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Article ; Online: FOXO1 Couples KGF and PI-3K/AKT Signaling to NKX2.1-Regulated Differentiation of Alveolar Epithelial Cells.

Zhong, Qian / Liu, Yixin / Correa, Michele Ramos / Marconett, Crystal Nicole / Minoo, Parviz / Li, Changgong / Ann, David K / Zhou, Beiyun / Borok, Zea

Cells

2022 Volume 11, Issue 7

Abstract: NKX2.1 is a master regulator of lung morphogenesis and cell specification; however, interactions of NKX2.1 with various transcription factors to regulate cell-specific gene expression and cell fate in the distal lung remain incompletely understood. FOXO1 ...

Abstract	NKX2.1 is a master regulator of lung morphogenesis and cell specification; however, interactions of NKX2.1 with various transcription factors to regulate cell-specific gene expression and cell fate in the distal lung remain incompletely understood. FOXO1 is a key regulator of stem/progenitor cell maintenance/differentiation in several tissues but its role in the regulation of lung alveolar epithelial progenitor homeostasis has not been evaluated. We identified a novel role for FOXO1 in alveolar epithelial cell (AEC) differentiation that results in the removal of NKX2.1 from surfactant gene promoters and the subsequent loss of surfactant expression in alveolar epithelial type I-like (AT1-like) cells. We found that the FOXO1 forkhead domain potentiates a loss of surfactant gene expression through an interaction with the NKX2.1 homeodomain, disrupting NKX2.1 binding to the
MeSH term(s)	Alveolar Epithelial Cells/metabolism ; Epithelial Cells/metabolism ; Fibroblast Growth Factor 7/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Pulmonary Surfactants/metabolism ; Surface-Active Agents/metabolism
Chemical Substances	Pulmonary Surfactants ; Surface-Active Agents ; Fibroblast Growth Factor 7 (126469-10-1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2022-03-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11071122
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Host-Intrinsic Interferon Status in Infection and Immunity.

Liu, Beiyun C / Sarhan, Joseph / Poltorak, Alexander

Trends in molecular medicine

2018 Volume 24, Issue 8, Page(s) 658–668

Abstract: Most genetic ablations of interferon (IFN) signaling abolish both the experimentally induced IFN response and constitutive IFN, whose effects are well established in autoimmunity but understudied during infection. In host-pathogen interactions, most IFN- ... ...

Abstract	Most genetic ablations of interferon (IFN) signaling abolish both the experimentally induced IFN response and constitutive IFN, whose effects are well established in autoimmunity but understudied during infection. In host-pathogen interactions, most IFN-mediated responses are attributed to infection-driven IFN. However, IFNs confer their activity by regulating networks of interferon-stimulated genes (ISGs), a process that requires de novo transcription and translation of both IFN and downstream ISGs through feedback of IFN receptor signaling. Due to the temporal requirement for IFN activity, many rapid antimicrobial responses may instead result from pre-established IFN signature stemming from host-intrinsic processes. Addressing the permeating effects of constitutive IFN is therefore needed to accurately describe immunity as host intrinsic or pathogen induced.
MeSH term(s)	Animals ; Autoimmunity ; Biomarkers ; Disease Models, Animal ; Disease Susceptibility ; Homeostasis ; Host-Pathogen Interactions/immunology ; Humans ; Immune System/cytology ; Immune System/immunology ; Immune System/metabolism ; Immunity ; Immunomodulation ; Infection/etiology ; Infection/metabolism ; Interferons/metabolism ; Ligands ; Mice ; Signal Transduction
Chemical Substances	Biomarkers ; Ligands ; Interferons (9008-11-1)
Language	English
Publishing date	2018-07-07
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2036490-8
ISSN	1471-499X ; 1471-4914
ISSN (online)	1471-499X
ISSN	1471-4914
DOI	10.1016/j.molmed.2018.06.004
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Zs.A 4345: Show issues

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Article ; Online: Randomized Phase II Study of Two Doses of Pixantrone in Patients with Metastatic Breast Cancer (NCCTG N1031, Alliance).

Sideras, Kostandinos / Hillman, David W / Giridhar, Karthik / Ginos, Brenda F / Tenglin, Richard C / Liu, Heshan / Chen, Beiyun / Tan, Winston / Gross, Gerald G / Mowat, Rex B / Dueck, Amylou C / Perez, Edith A / Moreno-Aspitia, Alvaro

The oncologist

2022

Abstract: Background: Anthracycline use in metastatic breast cancer (MBC) is hindered by cumulative exposure limits and risk of cardiotoxicity. Pixantrone, a novel aza-anthracenedione with structural similarities to mitoxantrone and anthracyclines, is theorized ... ...

