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Age-dependent changes on TGFβ1 Smad3 pathway modify the pattern of microglial cell activation

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What this work says

Outgoing claims: the papers this work cites, builds on, or argues with.

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Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration
inferredcites →https://doi.org/10.1002/glia.22343openalex-snapshot
TGF‐β signaling through SMAD2/3 induces the quiescent microglial phenotype within the CNS environment
inferredcites →https://doi.org/10.1002/jnr.10351openalex-snapshot
Gene expression profiling of 12633 genes in Alzheimer hippocampal CA1: Transcription and neurotrophic factor down‐regulation and up‐regulation of apoptotic and pro‐inflammatory signaling
inferredcites →https://doi.org/10.1002/jnr.21072openalex-snapshot
Ectopic expression of phospho‐Smad2 in Alzheimer's disease: Uncoupling of the transforming growth factor‐β pathway?
inferredcites →https://doi.org/10.1002/jnr.23082openalex-snapshot
Transforming growth factor‐β stimulates β amyloid uptake by microglia through Smad3‐dependent mechanisms
inferredcites →https://doi.org/10.1007/bf03033906openalex-snapshot
Glial cell dysregulation: a new perspective on Alzheimer disease
inferredcites →https://doi.org/10.1007/bf03033981openalex-snapshot
Pro- and anti-inflammatory cytokines regulate the ERK pathway: Implication of the timing for the activation of microglial cells
inferredcites →https://doi.org/10.1007/s10072-006-0562-6openalex-snapshot
Increased intrathecal TGF-β1, but not IL-12, IFN-γ and IL-10 levels in Alzheimer’s disease patients
inferredcites →https://doi.org/10.1016/j.bbi.2010.05.011openalex-snapshot
Protracted downregulation of CX3CR1 on microglia of aged mice after lipopolysaccharide challenge
inferredcites →https://doi.org/10.1016/j.cellsig.2006.11.008openalex-snapshot
SMAD3 expression is regulated by mitogen-activated protein kinase kinase-1 in epithelial and smooth muscle cells
inferredcites →https://doi.org/10.1016/j.ijdevneu.2005.11.014openalex-snapshot
Contribution of inflammatory processes to Alzheimer's disease: molecular mechanisms
inferredcites →https://doi.org/10.1016/j.imlet.2007.09.002openalex-snapshot
Altered plasma cytokine levels in Alzheimer's disease: Correlation with the disease progression
inferredcites →https://doi.org/10.1016/j.jneumeth.2011.08.027openalex-snapshot
Proliferating culture of aged microglia for the study of neurodegenerative diseases
inferredcites →https://doi.org/10.1016/j.jneuroim.2007.07.020openalex-snapshot
NGF promotes microglial migration through the activation of its high affinity receptor: Modulation by TGF-β
inferredcites →https://doi.org/10.1016/j.nbd.2005.01.003openalex-snapshot
Transforming growth factor-β1 produced by hippocampal cells modulates microglial reactivity in culture
inferredcites →https://doi.org/10.1016/j.nbd.2005.01.007openalex-snapshot
Protection of rat primary hippocampal cultures from Aβ cytotoxicity by pro-inflammatory molecules is mediated by astrocytes
inferredcites →https://doi.org/10.1016/j.neulet.2004.06.001openalex-snapshot
Increased cerebrospinal fluid levels of transforming growth factor-β1 in Alzheimer’s disease
inferredcites →https://doi.org/10.1016/j.neurobiolaging.2007.12.005openalex-snapshot
Mitochondrial dysfunction: An early event in Alzheimer pathology accumulates with age in AD transgenic mice
inferredcites →https://doi.org/10.1016/j.neuroscience.2008.11.002openalex-snapshot
Reduction of β-amyloid-induced neurotoxicity on hippocampal cell cultures by moderate acidosis is mediated by transforming growth factor β
inferredcites →https://doi.org/10.1016/s0896-6273(00)80187-7openalex-snapshot
Microglial Cells Internalize Aggregates of the Alzheimer's Disease Amyloid β-Protein Via a Scavenger Receptor
inferredcites →https://doi.org/10.1023/b:nere.0000023615.89699.63openalex-snapshot
Gene Expression Profiling in Fetal, Aged, and Alzheimer Hippocampus: A Continuum of Stress-Related Signaling
inferredcites →https://doi.org/10.1038/39321openalex-snapshot
Amyloidogenic role of cytokine TGF-β1 in transgenic mice and in Alzheimer's disease
inferredcites →https://doi.org/10.1038/87945openalex-snapshot
TGF-β1 promotes microglial amyloid-β clearance and reduces plaque burden in transgenic mice
inferredcites →https://doi.org/10.1038/nature02006openalex-snapshot
Smad-dependent and Smad-independent pathways in TGF-β family signalling
inferredcites →https://doi.org/10.1038/nm1781openalex-snapshot
Blocking TGF-β–Smad2/3 innate immune signaling mitigates Alzheimer-like pathology
inferredcites →https://doi.org/10.1038/nrm2297openalex-snapshot
TGFβ–SMAD signal transduction: molecular specificity and functional flexibility
inferredcites →https://doi.org/10.1038/nrn2038openalex-snapshot
Microglia-mediated neurotoxicity: uncovering the molecular mechanisms
inferredcites →https://doi.org/10.1038/sj.emboj.7601818openalex-snapshot
TGF‐β activates Erk MAP kinase signalling through direct phosphorylation of ShcA
inferredcites →https://doi.org/10.1042/bj20040682openalex-snapshot
Sp1 and Smad transcription factors co-operate to mediate TGF-β-dependent activation of amyloid-β precursor protein gene transcription
inferredcites →https://doi.org/10.1042/bst0351119openalex-snapshot
Mechanisms of inflammatory neurodegeneration: iNOS and NADPH oxidase
inferredcites →https://doi.org/10.1074/jbc.m004536200openalex-snapshot
Transforming Growth Factor-β1 Inhibition of Macrophage Activation Is Mediated via Smad3
inferredcites →https://doi.org/10.1074/jbc.m300819200openalex-snapshot
Transforming Growth Factor-β1 Potentiates Amyloid-β Generation in Astrocytes and in Transgenic Mice
inferredcites →https://doi.org/10.1074/jbc.m414686200openalex-snapshot
Expression of Scavenger Receptors in Glial Cells
inferredcites →https://doi.org/10.1089/ars.2011.4082openalex-snapshot
Alzheimer's Disease: Redox Dysregulation As a Common Denominator for Diverse Pathogenic Mechanisms
inferredcites →https://doi.org/10.1093/emboj/cdf366openalex-snapshot
TGF‐β receptor‐activated p38 MAP kinase mediates Smad‐independent TGF‐β responses
inferredcites →https://doi.org/10.1111/j.1460-9568.2006.05109.xopenalex-snapshot
Altered subcellular location of phosphorylated Smads in Alzheimer's disease
inferredcites →https://doi.org/10.1111/j.1471-4159.2009.06537.xopenalex-snapshot
Aging‐dependent changes of microglial cells and their relevance for neurodegenerative disorders
inferredcites →https://doi.org/10.1111/j.1471-4159.2012.07887.xopenalex-snapshot
Modulation of interferon‐γ‐induced glial cell activation by transforming growth factor β1: A role for STAT1 and MAPK pathways
inferredcites →https://doi.org/10.1126/science.1072994openalex-snapshot
The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics
inferredcites →https://doi.org/10.1136/jnnp.2003.034454openalex-snapshot
Association of a polymorphism of the transforming growth factor- 1 gene with cerebral amyloid angiopathy
inferredcites →https://doi.org/10.1159/000110642openalex-snapshot
Modulation by Astrocytes of Microglial Cell-Mediated Neuroinflammation: Effect on the Activation of Microglial Signaling Pathways
inferredcites →https://doi.org/10.1172/jci27341openalex-snapshot
Deficiency in neuronal TGF-β signaling promotes neurodegeneration and Alzheimer’s pathology
inferredcites →https://doi.org/10.3233/jad-2008-15104openalex-snapshot
Proinflammatory Stimuli are Needed for Induction of Microglial Cell-Mediated AβPP244–C and Aβ-Neurotoxicity in Hippocampal Cultures
inferredcites →https://doi.org/10.3233/jad-2011-101014openalex-snapshot
Microglia Demonstrate Age-Dependent Interaction with Amyloid-β Fibrils
inferredcites →https://doi.org/10.3233/jad-2012-120721openalex-snapshot
Transforming Growth Factor β1 Modulates Amyloid β-Induced Glial Activation through the Smad3-Dependent Induction of MAPK Phosphatase-1
inferredcites →https://doi.org/10.4049/jimmunol.173.2.962openalex-snapshot
TGF-β1 Disrupts Endotoxin Signaling in Microglial Cells through Smad3 and MAPK Pathways

