL BIOLOGY | BIOPHYSICS | CEREBELLUM | SYNAPSE FORMATION | GLOBULAR DOMAIN | CBLN1 | Protein Structure, Tertiary | Amino Acid Sequence | Adiponectin - chemistry | Calcium - metabolism | Protein Multimerization | Molecular Sequence Data | Complement C1q - genetics | Complement C1q - metabolism | Protein Binding | Adiponectin - metabolism | Mutation | Protein Stability | Complement C1q - chemistry | Oligomers | Physiological aspects | Muscle proteins | Protein binding | Index Medicus
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12. Full Text IgG Fc domains that bind C1q but not effector Fc gamma receptors delineate the importance of complement-mediated effector functions
by Lee, CH and Romain, G and Yan, WP and Watanabe, M and Charab, W and Todorova, B and Lee, J and Triplett, K and Donkor, M and Lungu, OI and Lux, A and Marshall, N and Lindorfer, MA and Goff, ORL and Balbino, B and Kang, TH and Tanno, H and Delidakis, G and Alford, C and Taylor, RP and Nimmerjahn, F and Varadarajan, N and Bruhns, P and Zhang, YJ and Georgiou, G and Argonne National Lab. (ANL), Argonne, IL (United States). Advanced Photon Source (APS)
NATURE IMMUNOLOGY, ISSN 1529-2908, 08/2017, Volume 18, Issue 8, pp. 889 - 889
Engineered crystallizable fragment (Fc) regions of antibody domains, which assume a unique and unprecedented asymmetric structure within the homodimeric Fc... 
DEPENDENT CELLULAR CYTOTOXICITY | MOUSE COMPLEMENT | CELLS | ACTIVATION | AFFINITY | RITUXIMAB | GLYCOSYLATION | IMMUNOLOGY | MONOCLONAL-ANTIBODIES | THERAPEUTIC ACTIVITY | HUMAN CD20 | Surface Plasmon Resonance | Precursor Cell Lymphoblastic Leukemia-Lymphoma - immunology | Immunoglobulin Fc Fragments - metabolism | Complement C1q - immunology | Humans | Crystallography, X-Ray | Complement C1q - metabolism | Receptors, IgG - metabolism | Precursor Cell Lymphoblastic Leukemia-Lymphoma - drug therapy | Tandem Mass Spectrometry | Immunoglobulin Fc Fragments - immunology | Burkitt Lymphoma - immunology | Immunoglobulin G - immunology | Immunotherapy | Mass Spectrometry | Lymphoma, B-Cell - immunology | Chromatography, Liquid | Lymphoma, Large B-Cell, Diffuse - immunology | Burkitt Lymphoma - drug therapy | Lymphoma, B-Cell - drug therapy | Lymphoma, Large B-Cell, Diffuse - drug therapy | Enzyme-Linked Immunosorbent Assay | Crystallization | Phagocytosis - immunology | Antibodies, Monoclonal | Receptors, IgG - immunology | Neoplasms - drug therapy | Animals | Neoplasms - immunology | Cell Line, Tumor | Mice | Chromatography, Gel | Cytotoxicity, Immunologic - immunology | In Vitro Techniques | Immunoglobulin G - metabolism | Index Medicus
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13. Full Text C1q and HMGB1 reciprocally regulate human macrophage polarization
by Son, Myoungsun and Son, Myoungsun and Porat, Amit and Porat, Amit and He, Mingzhu and He, Mingzhu and Suurmond, Jolien and Suurmond, Jolien and Santiago-Schwarz, Frances and Santiago-Schwarz, Frances and Andersson, Ulf and Andersson, Ulf and Coleman, Thomas R and Coleman, Thomas R and Volpe, Bruce T and Volpe, Bruce T and Tracey, Kevin J and Tracey, Kevin J and Al-Abed, Yousef and Al-Abed, Yousef and Diamond, Betty and Diamond, Betty
Blood, ISSN 0006-4971, 11/2016, Volume 128, Issue 18, pp. 2218 - 2228
A healthy immune system results from a balance of stimulatory and inhibitory pathways that allow effective responses to acute insults, without descending into... 
PATHOGENESIS | GROUP BOX 1 | SYSTEMIC-LUPUS-ERYTHEMATOSUS | ACTIVATION | DENDRITIC CELLS | COMPLEMENT PROTEIN C1Q | APOPTOTIC CELLS | RECEPTOR | CONTAINING IMMUNE-COMPLEXES | END-PRODUCTS RAGE | HEMATOLOGY | Cell Differentiation - immunology | Cell Polarity | Signal Transduction - immunology | Macrophages - metabolism | Complement C1q - immunology | HMGB1 Protein - metabolism | Humans | HMGB1 Protein - immunology | Macrophages - cytology | Complement C1q - metabolism | Macrophages - immunology | Index Medicus | Abridged Index Medicus | Immunobiology
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