NDLI: TLR4-mediated AKT activation is MyD88/TRIF dependent and critical for induction of oxidative phosphorylation and mitochondrial transcription factor A in murine macrophages.

Please wait, while we are loading the content...

A novel NKR-P1B(bright) NK cell subset expresses an activated CD25(+)CX(3)CR1(+)CD62L(-)CD11b(-)CD27(-) phenotype and is prevalent in blood, liver, and gut-associated lymphoid organs of rats.

Tyrosine phosphorylation-independent regulation of lipopolysaccharide-mediated response by the transmembrane adaptor protein LAB.

Removal of syndecan-1 promotes TRAIL-induced apoptosis in myeloma cells.

Recognition and prevention of tumor metastasis by the NK receptor NKp46/NCR1.

Chronic shift-lag alters the circadian clock of NK cells and promotes lung cancer growth in rats.

TLR4-mediated AKT activation is MyD88/TRIF dependent and critical for induction of oxidative phosphorylation and mitochondrial transcription factor A in murine macrophages.

TREM2 and ß-catenin regulate bone homeostasis by controlling the rate of osteoclastogenesis.

Three novel acetylation sites in the Foxp3 transcription factor regulate the suppressive activity of regulatory T cells.

Cellular and molecular requirements for rejection of B16 melanoma in the setting of regulatory T cell depletion and homeostatic proliferation.

Spatiotemporal inhibition of innate immunity signaling by the Tbc1d23 RAB-GAP.

Selective dependence of H2-M3-restricted CD8 responses on IL-15.

The adaptor protein SLP-76 regulates HIV-1 release and cell-to-cell transmission in T cells.

E3 ubiquitin ligase tripartite motif 38 negatively regulates TLR-mediated immune responses by proteasomal degradation of TNF receptor-associated factor 6 in macrophages.

Cutting edge: the 'death' adaptor CRADD/RAIDD targets BCL10 and suppresses agonist-induced cytokine expression in T lymphocytes.

Analysis of NLRP3 in the development of allergic airway disease in mice.

The impact of a large and frequent deletion in the human TCR ß locus on antiviral immunity.

Midkine inhibits inducible regulatory T cell differentiation by suppressing the development of tolerogenic dendritic cells.

Stromal TIMP3 regulates liver lymphocyte populations and provides protection against Th1 T cell-driven autoimmune hepatitis.

A new hypersensitive site, HS10, and the enhancers E3′ and Ed, differentially regulate Igκ gene expression

Germinal center alloantibody responses are mediated exclusively by indirect-pathway CD4 T follicular helper cells.

Downregulation of the Na/K-ATPase pump by leptospiral glycolipoprotein activates the NLRP3 inflammasome.

A TRIF-independent branch of TLR3 signaling.

Targeting TNF- to neoangiogenic vessels enhances lymphocyte infiltration in tumors and increases the therapeutic potential of immunotherapy.

Alternaria induces STAT6-dependent acute airway eosinophilia and epithelial FIZZ1 expression that promotes airway fibrosis and epithelial thickness.

Cutting edge: the role of IFN- receptor and MyD88 signaling in induction of IL-15 expression in vivo.

Frequency of epitope-specific naive CD4(+) T cells correlates with immunodominance in the human memory repertoire.

JAB1 is essential for B cell development and germinal center formation and inversely regulates Fas ligand and Bcl6 expression.

Innate NK cells and macrophages recognize and reject allogeneic nonself in vivo via different mechanisms.

Cutting edge: paradoxical roles of BST2/tetherin in promoting type I IFN response and viral infection.

Class B scavenger receptor types I and II and CD36 targeting improves sepsis survival and acute outcomes in mice.

The tick salivary protein sialostatin L inhibits the Th9-derived production of the asthma-promoting cytokine IL-9 and is effective in the prevention of experimental asthma.

Impaired NLRP3 inflammasome function in elderly mice during influenza infection is rescued by treatment with nigericin.

Modulation of antigen presentation and B cell receptor signaling in B cells of beige mice.

The development of colitogenic CD4(+) T cells is regulated by IL-7 in collaboration with NK cell function in a murine model of colitis.

Significant role of IL-1 signaling, but limited role of inflammasome activation, in oviduct pathology during Chlamydia muridarum genital infection.

IκB kinase ß is required for activation of NF-κB and AP-1 in CD3/CD28-stimulated primary CD4(+) T cells.

Neonatal rhinovirus infection induces mucous metaplasia and airways hyperresponsiveness.

Adiponectin induces dendritic cell activation via PLCÎ³/JNK/NF-κB pathways, leading to Th1 and Th17 polarization.

Suppression of the NF-κB pathway by diesel exhaust particles impairs human antimycobacterial immunity.

Human cytomegalovirus UL40 signal peptide regulates cell surface expression of the NK cell ligands HLA-E and gpUL18.

Hapivirins and Diprovirins: Novel θ-Defensin Analogs With Potent Activity Against Influenza A $Virus^{}$

Maximal adjuvant activity of nasally delivered IL-1 requires adjuvant-responsive CD11c(+) cells and does not correlate with adjuvant-induced in vivo cytokine production.

Germline deletion of Igh 3' regulatory region elements hs 5, 6, 7 (hs5-7) affects B cell-specific regulation, rearrangement, and insulation of the Igh locus.

Characterization of a PIAS4 homologue from zebrafish: insights into its conserved negative regulatory mechanism in the TRIF, MAVS, and IFN signaling pathways during vertebrate evolution.

MHC class II tetramers.

