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Article ; Online: Macrophages from Rosa26-Integrated Cas9-Expressing C57BL/6J Mice Have a Putative TRIF-Mediated Defect in the TLR-3/4 Signaling.

Raychowdhury, Raktima / Gentili, Matteo / Cui, Ang / Schweitzer, Lawrence D / Li, Bo / Hacohen, Nir

ImmunoHorizons

2021 Volume 5, Issue 10, Page(s) 818–829

Abstract: In this study, we report that the TLR4 ligand, LPS, and TLR3 ligand polyinosinic:polycytidylic acid failed to activate IRF3 or STAT1 in bone marrow-derived macrophages (BMMs) isolated from two independently generated lines of Rosa26-integrated Cas9- ... ...

Abstract	In this study, we report that the TLR4 ligand, LPS, and TLR3 ligand polyinosinic:polycytidylic acid failed to activate IRF3 or STAT1 in bone marrow-derived macrophages (BMMs) isolated from two independently generated lines of Rosa26-integrated Cas9-expressing C57BL/6J (B6) mice. RNA-sequencing analysis reveals that hundreds to thousands of genes including IFN-stimulated genes were differentially expressed in BMMs from these Cas9 strains compared with B6 upon LPS stimulation. Furthermore, the NF-κB signaling axis and TRIF-mediated necroptosis were also strongly reduced in response to LPS and polyinosinic:polycytidylic acid. In contrast, there were no defects in the responses of BMMs to ligands of the RIG-I, STING, TLR2, TLR9, and IFN receptors. Defects in TLR3 and TLR4 signaling were observed in mice with the B6 but not 129 background, and when Cas9 was integrated at the Rosa26 but not H11 locus. However, integration at the Rosa26 site, CAG promoter-driven Cas9 or eGFP were not individually sufficient to cause the defect. Taken together, the results of this study suggest a putative TRIF-mediated defect in TLR-3/4 signaling in BMMs from commercially available and widely used B6-Cas9-expressing mice.
MeSH term(s)	Adaptor Proteins, Vesicular Transport/metabolism ; Animals ; CRISPR-Associated Protein 9/genetics ; Cells, Cultured ; Female ; Lipopolysaccharides/immunology ; Macrophages/immunology ; Macrophages/metabolism ; Mice, Inbred C57BL ; Mice, Transgenic ; Models, Animal ; Necroptosis/immunology ; Poly I-C/immunology ; Primary Cell Culture ; RNA, Untranslated/genetics ; Signal Transduction/genetics ; Signal Transduction/immunology ; Toll-Like Receptor 3/metabolism ; Toll-Like Receptor 4/metabolism ; Mice
Chemical Substances	Adaptor Proteins, Vesicular Transport ; Gt(ROSA)26Sor non-coding RNA, mouse ; Lipopolysaccharides ; RNA, Untranslated ; TICAM-1 protein, mouse ; TLR3 protein, mouse ; Tlr4 protein, mouse ; Toll-Like Receptor 3 ; Toll-Like Receptor 4 ; CRISPR-Associated Protein 9 (EC 3.1.-) ; Poly I-C (O84C90HH2L)
Language	English
Publishing date	2021-10-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2573-7732
ISSN (online)	2573-7732
DOI	10.4049/immunohorizons.2100010
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Article ; Online: IRF3 inhibits IFN-γ-mediated restriction of intracellular pathogens in macrophages independently of IFNAR.

Maciag, Karolina / Raychowdhury, Raktima / Smith, Karen / Schneider, Alexis M / Coers, Jörn / Mumbach, Maxwell R / Schwartz, Schraga / Hacohen, Nir

Journal of leukocyte biology

2021 Volume 112, Issue 2, Page(s) 257–271

Abstract: Macrophages use an array of innate immune sensors to detect intracellular pathogens and to tailor effective antimicrobial responses. In addition, extrinsic activation with the cytokine IFN-γ is often required as well to tip the scales of the host- ... ...

