LIVIVO - Search results -

Search results

Result 1 - 10 of total 70

Search options

Article ; Online: Aberrantly activated TAK1 links neuroinflammation and neuronal loss in Alzheimer's disease mouse models.

Sai, Kazuhito / Nakanishi, Aoi / Scofield, Kimberly M / Tokarz, Debra A / Linder, Keith E / Cohen, Todd J / Ninomiya-Tsuji, Jun

Journal of cell science

2023 Volume 136, Issue 6

Abstract: Neuroinflammation is causally associated with Alzheimer's disease (AD) pathology. Reactive glia cells secrete various neurotoxic factors that impair neuronal homeostasis eventually leading to neuronal loss. Although the glial activation mechanism in AD ... ...

Abstract	Neuroinflammation is causally associated with Alzheimer's disease (AD) pathology. Reactive glia cells secrete various neurotoxic factors that impair neuronal homeostasis eventually leading to neuronal loss. Although the glial activation mechanism in AD has been relatively well studied, how it perturbs intraneuronal signaling, which ultimately leads to neuronal cell death, remains poorly understood. Here, we report that compound stimulation with the neurotoxic factors TNF and glutamate aberrantly activates neuronal TAK1 (also known as MAP3K7), which promotes the pathogenesis of AD in mouse models. Glutamate-induced Ca2+ influx shifts TNF signaling to hyper-activate TAK1 enzymatic activity through Ca2+/calmodulin-dependent protein kinase II, which leads to necroptotic cellular damage. Genetic ablation and pharmacological inhibition of TAK1 ameliorated AD-associated neuronal loss and cognitive impairment in the AD model mice. Our findings provide a molecular mechanism linking cytokines, Ca2+ signaling and neuronal necroptosis in AD.
MeSH term(s)	Animals ; Mice ; Alzheimer Disease/genetics ; Calcium ; Cytokines/metabolism ; Neuroinflammatory Diseases ; Signal Transduction/physiology
Chemical Substances	Calcium (SY7Q814VUP) ; Cytokines ; MAP kinase kinase kinase 7 (EC 2.7.11.25)
Language	English
Publishing date	2023-03-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.260102
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1200: 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 14: Show issues

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: TAK1 inhibition elicits mitochondrial ROS to block intracellular bacterial colonization.

López-Pérez, Wilfred / Sai, Kazuhito / Sakamachi, Yosuke / Parsons, Cameron / Kathariou, Sophia / Ninomiya-Tsuji, Jun

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

2021 Volume 118, Issue 25

Abstract: Mitogen-activated protein kinase kinase kinase 7 (MAP3K7), known as TAK1, is an intracellular signaling intermediate of inflammatory responses. However, a series of ... ...

Abstract	Mitogen-activated protein kinase kinase kinase 7 (MAP3K7), known as TAK1, is an intracellular signaling intermediate of inflammatory responses. However, a series of mouse
MeSH term(s)	Animals ; Bacteria/growth & development ; Caspase 3/metabolism ; Colony Count, Microbial ; Hydrogen Sulfide/pharmacology ; Intracellular Space/microbiology ; MAP Kinase Kinase Kinases/antagonists & inhibitors ; MAP Kinase Kinase Kinases/metabolism ; Mice ; Mitochondria/metabolism ; Reactive Oxygen Species/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Salmonella/drug effects ; Salmonella/growth & development ; Yersinia/drug effects
Chemical Substances	Reactive Oxygen Species ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Ripk3 protein, mouse (EC 2.7.11.1) ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; MAP kinase kinase kinase 7 (EC 2.7.11.25) ; Caspase 3 (EC 3.4.22.-) ; Hydrogen Sulfide (YY9FVM7NSN)
Language	English
Publishing date	2021-06-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2023647118
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1148: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Necroptosis mediators RIPK3 and MLKL suppress intracellular

Sai, Kazuhito / Parsons, Cameron / House, John S / Kathariou, Sophia / Ninomiya-Tsuji, Jun

The Journal of cell biology

2019 Volume 218, Issue 6, Page(s) 1994–2005

Abstract: RIPK3, a key mediator of necroptosis, has been implicated in the host defense against viral infection primary in immune cells. However, gene expression analysis revealed that RIPK3 is abundantly expressed not only in immune organs but also in the ... ...