Year: 2012 Volume: 188 Issue: 5

Year: 2012 Volume: 188 Issue: 4

Year: 2012 Volume: 188 Issue: 3

Year: 2012 Volume: 188 Issue: 2

Year: 2012 Volume: 188 Issue: 1

Year: 2011 Volume: 187

Year: 2011 Volume: 186

Year: 2010 Volume: 185

Year: 2010 Volume: 184

Year: 2009 Volume: 183

Year: 2009 Volume: 182

Year: 2008 Volume: 181

TLR4-mediated AKT activation is MyD88/TRIF dependent and critical for induction of oxidative phosphorylation and mitochondrial transcription factor A in murine macrophages.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Hüttemann, Maik Lee, Icksoo Nuñez, Gabriel Bauerfeld, Christian P. Franchi, Luigi Pirockinaite, Gaila Birnbaum, Morris J. Samavati, Lobelia Rastogi, Ruchi Monks, Bobby
Description	Country affiliation: United States Author Affiliation: Bauerfeld CP ( Department of Pediatrics, St. John Hospital and Medical Center, Detroit, MI 48236, USA.)
Abstract	Mitochondria play a critical role in cell survival and death. Mitochondrial recovery during inflammatory processes such as sepsis is associated with cell survival. Recovery of cellular respiration, mitochondrial biogenesis, and function requires coordinated expression of transcription factors encoded by nuclear and mitochondrial genes, including mitochondrial transcription factor A (T-fam) and cytochrome c oxidase (COX, complex IV). LPS elicits strong host defenses in mammals with pronounced inflammatory responses, but also triggers activation of survival pathways such as AKT pathway. AKT/PKB is a serine/threonine protein kinase that plays an important role in cell survival, protein synthesis, and controlled inflammation in response to TLRs. Hence we investigated the role of LPS-mediated AKT activation in mitochondrial bioenergetics and function in cultured murine macrophages (B6-MCL) and bone marrow-derived macrophages. We show that LPS challenge led to increased expression of T-fam and COX subunits I and IV in a time-dependent manner through early phosphorylation of the PI3K/AKT pathway. PI3K/AKT pathway inhibitors abrogated LPS-mediated T-fam and COX induction. Lack of induction was associated with decreased ATP production, increased proinflammatory cytokines (TNF- ), NO production, and cell death. The TLR4-mediated AKT activation and mitochondrial biogenesis required activation of adaptor protein MyD88 and Toll/IL-1R domain-containing adaptor-inducing IFN-ß. Importantly, using a genetic approach, we show that the AKT1 isoform is pivotal in regulating mitochondrial biogenesis in response to TLR4 agonist.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1102157
Journal	The Journal of Immunology
Issue Number	6
Volume Number	188
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-03-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Macrophages Metabolism Mitochondria Oxidative Phosphorylation Proto-oncogene Proteins C-akt Signal Transduction Physiology Toll-like Receptor 4 Adaptor Proteins, Vesicular Transport Immunology Animals Cell Survival Dna-binding Proteins Enzyme Activation Enzyme-linked Immunosorbent Assay High Mobility Group Proteins Immunoblotting Lipopolysaccharides Membrane Potential, Mitochondrial Mice Mice, Knockout Myeloid Differentiation Factor 88 Real-time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

The Asp299Gly polymorphism alters TLR4 signaling by interfering with recruitment of MyD88 and TRIF.

Dual signaling of MyD88 and TRIF is critical for maximal TLR4-induced dendritic cell maturation.

TRIF signaling is essential for TLR4-driven IgE class switching.

Melatonin modulates TLR4-mediated inflammatory genes through MyD88- and TRIF-dependent signaling pathways in lipopolysaccharide-stimulated RAW264.7 cells.

Cutting edge: Endoplasmic reticulum stress licenses macrophages to produce mature IL-1ß in response to TLR4 stimulation through a caspase-8- and TRIF-dependent pathway.

IFN-beta production by TLR4-stimulated innate immune cells is negatively regulated by GSK3-beta.

MyD88 and Trif target Beclin 1 to trigger autophagy in macrophages.

TLR4-mediated AKT Activation is MyD88/TRIF-dependent and Critical for Induction of OxPhos and Mitochondrial Transcription Factor A in Murine Macrophages

Mycobacterial phosphatidylinositol mannosides negatively regulate host Toll-like receptor 4, MyD88-dependent proinflammatory cytokines, and TRIF-dependent co-stimulatory molecule expression.

TLR4-mediated AKT activation is MyD88/TRIF dependent and critical for induction of oxidative phosphorylation and mitochondrial transcription factor A in murine macrophages.

Similar Documents

The Asp299Gly polymorphism alters TLR4 signaling by interfering with recruitment of MyD88 and TRIF.

Dual signaling of MyD88 and TRIF is critical for maximal TLR4-induced dendritic cell maturation.

TRIF signaling is essential for TLR4-driven IgE class switching.

Melatonin modulates TLR4-mediated inflammatory genes through MyD88- and TRIF-dependent signaling pathways in lipopolysaccharide-stimulated RAW264.7 cells.

Cutting edge: Endoplasmic reticulum stress licenses macrophages to produce mature IL-1ß in response to TLR4 stimulation through a caspase-8- and TRIF-dependent pathway.

IFN-beta production by TLR4-stimulated innate immune cells is negatively regulated by GSK3-beta.

MyD88 and Trif target Beclin 1 to trigger autophagy in macrophages.

TLR4-mediated AKT Activation is MyD88/TRIF-dependent and Critical for Induction of OxPhos and Mitochondrial Transcription Factor A in Murine Macrophages

Mycobacterial phosphatidylinositol mannosides negatively regulate host Toll-like receptor 4, MyD88-dependent proinflammatory cytokines, and TRIF-dependent co-stimulatory molecule expression.

TLR4-mediated AKT activation is MyD88/TRIF dependent and critical for induction of oxidative phosphorylation and mitochondrial transcription factor A in murine macrophages.