Abstract	Macrophages use an array of innate immune sensors to detect intracellular pathogens and to tailor effective antimicrobial responses. In addition, extrinsic activation with the cytokine IFN-γ is often required as well to tip the scales of the host-pathogen balance toward pathogen restriction. However, little is known about how host-pathogen sensing impacts the antimicrobial IFN-γ-activated state. It was observed that in the absence of IRF3, a key downstream component of pathogen sensing pathways, IFN-γ-primed macrophages more efficiently restricted the intracellular bacterium Legionella pneumophila and the intracellular protozoan parasite Trypanosoma cruzi. This effect did not require IFNAR, the receptor for Type I IFNs known to be induced by IRF3, nor the sensing adaptors MyD88/TRIF, MAVS, or STING. This effect also did not involve differential activation of STAT1, the major signaling protein downstream of both Type 1 and Type 2 IFN receptors. IRF3-deficient macrophages displayed a significantly altered IFN-γ-induced gene expression program, with up-regulation of microbial restriction factors such as Nos2. Finally, we found that IFN-γ-primed but not unprimed macrophages largely excluded the activated form of IRF3 from the nucleus following bacterial infection. These data are consistent with a relationship of mutual inhibition between IRF3 and IFN-γ-activated programs, possibly as a component of a partially reversible mechanism for modulating the activity of potent innate immune effectors (such as Nos2) in the context of intracellular infection.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Interferon Regulatory Factor-3/metabolism ; Interferon-gamma/metabolism ; Legionella pneumophila/pathogenicity ; Macrophages/metabolism ; Nitric Oxide Synthase Type II/metabolism ; Trypanosoma cruzi/pathogenicity
Chemical Substances	Adaptor Proteins, Signal Transducing ; Interferon Regulatory Factor-3 ; Interferon-gamma (82115-62-6) ; Nitric Oxide Synthase Type II (EC 1.14.13.39)
Language	English
Publishing date	2021-11-26
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1002/JLB.3A0218-069RR
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Zs.A 603: Show issues

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Article ; Online: Loss of the Nuclear Protein RTF2 Enhances Influenza Virus Replication.

Chia, Bing Shao / Li, Bo / Cui, Ang / Eisenhaure, Thomas / Raychowdhury, Raktima / Lieb, David / Hacohen, Nir

Journal of virology

2020 Volume 94, Issue 22

Abstract: While hundreds of genes are induced by type I interferons, their roles in restricting the influenza virus life cycle remain mostly unknown. Using a loss-of-function CRISPR screen in cells prestimulated with interferon beta (IFN-β), we identified a small ... ...

Abstract	While hundreds of genes are induced by type I interferons, their roles in restricting the influenza virus life cycle remain mostly unknown. Using a loss-of-function CRISPR screen in cells prestimulated with interferon beta (IFN-β), we identified a small number of factors required for restricting influenza A virus replication. In addition to known components of the interferon signaling pathway, we found that replication termination factor 2 (RTF2) restricts influenza virus at the nuclear stage (and perhaps other stages) of the viral life cycle, based on several lines of evidence. First, a deficiency in RTF2 leads to higher levels of viral primary transcription, even in the presence of cycloheximide to block genome replication and secondary transcription. Second, cells that lack RTF2 have enhanced activity of a viral reporter that depends solely on four viral proteins that carry out replication and transcription in the nucleus. Third, when the RTF2 protein is mislocalized outside the nucleus, it is not able to restrict replication. Finally, the absence of RTF2 leads not only to enhanced viral transcription but also to reduced expression of antiviral factors in response to interferon. RTF2 thus inhibits primary influenza virus transcription, likely acts in the nucleus, and contributes to the upregulation of antiviral effectors in response to type I interferons.
MeSH term(s)	A549 Cells ; Animals ; Antiviral Agents ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Cycle Proteins/pharmacology ; Cell Line ; Chlorocebus aethiops ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; DNA-Binding Proteins/pharmacology ; Gene Knockout Techniques ; HEK293 Cells ; Host-Pathogen Interactions ; Humans ; Immunity, Innate ; Influenza A virus/drug effects ; Influenza A virus/physiology ; Influenza, Human/metabolism ; Influenza, Human/virology ; Interferon Type I/immunology ; Interferon-beta/immunology ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Transcriptome ; Vero Cells ; Viral Proteins ; Virus Replication/drug effects
Chemical Substances	Antiviral Agents ; Cell Cycle Proteins ; DNA-Binding Proteins ; Interferon Type I ; Nuclear Proteins ; RTF2 protein, human ; Viral Proteins ; Interferon-beta (77238-31-4)
Language	English
Publishing date	2020-10-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.00319-20
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Article: Systematically characterizing the roles of E3-ligase family members in inflammatory responses with massively parallel Perturb-seq.

