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  1. Article ; Online: The IRAK1/IRF5 axis initiates IL-12 response by dendritic cells and control of Toxoplasma gondii infection.

    Pereira, Milton / Ramalho, Theresa / Andrade, Warrison A / Durso, Danielle F / Souza, Maria C / Fitzgerald, Katherine A / Golenbock, Douglas T / Silverman, Neal / Gazzinelli, Ricardo T

    Cell reports

    2024  Volume 43, Issue 2, Page(s) 113795

    Abstract: Activation of endosomal Toll-like receptor (TLR) 7, TLR9, and TLR11/12 is a key event in the resistance against the parasite Toxoplasma gondii. Endosomal TLR engagement leads to expression of interleukin (IL)-12 via the myddosome, a protein complex ... ...

    Abstract Activation of endosomal Toll-like receptor (TLR) 7, TLR9, and TLR11/12 is a key event in the resistance against the parasite Toxoplasma gondii. Endosomal TLR engagement leads to expression of interleukin (IL)-12 via the myddosome, a protein complex containing MyD88 and IL-1 receptor-associated kinase (IRAK) 4 in addition to IRAK1 or IRAK2. In murine macrophages, IRAK2 is essential for IL-12 production via endosomal TLRs but, surprisingly, Irak2
    MeSH term(s) Animals ; Mice ; Dendritic Cells ; Interferon Regulatory Factors/genetics ; Interleukin-1 Receptor-Associated Kinases ; Interleukin-12 ; Toxoplasmosis
    Chemical Substances Interferon Regulatory Factors ; Interleukin-1 Receptor-Associated Kinases (EC 2.7.11.1) ; Interleukin-12 (187348-17-0) ; Irf5 protein, mouse ; Irak1 protein, mouse (EC 2.7.11.1)
    Language English
    Publishing date 2024-02-15
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2024.113795
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The IRAK4 scaffold integrates TLR4-driven TRIF and MYD88 signaling pathways.

    Pereira, Milton / Durso, Danielle F / Bryant, Clare E / Kurt-Jones, Evelyn A / Silverman, Neal / Golenbock, Douglas T / Gazzinelli, Ricardo T

    Cell reports

    2022  Volume 40, Issue 7, Page(s) 111225

    Abstract: Interleukin-1 receptor-associated kinases (IRAKs) -4, -2, and -1 are involved in transducing signals from Toll-like receptors (TLRs) via the adaptor myeloid differentiation primary-response protein 88 (MYD88). How MYD88/IRAK4/2/1 complexes are formed, ... ...

    Abstract Interleukin-1 receptor-associated kinases (IRAKs) -4, -2, and -1 are involved in transducing signals from Toll-like receptors (TLRs) via the adaptor myeloid differentiation primary-response protein 88 (MYD88). How MYD88/IRAK4/2/1 complexes are formed, their redundancies, and potential non-enzymatic roles are subjects of debate. Here, we examine the hierarchical requirements for IRAK proteins in the context of TLR4 activation and confirmed that the kinase activity of IRAK4 is essential for MYD88 signaling. Surprisingly, the IRAK4 scaffold is required for activation of the E3 ubiquitin ligase TNF receptor-associated factor 6 (TRAF6) by both MYD88 and TIR domain-containing adaptor protein inducing IFN-β (TRIF), a unique adaptation in the TLR4 response. IRAK4 scaffold is, therefore, essential in integrating MYD88 and TRIF in TLR4 signaling.
    MeSH term(s) Adaptor Proteins, Signal Transducing/metabolism ; Adaptor Proteins, Vesicular Transport/metabolism ; Humans ; Interleukin-1 Receptor-Associated Kinases/metabolism ; Myeloid Differentiation Factor 88/metabolism ; Signal Transduction/physiology ; Toll-Like Receptor 3/metabolism ; Toll-Like Receptor 4/metabolism
    Chemical Substances Adaptor Proteins, Signal Transducing ; Adaptor Proteins, Vesicular Transport ; Myeloid Differentiation Factor 88 ; TLR4 protein, human ; Toll-Like Receptor 3 ; Toll-Like Receptor 4 ; IRAK4 protein, human (EC 2.7.11.1) ; Interleukin-1 Receptor-Associated Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2022-07-29
    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.2022.111225
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Caspase-8 mediates inflammation and disease in rodent malaria.