What points at this work

Incoming claims: where this work appears in other papers’ reference lists and arguments.

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Additional file 1 of Substantia nigra Smad3 signaling deficiency: relevance to aging and Parkinson’s disease and roles of microglia, proinflammatory factors, and MAPK
inferred← citeshttps://doi.org/10.6084/m9.figshare.13245320openalex-snapshot
Additional file 2 of Substantia nigra Smad3 signaling deficiency: relevance to aging and Parkinson’s disease and roles of microglia, proinflammatory factors, and MAPK
inferred← citeshttps://doi.org/10.6084/m9.figshare.13245323openalex-snapshot
Additional file 3 of Substantia nigra Smad3 signaling deficiency: relevance to aging and Parkinson’s disease and roles of microglia, proinflammatory factors, and MAPK
inferred← citeshttps://doi.org/10.6084/m9.figshare.13245329openalex-snapshot
Additional file 4 of Substantia nigra Smad3 signaling deficiency: relevance to aging and Parkinson’s disease and roles of microglia, proinflammatory factors, and MAPK
inferred← citeshttps://doi.org/10.6084/m9.figshare.13245332openalex-snapshot
Additional file 5 of Substantia nigra Smad3 signaling deficiency: relevance to aging and Parkinson’s disease and roles of microglia, proinflammatory factors, and MAPK
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