bioRxiv : the preprint server for biology

2023

Abstract: E3 ligases regulate key processes, but many of their roles remain unknown. Using Perturb-seq, we interrogated the function of 1,130 E3 ligases, partners and substrates in the inflammatory response in primary dendritic cells (DCs). Dozens impacted the ... ...

Abstract	E3 ligases regulate key processes, but many of their roles remain unknown. Using Perturb-seq, we interrogated the function of 1,130 E3 ligases, partners and substrates in the inflammatory response in primary dendritic cells (DCs). Dozens impacted the balance of DC1, DC2, migratory DC and macrophage states and a gradient of DC maturation. Family members grouped into co-functional modules that were enriched for physical interactions and impacted specific programs through substrate transcription factors. E3s and their adaptors co-regulated the same processes, but partnered with different substrate recognition adaptors to impact distinct aspects of the DC life cycle. Genetic interactions were more prevalent within than between modules, and a deep learning model, comβVAE, predicts the outcome of new combinations by leveraging modularity. The E3 regulatory network was associated with heritable variation and aberrant gene expression in immune cells in human inflammatory diseases. Our study provides a general approach to dissect gene function.
Language	English
Publishing date	2023-01-24
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.01.23.525198
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Article ; Online: Extranuclear DNA accumulates in aged cells and contributes to senescence and inflammation.

Lan, Yuk Yuen / Heather, James M / Eisenhaure, Thomas / Garris, Christopher Stuart / Lieb, David / Raychowdhury, Raktima / Hacohen, Nir

Aging cell

2019 Volume 18, Issue 2, Page(s) e12901

Abstract: Systemic inflammation is central to aging-related conditions. However, the intrinsic factors that induce inflammation are not well understood. We previously identified a cell-autonomous pathway through which damaged nuclear DNA is trafficked to the ... ...

Abstract	Systemic inflammation is central to aging-related conditions. However, the intrinsic factors that induce inflammation are not well understood. We previously identified a cell-autonomous pathway through which damaged nuclear DNA is trafficked to the cytosol where it activates innate cytosolic DNA sensors that trigger inflammation. These results led us to hypothesize that DNA released after cumulative damage contributes to persistent inflammation in aging cells through a similar mechanism. Consistent with this notion, we found that older cells harbored higher levels of extranuclear DNA compared to younger cells. Extranuclear DNA was exported by a leptomycin B-sensitive process, degraded through the autophagosome-lysosomal pathway and triggered innate immune responses through the DNA-sensing cGAS-STING pathway. Patient cells from the aging diseases ataxia and progeria also displayed extranuclear DNA accumulation, increased pIRF3 and pTBK1, and STING-dependent p16 expression. Removing extranuclear DNA in old cells using DNASE2A reduced innate immune responses and senescence-associated (SA) β-gal enzyme activity. Cells and tissues of Dnase2a
MeSH term(s)	Animals ; Cell Nucleus/metabolism ; Cells, Cultured ; Cellular Senescence ; DNA/metabolism ; Endodeoxyribonucleases/deficiency ; Endodeoxyribonucleases/metabolism ; Humans ; Inflammation/metabolism ; Mice ; Mice, Knockout
Chemical Substances	DNA (9007-49-2) ; Endodeoxyribonucleases (EC 3.1.-) ; deoxyribonuclease II (EC 3.1.22.1)
Language	English
Publishing date	2019-01-31
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.12901
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Zs.A 6581: Show issues

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Article ; Online: An Integrative Framework Reveals Signaling-to-Transcription Events in Toll-like Receptor Signaling.