    Pereira, Larissa M N / Assis, Patrícia A / de Araújo, Natalia M / Durso, Danielle F / Junqueira, Caroline / Ataíde, Marco Antônio / Pereira, Dhelio B / Lien, Egil / Fitzgerald, Katherine A / Zamboni, Dario S / Golenbock, Douglas T / Gazzinelli, Ricardo T

    Nature communications

    2020  Volume 11, Issue 1, Page(s) 4596

    Abstract: Earlier studies indicate that either the canonical or non-canonical pathways of inflammasome activation have a limited role on malaria pathogenesis. Here, we report that caspase-8 is a central mediator of systemic inflammation, septic shock in the ... ...

    Abstract Earlier studies indicate that either the canonical or non-canonical pathways of inflammasome activation have a limited role on malaria pathogenesis. Here, we report that caspase-8 is a central mediator of systemic inflammation, septic shock in the Plasmodium chabaudi-infected mice and the P. berghei-induced experimental cerebral malaria (ECM). Importantly, our results indicate that the combined deficiencies of caspases-8/1/11 or caspase-8/gasdermin-D (GSDM-D) renders mice impaired to produce both TNFα and IL-1β and highly resistant to lethality in these models, disclosing a complementary, but independent role of caspase-8 and caspases-1/11/GSDM-D in the pathogenesis of malaria. Further, we find that monocytes from malaria patients express active caspases-1, -4 and -8 suggesting that these inflammatory caspases may also play a role in the pathogenesis of human disease.
    MeSH term(s) Animals ; Brain/pathology ; Caspase 1/metabolism ; Caspase 8/metabolism ; Dendritic Cells/metabolism ; Enzyme Activation ; Extracellular Matrix/metabolism ; Gene Expression Regulation ; Humans ; Inflammation/pathology ; Interferon-gamma/metabolism ; Interleukin-1beta/metabolism ; Lipopolysaccharides ; Malaria, Cerebral/enzymology ; Malaria, Cerebral/genetics ; Mice, Inbred C57BL ; Monocytes/metabolism ; Plasmodium chabaudi/physiology ; Spleen/metabolism ; Toll-Like Receptors/metabolism
    Chemical Substances Interleukin-1beta ; Lipopolysaccharides ; Toll-Like Receptors ; Interferon-gamma (82115-62-6) ; Caspase 8 (EC 3.4.22.-) ; Caspase 1 (EC 3.4.22.36)
    Language English
    Publishing date 2020-09-14
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-020-18295-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Author Correction: Caspase-8 mediates inflammation and disease in rodent malaria.

    Pereira, Larissa M N / Assis, Patrícia A / de Araújo, Natalia M / Durso, Danielle F / Junqueira, Caroline / Ataíde, Marco Antônio / Pereira, Dhelio B / Lien, Egil / Fitzgerald, Katherine A / Zamboni, Dario S / Golenbock, Douglas T / Gazzinelli, Ricardo T

    Nature communications

    2020  Volume 11, Issue 1, Page(s) 5673

    Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper. ...

    Abstract An amendment to this paper has been published and can be accessed via a link at the top of the paper.
    Language English
    Publishing date 2020-11-03
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-020-19620-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: A Meta-Analysis of Brain DNA Methylation Across Sex, Age, and Alzheimer's Disease Points for Accelerated Epigenetic Aging in Neurodegeneration.

    Pellegrini, Camilla / Pirazzini, Chiara / Sala, Claudia / Sambati, Luisa / Yusipov, Igor / Kalyakulina, Alena / Ravaioli, Francesco / Kwiatkowska, Katarzyna M / Durso, Danielle F / Ivanchenko, Mikhail / Monti, Daniela / Lodi, Raffaele / Franceschi, Claudio / Cortelli, Pietro / Garagnani, Paolo / Bacalini, Maria Giulia

    Frontiers in aging neuroscience

    2021  Volume 13, Page(s) 639428

    Abstract: Alzheimer's disease (AD) is characterized by specific alterations of brain DNA methylation (DNAm) patterns. Age and sex, two major risk factors for AD, are also known to largely affect the epigenetic profiles in brain, but their contribution to AD- ... ...

