about
Simple combinations of lineage-determining transcription factors prime cis-regulatory elements required for macrophage and B cell identitiesRegulated accumulation of desmosterol integrates macrophage lipid metabolism and inflammatory responsesExploiting genomics and natural genetic variation to decode macrophage enhancersThe selection and function of cell type-specific enhancers53BP1 and USP28 mediate p53 activation and G1 arrest after centrosome loss or extended mitotic duration.Mutant Huntingtin promotes autonomous microglia activation via myeloid lineage-determining factorsNCoR repression of LXRs restricts macrophage biosynthesis of insulin-sensitizing omega 3 fatty acids.Mechanisms establishing TLR4-responsive activation states of inflammatory response genes.Coronin 2A mediates actin-dependent de-repression of inflammatory response genes.Reprogramming transcription by distinct classes of enhancers functionally defined by eRNAFunctional roles of enhancer RNAs for oestrogen-dependent transcriptional activationEnvironment drives selection and function of enhancers controlling tissue-specific macrophage identities.Global changes in the nuclear positioning of genes and intra- and interdomain genomic interactions that orchestrate B cell fate.Affinity and dose of TCR engagement yield proportional enhancer and gene activity in CD4+ T cells.Tissue damage drives co-localization of NF-κB, Smad3, and Nrf2 to direct Rev-erb sensitive wound repair in mouse macrophagesRev-Erbs repress macrophage gene expression by inhibiting enhancer-directed transcription.25-Hydroxycholesterol activates the integrated stress response to reprogram transcription and translation in macrophages.Vespucci: a system for building annotated databases of nascent transcripts.Effect of natural genetic variation on enhancer selection and function.Control of proinflammatory gene programs by regulated trimethylation and demethylation of histone H4K20.Loss of CMAH during Human Evolution Primed the Monocyte-Macrophage Lineage toward a More Inflammatory and Phagocytic State.Transcriptional networks specifying homeostatic and inflammatory programs of gene expression in human aortic endothelial cells.Mutant p53 shapes the enhancer landscape of cancer cells in response to chronic immune signaling.Remodeling of the enhancer landscape during macrophage activation is coupled to enhancer transcription.An environment-dependent transcriptional network specifies human microglia identity.Thrombospondin1 (TSP1) replacement prevents cerebral cavernous malformations.Histone demethylase LSD1 regulates hematopoietic stem cells homeostasis and protects from death by endotoxic shock.Massively Parallel Sequencing of Peritoneal and Splenic B Cell Repertoires Highlights Unique Properties of B-1 Cell Antibodies.Cell-specific discrimination of desmosterol and desmosterol mimetics confers selective regulation of LXR and SREBP in macrophages.Deconvolution of pro- and antiviral genomic responses in Zika virus-infected and bystander macrophagesMARGE: Mutation Analysis for Regulatory Genomic ElementsPHLPP1 counter-regulates STAT1-mediated inflammatory signalingSF2523: Dual PI3K/BRD4 Inhibitor Blocks Tumor Immunosuppression and Promotes Adaptive Immune Responses in CancerBrain cell type-specific enhancer-promoter interactome maps and disease-risk associationCx3cr1-deficient microglia exhibit a premature aging transcriptomeZNF263 is a transcriptional regulator of heparin and heparan sulfate biosynthesisThe coming of age of Langerhans cell histiocytosisTranscriptomic and epigenetic mechanisms underlying myeloid diversity in the lungMacrophage Syk-PI3Kγ Inhibits Antitumor Immunity: SRX3207, a Novel Dual Syk-PI3K Inhibitory Chemotype Relieves Tumor Immunosuppression
P50
Q24617969-5488EFED-B206-4015-B365-809FD0946BE5Q24631052-1B29644E-7A62-480F-A19C-6AD8C88464C5Q26825066-B3497B46-E665-4364-9E6D-2864BED48E18Q28081960-716A0D35-7FFB-48A5-A76C-0B2511C5B735Q30786652-9D4D785F-F43E-4DF2-B2F8-F7172DF10BB5Q33959395-ECDE3264-3884-4220-A50B-EA3305218AF5Q34040157-60DACDE8-00E3-43A3-AC21-ADB626AEBCF3Q34102791-83260875-2D62-4274-860C-0A70287D00CBQ34165410-361A724F-4AFA-444D-988F-EDEDA92225F9Q34185076-F8F51D48-99C0-423F-A774-F2602674F7C4Q34348069-1C29CD91-31CC-4158-B70F-D805DC80F0D7Q34452301-03A7BA6E-5F7F-4D41-82BF-250ED879BAD8Q36409603-8E0BD24C-CF82-4511-AA14-32563F1E8BF2Q37062660-AD4F0344-898E-41AC-8B9F-4706CEE66E27Q37131362-C9EFB16F-21B1-4F5A-813C-274BFE1870FFQ37340291-7119C164-B32F-43C3-8886-7D4D68C48A15Q37388798-1369CF9D-AEA7-4FDA-95CF-52AAA3785853Q37606961-2AF15B6A-791E-407D-8E7A-D2BA48747AEDQ38866012-867097E3-ACC5-4772-861A-F82CCD4FF311Q39291348-F0C41C1D-304C-4D9F-A3A9-AE080986CA2DQ40349870-60EBFF47-89B4-4181-85E7-7EDC92D59176Q41854365-AE21CB11-685F-47DD-B96B-F87F5759DF2DQ42367753-5EE50532-9996-4556-AEB6-16B99CF74A85Q42972194-81E1CB82-119C-4136-87E4-551C8B803F8FQ44102400-C0F8C436-C2B8-47FA-986A-E24CBE61129CQ46147842-B7543BDC-DBE4-4569-8AA7-ECE62D69EC27Q47562688-C95E9870-E427-45E7-89D1-7DE4EEE94170Q48147788-4ECED5DC-4787-4E85-B245-63F7F487A6FDQ52720528-44CC9674-757F-4310-8749-13EE548A9874Q58749402-D0CF7E5C-A3BA-4088-973B-CBE8B97ABD86Q59708326-9A219EF0-6799-4DA4-8D22-06DD95D3EAC3Q83230317-04EFAAA5-3C11-4430-9FD3-4501AA31575AQ90281946-C75250E6-916F-408B-A856-5A7E98ABCC07Q91286474-621D3D67-EABC-4D85-9B76-13DB8D074472Q91618150-A1FEDD8C-EA7D-404F-922B-CDC37B83E560Q91816217-3C44DEC9-49D4-4D59-AC0D-3E07F92AEA79Q91934621-E7969A7C-53DE-46FC-8426-F02E8E19118BQ92784696-E121144A-5603-4EB7-93FA-891973FF834CQ92889441-C72AA924-7FBA-4FF7-844A-6100D35A735E
P50
description
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
Christopher K Glass
@ast
Christopher K Glass
@en
Christopher K Glass
@es
Christopher K Glass
@nl
Christopher K Glass
@sl
type
label
Christopher K Glass
@ast
Christopher K Glass
@en
Christopher K Glass
@es
Christopher K Glass
@nl
Christopher K Glass
@sl
prefLabel
Christopher K Glass
@ast
Christopher K Glass
@en
Christopher K Glass
@es
Christopher K Glass
@nl
Christopher K Glass
@sl
P106
P21
P31
P496
0000-0003-4344-3592