Mertins, Philipp / Przybylski, Dariusz / Yosef, Nir / Qiao, Jana / Clauser, Karl / Raychowdhury, Raktima / Eisenhaure, Thomas M / Maritzen, Tanja / Haucke, Volker / Satoh, Takashi / Akira, Shizuo / Carr, Steven A / Regev, Aviv / Hacohen, Nir / Chevrier, Nicolas

Cell reports

2017 Volume 19, Issue 13, Page(s) 2853–2866

Abstract: Building an integrated view of cellular responses to environmental cues remains a fundamental challenge due to the complexity of intracellular networks in mammalian cells. Here, we introduce an integrative biochemical and genetic framework to dissect ... ...

Abstract	Building an integrated view of cellular responses to environmental cues remains a fundamental challenge due to the complexity of intracellular networks in mammalian cells. Here, we introduce an integrative biochemical and genetic framework to dissect signal transduction events using multiple data types and, in particular, to unify signaling and transcriptional networks. Using the Toll-like receptor (TLR) system as a model cellular response, we generate multifaceted datasets on physical, enzymatic, and functional interactions and integrate these data to reveal biochemical paths that connect TLR4 signaling to transcription. We define the roles of proximal TLR4 kinases, identify and functionally test two dozen candidate regulators, and demonstrate a role for Ap1ar (encoding the Gadkin protein) and its binding partner, Picalm, potentially linking vesicle transport with pro-inflammatory responses. Our study thus demonstrates how deciphering dynamic cellular responses by integrating datasets on various regulatory layers defines key components and higher-order logic underlying signaling-to-transcription pathways.
MeSH term(s)	Dendritic Cells/metabolism ; Humans ; Phosphorylation ; Signal Transduction ; Toll-Like Receptors/metabolism
Chemical Substances	Toll-Like Receptors
Language	English
Publishing date	2017-06-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2017.06.016
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Article ; Online: A Regression-Based Analysis of Ribosome-Profiling Data Reveals a Conserved Complexity to Mammalian Translation.

Fields, Alexander P / Rodriguez, Edwin H / Jovanovic, Marko / Stern-Ginossar, Noam / Haas, Brian J / Mertins, Philipp / Raychowdhury, Raktima / Hacohen, Nir / Carr, Steven A / Ingolia, Nicholas T / Regev, Aviv / Weissman, Jonathan S

Molecular cell

2015 Volume 60, Issue 5, Page(s) 816–827

Abstract: A fundamental goal of genomics is to identify the complete set of expressed proteins. Automated annotation strategies rely on assumptions about protein-coding sequences (CDSs), e.g., they are conserved, do not overlap, and exceed a minimum length. ... ...