    Abstract Alzheimer's disease (AD) is characterized by specific alterations of brain DNA methylation (DNAm) patterns. Age and sex, two major risk factors for AD, are also known to largely affect the epigenetic profiles in brain, but their contribution to AD-associated DNAm changes has been poorly investigated. In this study we considered publicly available DNAm datasets of four brain regions (temporal, frontal, entorhinal cortex, and cerebellum) from healthy adult subjects and AD patients, and performed a meta-analysis to identify sex-, age-, and AD-associated epigenetic profiles. In one of these datasets it was also possible to distinguish 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC) profiles. We showed that DNAm differences between males and females tend to be shared between the four brain regions, while aging differently affects cortical regions compared to cerebellum. We found that the proportion of sex-dependent probes whose methylation is modified also during aging is higher than expected, but that differences between males and females tend to be maintained, with only a few probes showing age-by-sex interaction. We did not find significant overlaps between AD- and sex-associated probes, nor disease-by-sex interaction effects. On the contrary, we found that AD-related epigenetic modifications are significantly enriched in probes whose DNAm varies with age and that there is a high concordance between the direction of changes (hyper or hypo-methylation) in aging and AD, supporting accelerated epigenetic aging in the disease. In summary, our results suggest that age-associated DNAm patterns concur to the epigenetic deregulation observed in AD, providing new insights on how advanced age enables neurodegeneration.
    Language English
    Publishing date 2021-03-11
    Publishing country Switzerland
    Document type Systematic Review
    ZDB-ID 2558898-9
    ISSN 1663-4365
    ISSN 1663-4365
    DOI 10.3389/fnagi.2021.639428
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: A single FTO gene variant rs9939609 is associated with body weight evolution in a multiethnic extremely obese population that underwent bariatric surgery.

    Rodrigues, Gisele K / Resende, Cristina M M / Durso, Danielle F / Rodrigues, Lorena A A / Silva, José Luiz P / Reis, Rodrigo C / Pereira, Solange S / Ferreira, Daniela C / Franco, Gloria R / Alvarez-Leite, Jacqueline

    Nutrition (Burbank, Los Angeles County, Calif.)

    2015  Volume 31, Issue 11-12, Page(s) 1344–1350

    Abstract: Objectives: The rs9939609 single nucleotide polymorphism (SNP) in the fat mass and obesity-associated (FTO) gene is involved in obesity. Few studies have been conducted on patients who underwent bariatric surgery. The aim of this study was to evaluate ... ...

    Abstract Objectives: The rs9939609 single nucleotide polymorphism (SNP) in the fat mass and obesity-associated (FTO) gene is involved in obesity. Few studies have been conducted on patients who underwent bariatric surgery. The aim of this study was to evaluate the influence of FTO SNPs on body weight, body composition, and weight regain during a 60-mo follow-up period after bariatric surgery.
    Methods: The rs9939609 was genotyped in 146 individuals using a real-time polymerase chain reaction TaqMan assay. Data for lifestyle, comorbidities, body weight, body mass index (BMI), excess weight loss (EWL), and body composition were obtained before and 6, 12, 18, 24, 36, 48, and 60 mo after surgery. Data were analyzed by comparing two groups of patients according to rs9939609 FTO gene polymorphism. Mixed-regression models were constructed to evaluate the dynamics of body weight, BMI, and EWL over time in female patients.
    Results: No differences were observed between the groups during the first 24 mo after surgery. After 36, 48, and 60 mo, body weight, fat mass, and BMI were higher, whereas fat-free mass and EWL were lower in the FTO-SNP patient group. Weight regain was more frequent and occurred sooner in the FTO-SNP group.
    Conclusions: There is a different evolution of weight loss in obese carriers of the FTO gene variant rs9939609 after bariatric surgery. However, this pattern was evident at only 2 y postbariatric surgery, inducing a lower proportion of surgery success and a greater and earlier weight regain.
    MeSH term(s) Adolescent ; Adult ; Alpha-Ketoglutarate-Dependent Dioxygenase FTO ; Bariatric Surgery ; Body Composition ; Body Mass Index ; Body Weight Maintenance ; Ethnic Groups ; Female ; Genetic Predisposition to Disease ; Genotype ; Humans ; Male ; Middle Aged ; Obesity, Morbid/genetics ; Obesity, Morbid/surgery ; Polymorphism, Single Nucleotide ; Proteins/genetics ; Treatment Outcome ; Weight Loss ; Young Adult
    Chemical Substances Proteins ; Alpha-Ketoglutarate-Dependent Dioxygenase FTO (EC 1.14.11.33) ; FTO protein, human (EC 1.14.11.33)
    Language English
    Publishing date 2015-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 639259-3
    ISSN 1873-1244 ; 0899-9007
    ISSN (online) 1873-1244
    ISSN 0899-9007
    DOI 10.1016/j.nut.2015.05.020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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