Abstract	RIPK3, a key mediator of necroptosis, has been implicated in the host defense against viral infection primary in immune cells. However, gene expression analysis revealed that RIPK3 is abundantly expressed not only in immune organs but also in the gastrointestinal tract, particularly in the small intestine. We found that orally inoculated
MeSH term(s)	Animals ; Female ; Humans ; Listeria/growth & development ; Listeria/immunology ; Listeria/metabolism ; Listeriosis/metabolism ; Listeriosis/microbiology ; Listeriosis/pathology ; Listeriosis/prevention & control ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Necroptosis ; Protein Kinases/physiology ; Receptor-Interacting Protein Serine-Threonine Kinases/genetics ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases/physiology
Chemical Substances	MLKL protein, mouse (EC 2.7.-) ; Protein Kinases (EC 2.7.-) ; RIPK3 protein, human (EC 2.7.11.1) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Ripk3 protein, mouse (EC 2.7.11.1)
Language	English
Publishing date	2019-04-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	218154-x
ISSN	1540-8140 ; 0021-9525
ISSN (online)	1540-8140
ISSN	0021-9525
DOI	10.1083/jcb.201810014
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ub I Zs.190: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Erratum: Noncanonical cell death program independent of caspase activation cascade and necroptotic modules is elicited by loss of TGFβ-activated kinase 1.

Mihaly, September R / Sakamachi, Yosuke / Ninomiya-Tsuji, Jun / Morioka, Sho

Scientific reports

2017 Volume 7, Issue 1, Page(s) 10695

Abstract: A correction to this article has been published and is linked from the HTML version of this paper. The error has been fixed in the paper. ...

Abstract	A correction to this article has been published and is linked from the HTML version of this paper. The error has been fixed in the paper.
Language	English
Publishing date	2017-09-06
Publishing country	England
Document type	Journal Article ; Published Erratum
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-09609-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Noncanonical cell death program independent of caspase activation cascade and necroptotic modules is elicited by loss of TGFβ-activated kinase 1.

Mihaly, September R / Sakamachi, Yosuke / Ninomiya-Tsuji, Jun / Morioka, Sho

Scientific reports

2017 Volume 7, Issue 1, Page(s) 2918

Abstract: Programmed cell death (PCD) occurs in several forms including apoptosis and necroptosis. Apoptosis is executed by the activation of caspases, while necroptosis is dependent on the receptor interacting protein kinase 3 (RIPK3). Precise control of cell ... ...

Abstract	Programmed cell death (PCD) occurs in several forms including apoptosis and necroptosis. Apoptosis is executed by the activation of caspases, while necroptosis is dependent on the receptor interacting protein kinase 3 (RIPK3). Precise control of cell death is crucial for tissue homeostasis. Indeed, necroptosis is triggered by caspase inhibition to ensure cell death. Here we identified a previously uncharacterized cell death pathway regulated by TAK1, which is unexpectedly provoked by inhibition of caspase activity and necroptosis cascades. Ablation of TAK1 triggers spontaneous death in macrophages. Simultaneous inhibition of caspases and RIPK3 did not completely restore cell viability. Previous studies demonstrated that loss of TAK1 in fibroblasts causes TNF-induced apoptosis and that additional inhibition of caspase leads to necroptotic cell death. However, we surprisingly found that caspase and RIPK3 inhibitions do not completely suppress cell death in Tak1-deficient cells. Mechanistically, the execution of the third cell death pathway in Tak1-deficient macrophages and fibroblasts were mediated by RIPK1-dependent rapid accumulation of reactive oxygen species (ROS). Conversely, activation of RIPK1 was sufficient to induce cell death. Therefore, loss of TAK1 elicits noncanonical cell death which is mediated by RIPK1-induced oxidative stress upon caspase and necroptosis inhibition to further ensure induction of cell death.
Language	English
Publishing date	2017-06-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-03112-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Activated macrophage survival is coordinated by TAK1 binding proteins.