Abstract	Background: Anthracycline use in metastatic breast cancer (MBC) is hindered by cumulative exposure limits and risk of cardiotoxicity. Pixantrone, a novel aza-anthracenedione with structural similarities to mitoxantrone and anthracyclines, is theorized to exhibit less cardiotoxicity, mainly due to lack of iron binding. We conducted a randomized phase II study to evaluate the efficacy and safety of 2 dosing schedules of pixantrone in patients with refractory HER2-negative MBC. Methods: Intravenous pixantrone was administered at 180 mg/m2 every 3 weeks (group A) versus 85 mg/m2 on days 1, 8, and 15 of a 28-day cycle (group B). Primary endpoint was objective response rate (ORR) and secondary endpoints included progression-free survival (PFS), median 6-month PFS, overall survival (OS), safety, quality of life, and serial assessment of circulating tumor cells. A 20% ORR was targeted as sufficient for further testing of pixantrone in this patient population. Results: Forty-five patients were evaluable, with 2 confirmed partial responses in group A and 1 in group B. The trial was terminated due to insufficient activity. Overall median PFS and OS were 2.8 (95% confidence interval [CI]: 2.0-4.1) and 16.8 (95% CI: 8.9-21.6) months, respectively. Notable overall grade 3-4 adverse events were the following: neutrophil count decrease (62%), fatigue (16%), and decrease in ejection fraction (EF) (4%). Conclusion: Pixantrone has insufficient activity in the second- and third-line MBC setting. It appears, however, to have limited cardiotoxicity. (ClinicalTrials.gov ID: NCT01086605).
Language	English
Publishing date	2022-04-21
Publishing country	England
Document type	Journal Article
ZDB-ID	1409038-7
ISSN	1549-490X ; 1083-7159
ISSN (online)	1549-490X
ISSN	1083-7159
DOI	10.1093/oncolo/oyab065
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Zs.A 4845: 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.MO 494: Show issues

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Article ; Online: Development of human alveolar epithelial cell models to study distal lung biology and disease.

Tran, Evelyn / Shi, Tuo / Li, Xiuwen / Chowdhury, Adnan Y / Jiang, Du / Liu, Yixin / Wang, Hongjun / Yan, Chunli / Wallace, William D / Lu, Rong / Ryan, Amy L / Marconett, Crystal N / Zhou, Beiyun / Borok, Zea / Offringa, Ite A

iScience

2022 Volume 25, Issue 2, Page(s) 103780

Abstract: ... aquaporin 5 (AQP5), G-protein-coupled receptor class C group 5 member A (GPRC5A), and surface marker HTII280 ...

Abstract	Many acute and chronic diseases affect the distal lung alveoli. Alveolar epithelial cell (AEC) lines are needed to better model these diseases. We used de-identified human remnant transplant lungs to develop a method to establish AEC lines. The lines grow well in 2-dimensional (2D) culture as epithelial monolayers expressing lung progenitor markers. In 3-dimensional (3D) culture with fibroblasts, Matrigel, and specific media conditions, the cells form alveolar-like organoids expressing mature AEC markers including aquaporin 5 (AQP5), G-protein-coupled receptor class C group 5 member A (GPRC5A), and surface marker HTII280. Single-cell RNA sequencing of an AEC line in 2D versus 3D culture revealed increased cellular heterogeneity and induction of cytokine and lipoprotein signaling in 3D organoids. Our approach yields lung progenitor lines that retain the ability to differentiate along the alveolar cell lineage despite long-term expansion and provides a valuable system to model and study the distal lung
Language	English
Publishing date	2022-01-15
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2022.103780
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Article ; Online: Lessons for the Next Generation of Scientists from the Second Annual Arthur and Sandra Irving Cancer Immunology Symposium.

Alvarez-Breckenridge, Christopher / Anderson, Kristin G / Correia, Ana Luisa / Demehri, Shadmehr / Dinh, Huy Q / Dixon, Karen Olivia / Dunn, Gavin P / Evgin, Laura / Goc, Jeremy / Good, Zinaida / Hacohen, Nir / Han, Patrick / Hanč, Pavel / Hickey, John / Kersten, Kelly / Liu, Beiyun C / Buque, Aitziber / Miao, Yuxuan 'Phoenix' / Milner, J Justin /

Pritykin, Yuri / Pucci, Ferdinando / Scharping, Nicole E / Sudmeier, Lisa / Wang, Yufei / Wieland, Andreas / Williams, Michelle M

Cancer immunology research

2023 Volume 11, Issue 12, Page(s) 1571–1577

Abstract: The Arthur and Sandra Irving Cancer Immunology Symposium has been created as a platform for established cancer immunologists to mentor trainees and young investigators as they launch their research career in the field. By sharing their different paths to ...