Abstract	A fundamental goal of genomics is to identify the complete set of expressed proteins. Automated annotation strategies rely on assumptions about protein-coding sequences (CDSs), e.g., they are conserved, do not overlap, and exceed a minimum length. However, an increasing number of newly discovered proteins violate these rules. Here we present an experimental and analytical framework, based on ribosome profiling and linear regression, for systematic identification and quantification of translation. Application of this approach to lipopolysaccharide-stimulated mouse dendritic cells and HCMV-infected human fibroblasts identifies thousands of novel CDSs, including micropeptides and variants of known proteins, that bear the hallmarks of canonical translation and exhibit translation levels and dynamics comparable to that of annotated CDSs. Remarkably, many translation events are identified in both mouse and human cells even when the peptide sequence is not conserved. Our work thus reveals an unexpected complexity to mammalian translation suited to provide both conserved regulatory or protein-based functions.
MeSH term(s)	Amino Acid Sequence ; Animals ; Cells, Cultured ; Conserved Sequence ; Dendritic Cells/drug effects ; Humans ; Lipopolysaccharides/pharmacology ; Mice ; Open Reading Frames ; Proteome/metabolism ; Proteomics/methods ; Regression Analysis ; Ribosomes/metabolism
Chemical Substances	Lipopolysaccharides ; Proteome
Language	English
Publishing date	2015-12-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2015.11.013
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Zs.A 5055: Show issues

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Article ; Online: Genetic analysis of isoform usage in the human anti-viral response reveals influenza-specific regulation of

Genome research

2018 Volume 28, Issue 12, Page(s) 1812–1825

Abstract: While genetic variants are known to be associated with overall gene abundance in stimulated immune cells, less is known about their effects on alternative isoform usage. By analyzing RNA-seq profiles of monocyte-derived dendritic cells from 243 ... ...

Abstract	While genetic variants are known to be associated with overall gene abundance in stimulated immune cells, less is known about their effects on alternative isoform usage. By analyzing RNA-seq profiles of monocyte-derived dendritic cells from 243 individuals, we uncovered thousands of unannotated isoforms synthesized in response to influenza infection and type 1 interferon stimulation. We identified more than a thousand quantitative trait loci (QTLs) associated with alternate isoform usage (isoQTLs), many of which are independent of expression QTLs (eQTLs) for the same gene. Compared with eQTLs, isoQTLs are enriched for splice sites and untranslated regions, but depleted of sequences upstream of annotated transcription start sites. Both eQTLs and isoQTLs explain a significant proportion of the disease heritability attributed to common genetic variants. At the
MeSH term(s)	Adolescent ; Adult ; Alternative Splicing ; Aminopeptidases/genetics ; Chromosome Mapping ; Computational Biology/methods ; Dendritic Cells/metabolism ; Female ; Gene Expression Profiling ; Gene Expression Regulation ; Gene Ontology ; Genetic Predisposition to Disease ; Genetic Testing ; Genetic Variation ; Host-Pathogen Interactions/genetics ; Humans ; Influenza A virus ; Influenza, Human/genetics ; Influenza, Human/virology ; Interferon Type I/metabolism ; Male ; Middle Aged ; Models, Biological ; Molecular Sequence Annotation ; Monocytes/metabolism ; Quantitative Trait Loci ; Transcriptome ; Young Adult
Chemical Substances	Interferon Type I ; Aminopeptidases (EC 3.4.11.-) ; ERAP2 protein, human (EC 3.4.11.-)
Language	English
Publishing date	2018-11-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1284872-4
ISSN	1549-5469 ; 1088-9051 ; 1054-9803
ISSN (online)	1549-5469
ISSN	1088-9051 ; 1054-9803
DOI	10.1101/gr.240390.118
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Zs.A 3729: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 8: Show issues

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Article ; Online: Perturb-Seq: Dissecting Molecular Circuits with Scalable Single-Cell RNA Profiling of Pooled Genetic Screens.

Dixit, Atray / Parnas, Oren / Li, Biyu / Chen, Jenny / Fulco, Charles P / Jerby-Arnon, Livnat / Marjanovic, Nemanja D / Dionne, Danielle / Burks, Tyler / Raychowdhury, Raktima / Adamson, Britt / Norman, Thomas M / Lander, Eric S / Weissman, Jonathan S / Friedman, Nir / Regev, Aviv

Cell

2016 Volume 167, Issue 7, Page(s) 1853–1866.e17

Abstract: Genetic screens help infer gene function in mammalian cells, but it has remained difficult to assay complex phenotypes-such as transcriptional profiles-at scale. Here, we develop Perturb-seq, combining single-cell RNA sequencing (RNA-seq) and clustered ... ...