Mihaly, September R / Morioka, Sho / Ninomiya-Tsuji, Jun / Takaesu, Giichi

PloS one

2014 Volume 9, Issue 4, Page(s) e94982

Abstract: Macrophages play diverse roles in tissue homeostasis and immunity, and canonically activated macrophages are critically associated with acute inflammatory responses. It is known that activated macrophages undergo cell death after transient activation in ... ...

Abstract	Macrophages play diverse roles in tissue homeostasis and immunity, and canonically activated macrophages are critically associated with acute inflammatory responses. It is known that activated macrophages undergo cell death after transient activation in some settings, and the viability of macrophages impacts on inflammatory status. Here we report that TGFβ- activated kinase (TAK1) activators, TAK1-binding protein 1 (TAB1) and TAK1-binding protein 2 (TAB2), are critical molecules in the regulation of activated macrophage survival. While deletion of Tak1 induced cell death in bone marrow derived macrophages even without activation, Tab1 or Tab2 deletion alone did not profoundly affect survival of naïve macrophages. However, in lipopolysaccharide (LPS)-activated macrophages, even single deletion of Tab1 or Tab2 resulted in macrophage death with both necrotic and apoptotic features. We show that TAB1 and TAB2 were redundantly involved in LPS-induced TAK1 activation in macrophages. These results demonstrate that TAK1 activity is the key to activated macrophage survival. Finally, in an in vivo setting, Tab1 deficiency impaired increase of peritoneal macrophages upon LPS challenge, suggesting that TAK1 complex regulation of macrophages may participate in in vivo macrophage homeostasis. Our results demonstrate that TAB1 and TAB2 are required for activated macrophages, making TAB1 and TAB2 effective targets to control inflammation by modulating macrophage survival.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Cell Death/drug effects ; Cell Death/immunology ; Cell Survival/genetics ; GTPase-Activating Proteins/antagonists & inhibitors ; GTPase-Activating Proteins/genetics ; GTPase-Activating Proteins/metabolism ; Gene Deletion ; Lipopolysaccharides/immunology ; MAP Kinase Kinase Kinases/genetics ; Macrophage Activation/genetics ; Macrophage Activation/immunology ; Macrophages/immunology ; Macrophages/metabolism ; Mice ; Mice, Knockout
Chemical Substances	Adaptor Proteins, Signal Transducing ; GTPase-Activating Proteins ; Lipopolysaccharides ; Ralbp1 protein, mouse ; Tab1 protein, mouse ; Tab2 protein, mouse ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; MAP kinase kinase kinase 7 (EC 2.7.11.25)
Language	English
Publishing date	2014-04-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0094982
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: TAK1 binding protein 2 is essential for liver protection from stressors.

Ikeda, Yuka / Morioka, Sho / Matsumoto, Kunihiro / Ninomiya-Tsuji, Jun

PloS one

2014 Volume 9, Issue 2, Page(s) e88037

Abstract: The liver is the first line of defense from environmental stressors in that hepatocytes respond to and metabolize them. Hence, hepatocytes can be damaged by stressors. Protection against hepatic cell damage and cell death is important for liver function ... ...