Abstract	The Arthur and Sandra Irving Cancer Immunology Symposium has been created as a platform for established cancer immunologists to mentor trainees and young investigators as they launch their research career in the field. By sharing their different paths to success, the senior faculty mentors provide an invaluable resource to support the development of the next generation of leaders in the cancer immunology community. This Commentary describes some of the key topics that were discussed during the 2022 symposium: scientific and career trajectory, leadership, mentoring, collaborations, and publishing. For each of these topics, established investigators discussed the elements that facilitate success in these areas as well as mistakes that can hinder progress. Herein, we outline the critical points raised in these discussions for establishing a successful independent research career. These points are highly relevant for the broader scientific community.
MeSH term(s)	Humans ; Mentoring ; Mentors ; Physicians ; Research Personnel ; Neoplasms/therapy
Language	English
Publishing date	2023-10-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	2732489-8
ISSN	2326-6074 ; 2326-6066
ISSN (online)	2326-6074
ISSN	2326-6066
DOI	10.1158/2326-6066.CIR-23-0522
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Zs.A 7022: Show issues

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Article ; Online: Constitutive Interferon Attenuates RIPK1/3-Mediated Cytokine Translation

Hayley I. Muendlein / Joseph Sarhan / Beiyun C. Liu / Wilson M. Connolly / Stephen A. Schworer / Irina Smirnova / Amy Y. Tang / Vladimir Ilyukha / Jodie Pietruska / Soroush Tahmasebi / Nahum Sonenberg / Alexei Degterev / Alexander Poltorak

Cell Reports, Vol 30, Iss 3, Pp 699-713.e

2020 Volume 4

Abstract: Summary: Receptor-interacting protein kinase 1 (RIPK1) and 3 (RIPK3) are well known for their capacity to drive necroptosis via mixed-lineage kinase-like domain (MLKL). Recently, RIPK1/3 kinase activity has been shown to drive inflammation via activation ...

Abstract	Summary: Receptor-interacting protein kinase 1 (RIPK1) and 3 (RIPK3) are well known for their capacity to drive necroptosis via mixed-lineage kinase-like domain (MLKL). Recently, RIPK1/3 kinase activity has been shown to drive inflammation via activation of MAPK signaling. However, the regulatory mechanisms underlying this kinase-dependent cytokine production remain poorly understood. In the present study, we establish that the kinase activity of RIPK1/3 regulates cytokine translation in mouse and human macrophages. Furthermore, we show that this inflammatory response is downregulated by type I interferon (IFN) signaling, independent of type I IFN-promoted cell death. Specifically, low-level constitutive IFN signaling attenuates RIPK-driven activation of cap-dependent translation initiation pathway components AKT, mTORC1, 4E-BP and eIF4E, while promoting RIPK-dependent cell death. Altogether, these data characterize constitutive IFN signaling as a regulator of RIPK-dependent inflammation and establish cap-dependent translation as a crucial checkpoint in the regulation of cytokine production. : Balancing inflammatory responses is critical for host survival. Muendlein et al. show that constitutive type I IFN signaling inhibits translation machinery activated downstream of the kinase activity of RIPK1/3, preventing the production of a subset of inflammatory cytokines. This work identifies cap-dependent translation as a checkpoint in regulation of RIPK1/3-kinase-dependent inflammation. Keywords: inflammation, necroptosis, constitutive IFN, translation, macrophage, receptor-interacting protein kinases
Keywords	Biology (General) ; QH301-705.5
Subject code	571
Language	English
Publishing date	2020-01-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The N terminus of SKAP55 enables T cell adhesion to TCR and integrin ligands via distinct mechanisms.

Ophir, Michael J / Liu, Beiyun C / Bunnell, Stephen C

The Journal of cell biology

2013 Volume 203, Issue 6, Page(s) 1021–1041

Abstract: The T cell receptor (TCR) triggers the assembly of "SLP-76 microclusters," which mediate signals required for T cell activation. In addition to regulating integrin activation, we show that Src kinase-associated phosphoprotein of 55 kD (SKAP55) is ... ...