Abstract	Genetic screens help infer gene function in mammalian cells, but it has remained difficult to assay complex phenotypes-such as transcriptional profiles-at scale. Here, we develop Perturb-seq, combining single-cell RNA sequencing (RNA-seq) and clustered regularly interspaced short palindromic repeats (CRISPR)-based perturbations to perform many such assays in a pool. We demonstrate Perturb-seq by analyzing 200,000 cells in immune cells and cell lines, focusing on transcription factors regulating the response of dendritic cells to lipopolysaccharide (LPS). Perturb-seq accurately identifies individual gene targets, gene signatures, and cell states affected by individual perturbations and their genetic interactions. We posit new functions for regulators of differentiation, the anti-viral response, and mitochondrial function during immune activation. By decomposing many high content measurements into the effects of perturbations, their interactions, and diverse cell metadata, Perturb-seq dramatically increases the scope of pooled genomic assays.
MeSH term(s)	Animals ; Cell Cycle ; Clustered Regularly Interspaced Short Palindromic Repeats ; Feedback ; Gene Expression Profiling ; Gene Knockdown Techniques ; Humans ; K562 Cells ; Mice ; Mice, Transgenic ; Sequence Analysis, RNA/methods ; Single-Cell Analysis/methods ; Transcription Factors/metabolism
Chemical Substances	Transcription Factors
Language	English
Publishing date	2016-12-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2016.11.038
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Zs.A 1167: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 58: Show issues

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Article ; Online: High-resolution sequencing and modeling identifies distinct dynamic RNA regulatory strategies.

Rabani, Michal / Raychowdhury, Raktima / Jovanovic, Marko / Rooney, Michael / Stumpo, Deborah J / Pauli, Andrea / Hacohen, Nir / Schier, Alexander F / Blackshear, Perry J / Friedman, Nir / Amit, Ido / Regev, Aviv

Cell

2014 Volume 159, Issue 7, Page(s) 1698–1710

Abstract: Cells control dynamic transitions in transcript levels by regulating transcription, processing, and/or degradation through an integrated regulatory strategy. Here, we combine RNA metabolic labeling, rRNA-depleted RNA-seq, and DRiLL, a novel computational ...

Abstract	Cells control dynamic transitions in transcript levels by regulating transcription, processing, and/or degradation through an integrated regulatory strategy. Here, we combine RNA metabolic labeling, rRNA-depleted RNA-seq, and DRiLL, a novel computational framework, to quantify the level; editing sites; and transcription, processing, and degradation rates of each transcript at a splice junction resolution during the LPS response of mouse dendritic cells. Four key regulatory strategies, dominated by RNA transcription changes, generate most temporal gene expression patterns. Noncanonical strategies that also employ dynamic posttranscriptional regulation control only a minority of genes, but provide unique signal processing features. We validate Tristetraprolin (TTP) as a major regulator of RNA degradation in one noncanonical strategy. Applying DRiLL to the regulation of noncoding RNAs and to zebrafish embryogenesis demonstrates its broad utility. Our study provides a new quantitative approach to discover transcriptional and posttranscriptional events that control dynamic changes in transcript levels using RNA sequencing data.
MeSH term(s)	Animals ; Computer Simulation ; Dendritic Cells/metabolism ; Gene Expression Profiling/methods ; Kinetics ; Lipopolysaccharides/metabolism ; Mice ; RNA Processing, Post-Transcriptional ; RNA Stability ; RNA, Untranslated/metabolism ; Sequence Analysis, RNA/methods ; Transcription, Genetic ; Tristetraprolin/metabolism ; Zebrafish/embryology
Chemical Substances	Lipopolysaccharides ; RNA, Untranslated ; Tristetraprolin
Language	English
Publishing date	2014-12-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2014.11.015
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Zs.A 1167: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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