Abstract	The liver is the first line of defense from environmental stressors in that hepatocytes respond to and metabolize them. Hence, hepatocytes can be damaged by stressors. Protection against hepatic cell damage and cell death is important for liver function and homeostasis. TAK1 (MAP3K7) is an intermediate of stressors such as bacterial moieties-induced signal transduction pathways in several cell types. Tak1 deficiency has been reported to induce spontaneous hepatocellular carcinoma. However, the regulatory mechanism of TAK1 activity in liver stress response has not yet been defined. Here we report that activation of TAK1 through TAK1 binding protein 2 (TAB2) is required for liver protection from stressors. We found that a bacterial moiety, lipopolysaccharides (LPS), activated TAK1 in primary hepatocytes, which was diminished by deletion of TAB2. Mice having hepatocyte-specific deletion of the Tab2 gene exhibited only late-onset moderate liver lesions but were hypersensitive to LPS-induced liver injury. Furthermore, we show that a chemical stressor induced greatly exaggerated liver injury in hepatocyte-specific Tab2-deficient mice. These results demonstrate that TAB2 is a sensor of stress conditions in the liver and functions to protect the liver by activating the TAK1 pathway.
MeSH term(s)	Adaptor Proteins, Signal Transducing/physiology ; Alkylating Agents/toxicity ; Animals ; Apoptosis/drug effects ; Blotting, Western ; Chemical and Drug Induced Liver Injury/etiology ; Chemical and Drug Induced Liver Injury/metabolism ; Chemical and Drug Induced Liver Injury/prevention & control ; Diethylnitrosamine/toxicity ; Electrophoretic Mobility Shift Assay ; Female ; Hepatocytes/drug effects ; Hepatocytes/metabolism ; Hepatocytes/pathology ; Integrases/metabolism ; Lipopolysaccharides/toxicity ; MAP Kinase Kinase Kinases/physiology ; Male ; Mice ; Mice, Knockout ; Mice, Transgenic ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction
Chemical Substances	Adaptor Proteins, Signal Transducing ; Alkylating Agents ; Lipopolysaccharides ; RNA, Messenger ; Tab2 protein, mouse ; Diethylnitrosamine (3IQ78TTX1A) ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; MAP kinase kinase kinase 7 (EC 2.7.11.25) ; Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-)
Language	English
Publishing date	2014-02-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0088037
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: TAK1 Regulates the Nrf2 Antioxidant System Through Modulating p62/SQSTM1.

Hashimoto, Kazunori / Simmons, Alicia N / Kajino-Sakamoto, Rie / Tsuji, Yoshiaki / Ninomiya-Tsuji, Jun

Antioxidants & redox signaling

2016 Volume 25, Issue 17, Page(s) 953–964

Abstract: Aims: Nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2) is the master transcriptional regulator of antioxidant gene expression. On increased oxidative stress, an adaptor for Nrf2 degradation, Kelch-like ECH-associated protein 1 (Keap1), is ... ...

Abstract	Aims: Nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2) is the master transcriptional regulator of antioxidant gene expression. On increased oxidative stress, an adaptor for Nrf2 degradation, Kelch-like ECH-associated protein 1 (Keap1), is directly modulated by oxidants in the cytoplasm, which results in stabilization and activation of Nrf2. Nrf2 is also constitutively active, to some extent, in the absence of exogenous oxidative stress. We have previously demonstrated that intestinal epithelium-specific TGF-β-activated kinase 1 (TAK1) deletion downregulates the level of Nrf2 protein, resulting in an increase of reactive oxygen species (ROS) in a mouse model. We aim at determining the mechanism by which TAK1 modulates the level of Nrf2. Results: We found that TAK1 upregulated serine 351 phosphorylation of an autophagic adaptor protein, p62/Sequestosome-1 (SQSTM1), which facilitates interaction between p62/SQSTM1 and Keap1 and subsequent Keap1 degradation. This, ultimately, causes increased Nrf2. Tak1 deficiency reduced the phosphorylation of p62/SQSTM1, resulting in decreased steady-state levels of Nrf2 along with increased Keap1. We also found that this regulation is independent of the canonical redox-mediated Nrf2 activation mechanism. In Tak1-deficient intestinal epithelium, a synthetic phenolic electrophile, butylated hydroxyanisole still effectively upregulated Nrf2 and reduced ROS. Innovation: Our results identify for the first time that TAK1 is a modulator of p62/SQSTM1-dependent Keap1 degradation and maintains the steady state-level of Nrf2. Conclusion: TAK1 regulates Nrf2 through modulation of Keap-p62/SQSTM1 interaction. This regulation is important for homeostatic antioxidant protection in the intestinal epithelium. Antioxid. Redox Signal. 25, 953-964.
MeSH term(s)	Animals ; Antioxidants/metabolism ; Cell Line ; Gene Expression Regulation ; Humans ; Intestinal Mucosa/metabolism ; Kelch-Like ECH-Associated Protein 1/metabolism ; MAP Kinase Kinase Kinases/genetics ; MAP Kinase Kinase Kinases/metabolism ; Mice ; Mice, Knockout ; Models, Biological ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Oxidative Stress ; Protein Binding ; Proteolysis ; Reactive Oxygen Species/metabolism ; Sequestosome-1 Protein/metabolism
Chemical Substances	Antioxidants ; Kelch-Like ECH-Associated Protein 1 ; NF-E2-Related Factor 2 ; Reactive Oxygen Species ; Sequestosome-1 Protein ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; MAP kinase kinase kinase 7 (EC 2.7.11.25)
Language	English
Publishing date	2016-12-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2016.6663
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 5488: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Compound mutations in Bmpr1a and Tak1 synergize facial deformities via increased cell death.

