Zobrazeno 1 - 10
of 11
pro vyhledávání: '"Annemarie Steiner"'
Autor:
Annemarie Steiner, Katja Hrovat-Schaale, Ignazia Prigione, Chien-Hsiung Yu, Pawat Laohamonthonkul, Cassandra R. Harapas, Ronnie Ren Jie Low, Dominic De Nardo, Laura F. Dagley, Michael J. Mlodzianoski, Kelly L. Rogers, Thomas Zillinger, Gunther Hartmann, Michael P. Gantier, Marco Gattorno, Matthias Geyer, Stefano Volpi, Sophia Davidson, Seth L. Masters
Publikováno v:
Nature Communications, Vol 13, Iss 1, Pp 1-16 (2022)
Mutations in the coatomer complex I can result in endoplasmic reticulum stress and inflammatory consequences. Here authors define aberrant activation of the STING immunosensing pathway in a disturbed coatmer complex context and the therapeutic modula
Externí odkaz:
https://doaj.org/article/30fa6bbd687e41a1bd2b9d85bd46d601
Autor:
Sophia Davidson, Chien-Hsiung Yu, Annemarie Steiner, Frédéric Ebstein, Paul J. Baker, Valentina Jarur-Chamy, Katja Hrovat Schaale, Pawat Laohamonthonkul, Klara Kong, Dale J. Calleja, Cassandra R. Harapas, Katherine R. Balka, Jacob Mitchell, Jacob T. Jackson, Niall D. Geoghegan, Fiona Moghaddas, Kelly L. Rogers, Katrin D. Mayer-Barber, Adriana A. De Jesus, Dominic De Nardo, Benjamin T. Kile, Anthony J. Sadler, M. Cecilia Poli, Elke Krüger, Raphaela Goldbach Mansky, Seth L. Masters
Publikováno v:
Science Immunology. 7
Proteasome dysfunction can lead to autoinflammatory disease associated with elevated type I interferon (IFN-αβ) and NF-κB signaling; however, the innate immune pathway driving this is currently unknown. Here, we identified protein kinase R (PKR) a
Autor:
Cassandra R. Harapas, Elina Idiiatullina, Mahmoud Al-Azab, Katja Hrovat-Schaale, Thomas Reygaerts, Annemarie Steiner, Pawat Laohamonthonkul, Sophia Davidson, Chien-Hsiung Yu, Lee Booty, Seth L. Masters
Publikováno v:
Nature reviews. Immunology. 22(9)
A cell is delimited by numerous borders that define specific organelles. The walls of some organelles are particularly robust, such as in mitochondria or endoplasmic reticulum, but some are more fluid such as in phase-separated stress granules. Eithe
Autor:
Jorge Kalil, Fiona Moghaddas, Alice Grossi, Florian N. Gohr, Matthias Geyer, Sophia Davidson, Gunther Hartmann, Leonardo Oliveira Mendonça, Seth L. Masters, Fabio Fernandes Morato Castro, Isabella Ceccherini, Thomas Reygaerts, Eva Bartok, Thomas Zillinger, Alessandra Pontillo, Marco Gattorno, Francesco Caroli, Jonas Moecking, Florian I. Schmidt, Annemarie Steiner
Publikováno v:
Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual)
Universidade de São Paulo (USP)
instacron:USP
Universidade de São Paulo (USP)
instacron:USP
PurposeNLRC4-associated autoinflammatory disease (NLRC4-AID) is an autosomal dominant condition presenting with a range of clinical manifestations which can include macrophage activation syndrome (MAS) and severe enterocolitis. We now report the firs
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ce36065dcf90fc28870e501cb95804e2
Autor:
Annemarie Steiner, Katja Hrovat-Schaale, Ignazia Prigione, Chien-Hsiung Yu, Pawat Laohamonthonkul, Cassandra R. Harapas, Ronnie Ren Jie Low, Dominic De Nardo, Laura F. Dagley, Michael J. Mlodzianoski, Kelly L. Rogers, Thomas Zillinger, Gunther Hartmann, Michael P. Gantier, Marco Gattorno, Matthias Geyer, Stefano Volpi, Sophia Davidson, Seth L. Masters
Publikováno v:
Nature communications. 13(1)
Coatomer complex I (COPI) mediates retrograde vesicular trafficking from Golgi to the endoplasmic reticulum (ER) and within Golgi compartments. Deficiency in subunit alpha causes COPA syndrome and is associated with type I IFN signalling, although th
Autor:
Marco Gattorno, Laura F. Dagley, Sophia Davidson, Seth L. Masters, Annemarie Steiner, Dominic De Nardo, Katja Hrovat Schaale, Stefano Volpi, Chien-Hsiung Yu, Cassandra R. Harapas, Ignazia Prigione, Michael P. Gantier, Pawat Laohamonthonkul
COPA syndrome is caused by loss-of-function mutations in the COP-α subunit of coatomer protein complex I (COPI), which participates in retrograde vesicular trafficking of proteins from the Golgi to the endoplasmic reticulum (ER). Disease manifests e
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::4d3a7732c193093452d27a4ffa799d3a
https://doi.org/10.1101/2020.07.09.194399
https://doi.org/10.1101/2020.07.09.194399
Autor:
Annemarie, Steiner, Thomas, Reygaerts, Alessandra, Pontillo, Isabella, Ceccherini, Jonas, Moecking, Fiona, Moghaddas, Sophia, Davidson, Francesco, Caroli, Alice, Grossi, Fabio Fernandes Morato, Castro, Jorge, Kalil, Florian N, Gohr, Florian I, Schmidt, Eva, Bartok, Thomas, Zillinger, Gunther, Hartmann, Matthias, Geyer, Marco, Gattorno, Leonardo Oliveira, Mendonça, Seth L, Masters
Publikováno v:
Journal of clinical immunology. 42(2)
NLRC4-associated autoinflammatory disease (NLRC4-AID) is an autosomal dominant condition presenting with a range of clinical manifestations which can include macrophage activation syndrome (MAS) and severe enterocolitis. We now report the first homoz
Publikováno v:
Current Rheumatology Reports. 20
Type I interferons (IFNαβ) induce the expression of hundreds of genes; thus, it is unsurprising that the initiation, transmission, and resolution of the IFNαβ-mediated immune response is tightly controlled. Mutations that alter nucleic acid proce
Publikováno v:
Current Rheumatology Reports. 20
Autoinflammatory diseases are driven by abnormal innate immune activation. In the case of inflammasomopathies, these are all attributable to activation of an inflammasome complex, nucleated by an innate immune sensor such as NLRP3. This review will f
Publikováno v:
Current Rheumatology Reports. 20
The nuclear factor κB (NF-κB) pathway is tightly regulated through multiple posttranslational mechanisms including ubiquitination. Mutations in these regulatory pathways can cause disease and are the focus of this review. The linear ubiquitin chain