Abstract	The T cell receptor (TCR) triggers the assembly of "SLP-76 microclusters," which mediate signals required for T cell activation. In addition to regulating integrin activation, we show that Src kinase-associated phosphoprotein of 55 kD (SKAP55) is required for microcluster persistence and movement, junctional stabilization, and integrin-independent adhesion via the TCR. These functions require the dimerization of SKAP55 and its interaction with the adaptor adhesion and degranulation-promoting adaptor protein (ADAP). A "tandem dimer" containing two ADAP-binding SKAP55 Src homology 3 (SH3) domains stabilized SLP-76 microclusters and promoted T cell adhesion via the TCR, but could not support adhesion to integrin ligands. Finally, the SKAP55 dimerization motif (DM) enabled the coimmunoprecipitation of the Rap1-dependent integrin regulator Rap1-GTP-interacting adaptor molecule (RIAM), the recruitment of talin into TCR-induced adhesive junctions, and "inside-out" signaling to β1 integrins. Our data indicate that SKAP55 dimers stabilize SLP-76 microclusters, couple SLP-76 to the force-generating systems responsible for microcluster movement, and enable adhesion via the TCR by mechanisms independent of RIAM, talin, and β1 integrins.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Cell Adhesion ; Dimerization ; Humans ; Integrins/metabolism ; Jurkat Cells ; Ligands ; Phosphoproteins/chemistry ; Phosphoproteins/metabolism ; Phosphoproteins/physiology ; Protein Structure, Tertiary ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction ; T-Lymphocytes/cytology
Chemical Substances	Adaptor Proteins, Signal Transducing ; Integrins ; Ligands ; Phosphoproteins ; Receptors, Antigen, T-Cell ; SKAP1 protein, human ; SLP-76 signal Transducing adaptor proteins
Language	English
Publishing date	2013-12-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218154-x
ISSN	1540-8140 ; 0021-9525
ISSN (online)	1540-8140
ISSN	0021-9525
DOI	10.1083/jcb.201305088
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Article ; Online: Constitutive Interferon Attenuates RIPK1/3-Mediated Cytokine Translation.

Muendlein, Hayley I / Sarhan, Joseph / Liu, Beiyun C / Connolly, Wilson M / Schworer, Stephen A / Smirnova, Irina / Tang, Amy Y / Ilyukha, Vladimir / Pietruska, Jodie / Tahmasebi, Soroush / Sonenberg, Nahum / Degterev, Alexei / Poltorak, Alexander

Cell reports

2020 Volume 30, Issue 3, Page(s) 699–713.e4

Abstract: Receptor-interacting protein kinase 1 (RIPK1) and 3 (RIPK3) are well known for their capacity to drive necroptosis via mixed-lineage kinase-like domain (MLKL). Recently, RIPK1/3 kinase activity has been shown to drive inflammation via activation of MAPK ... ...

Abstract	Receptor-interacting protein kinase 1 (RIPK1) and 3 (RIPK3) are well known for their capacity to drive necroptosis via mixed-lineage kinase-like domain (MLKL). Recently, RIPK1/3 kinase activity has been shown to drive inflammation via activation of MAPK signaling. However, the regulatory mechanisms underlying this kinase-dependent cytokine production remain poorly understood. In the present study, we establish that the kinase activity of RIPK1/3 regulates cytokine translation in mouse and human macrophages. Furthermore, we show that this inflammatory response is downregulated by type I interferon (IFN) signaling, independent of type I IFN-promoted cell death. Specifically, low-level constitutive IFN signaling attenuates RIPK-driven activation of cap-dependent translation initiation pathway components AKT, mTORC1, 4E-BP and eIF4E, while promoting RIPK-dependent cell death. Altogether, these data characterize constitutive IFN signaling as a regulator of RIPK-dependent inflammation and establish cap-dependent translation as a crucial checkpoint in the regulation of cytokine production.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Cell Cycle Proteins/metabolism ; Cytokines/genetics ; Cytokines/metabolism ; Down-Regulation ; Eukaryotic Initiation Factor-4E/metabolism ; Female ; Humans ; Inflammation/pathology ; Interferons/metabolism ; Lipopolysaccharides/pharmacology ; Macrophage Activation/drug effects ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Mice, Inbred C57BL ; Protein Biosynthesis ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Signal Transduction
Chemical Substances	Adaptor Proteins, Signal Transducing ; Cell Cycle Proteins ; Cytokines ; Eif4ebp1 protein, mouse ; Eukaryotic Initiation Factor-4E ; Lipopolysaccharides ; RNA, Messenger ; Interferons (9008-11-1) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; RIPK1 protein, human (EC 2.7.11.1) ; RIPK3 protein, human (EC 2.7.11.1) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Ripk1 protein, mouse (EC 2.7.11.1) ; Ripk3 protein, mouse (EC 2.7.11.1)
Language	English
Publishing date	2020-01-22
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.2019.12.073
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Article ; Online: Constitutive Interferon Maintains GBP Expression Required for Release of Bacterial Components Upstream of Pyroptosis and Anti-DNA Responses.

Liu, Beiyun C / Sarhan, Joseph / Panda, Alexander / Muendlein, Hayley I / Ilyukha, Vladimir / Coers, Jörn / Yamamoto, Masahiro / Isberg, Ralph R / Poltorak, Alexander

Cell reports

2018 Volume 24, Issue 1, Page(s) 155–168.e5

Abstract: ... deficient for chromosome 3 GBPs were unable to mount a rapid IL-1/chemokine (C-X-C motif) ligand 1 (CXCL1 ...

Abstract	Legionella pneumophila elicits caspase-11-driven macrophage pyroptosis through guanylate-binding proteins (GBPs) encoded on chromosome 3. It has been proposed that microbe-driven IFN upregulates GBPs to facilitate pathogen vacuole rupture and bacteriolysis preceding caspase-11 activation. We show here that macrophage death occurred independently of microbial-induced IFN signaling and that GBPs are dispensable for pathogen vacuole rupture. Instead, the host-intrinsic IFN status sustained sufficient GBP expression levels to drive caspase-1 and caspase-11 activation in response to cytosol-exposed bacteria. In addition, endogenous GBP levels were sufficient for the release of DNA from cytosol-exposed bacteria, preceding the cyclic GMP-AMP synthase/stimulator of interferon genes (cGAS/STING) pathway for Ifnb induction. Mice deficient for chromosome 3 GBPs were unable to mount a rapid IL-1/chemokine (C-X-C motif) ligand 1 (CXCL1) response during Legionella-induced pneumonia, with defective bacterial clearance. Our results show that rapid GBP activity is controlled by host-intrinsic cytokine signaling and that GBP activities precede immune amplification responses, including IFN induction, inflammasome activation, and cell death.
MeSH term(s)	Animals ; Anti-Infective Agents/pharmacology ; Chromosomes, Mammalian/metabolism ; Cytosol/metabolism ; DNA, Bacterial/metabolism ; Female ; GTP-Binding Proteins/metabolism ; Humans ; Interferons/metabolism ; Janus Kinases/metabolism ; Legionella/metabolism ; Legionellosis/microbiology ; Macrophages/cytology ; Male ; Mice, Inbred C57BL ; Pneumonia/microbiology ; Pneumonia/pathology ; Pyroptosis ; Receptor, Interferon alpha-beta/metabolism ; STAT Transcription Factors/metabolism ; Signal Transduction ; Vacuoles/metabolism
Chemical Substances	Anti-Infective Agents ; DNA, Bacterial ; STAT Transcription Factors ; Receptor, Interferon alpha-beta (156986-95-7) ; Interferons (9008-11-1) ; Janus Kinases (EC 2.7.10.2) ; GTP-Binding Proteins (EC 3.6.1.-)
Language	English
Publishing date	2018-07-02
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.2018.06.012
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Article ; Online: Caspase-8 induces cleavage of gasdermin D to elicit pyroptosis during

Sarhan, Joseph / Liu, Beiyun C / Muendlein, Hayley I / Li, Peng / Nilson, Rachael / Tang, Amy Y / Rongvaux, Anthony / Bunnell, Stephen C / Shao, Feng / Green, Douglas R / Poltorak, Alexander

Proceedings of the National Academy of Sciences of the United States of America

2018 Volume 115, Issue 46, Page(s) E10888–E10897

Abstract: Cell death and inflammation are intimately linked ... ...

Abstract	Cell death and inflammation are intimately linked during
MeSH term(s)	Animals ; Apoptosis/physiology ; Apoptosis Regulatory Proteins/metabolism ; Bacterial Proteins/metabolism ; Caspase 8/metabolism ; Humans ; Interleukin-1/metabolism ; Intracellular Signaling Peptides and Proteins ; Lipopolysaccharides/pharmacology ; MAP Kinase Kinase Kinases/antagonists & inhibitors ; MAP Kinase Kinase Kinases/metabolism ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL ; Phosphate-Binding Proteins ; Pyroptosis/physiology ; Yersinia Infections/metabolism ; Yersinia Infections/pathology ; Yersinia pseudotuberculosis/metabolism
Chemical Substances	Apoptosis Regulatory Proteins ; Bacterial Proteins ; Gsdmd protein, mouse ; Interleukin-1 ; Intracellular Signaling Peptides and Proteins ; Lipopolysaccharides ; Phosphate-Binding Proteins ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; MAP kinase kinase kinase 7 (EC 2.7.11.25) ; Casp8 protein, mouse (EC 3.4.22.-) ; Caspase 8 (EC 3.4.22.-)
Language	English
Publishing date	2018-10-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1809548115
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