Liu, Xia / Hayano, Satoru / Pan, Haichun / Inagaki, Maiko / Ninomiya-Tsuji, Jun / Sun, Hongchen / Mishina, Yuji

Genesis (New York, N.Y. : 2000)

2018 Volume 56, Issue 3, Page(s) e23093

Abstract: BMP signaling plays a critical role in craniofacial development. Augmentation of BMPR1A signaling through neural crest-specific expression of constitutively active Bmpr1a (caBmpr1a) results in craniofacial deformities in mice. To investigate whether ... ...

Abstract	BMP signaling plays a critical role in craniofacial development. Augmentation of BMPR1A signaling through neural crest-specific expression of constitutively active Bmpr1a (caBmpr1a) results in craniofacial deformities in mice. To investigate whether deletion of Tak1 may rescue the craniofacial deformities caused by enhanced Smad-dependent signaling through caBMPR1A, we generated embryos to activate transcription of caBmpr1a transgene and ablate Tak1 in neural crest derivatives at the same time. We found that deformities of the double mutant mice showed more severe than those with each single mutation, including median facial cleft and cleft palate. We found higher levels of cell death in the medial nasal and the lateral nasal processes at E10.5 in association with higher levels of p53 in the double mutant embryos. We also found higher levels of pSmad1/5/9 in the lateral nasal processes at E10.5 in the double mutant embryos. Western analyses revealed that double mutant embryos showed similar degrees of upregulation of pSmad1/5/9 with caBmpr1a or Tak1-cKO embryos while the double mutant embryos showed higher levels of phospho-p38 than caBmpr1a or Tak1-cKO embryos at E17.5, but not at E10.5. It suggested that deletion of Tak1 aggravates the craniofacial deformities of the caBmpr1a mutants by increasing p53 and phospho-p38 at different stage of embryogenesis.
MeSH term(s)	Animals ; Apoptosis/genetics ; Biomarkers ; Bone Morphogenetic Protein Receptors, Type I/genetics ; Bone Morphogenetic Protein Receptors, Type I/metabolism ; Cell Death/genetics ; Craniofacial Abnormalities/diagnosis ; Craniofacial Abnormalities/genetics ; Genetic Association Studies ; Genotype ; Gestational Age ; Immunohistochemistry ; MAP Kinase Kinase Kinases/genetics ; MAP Kinase Kinase Kinases/metabolism ; Mice ; Mice, Transgenic ; Mutation ; Phenotype ; Signal Transduction ; Smad Proteins/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Biomarkers ; Smad Proteins ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; MAP kinase kinase kinase 7 (EC 2.7.11.25) ; Bmpr1a protein, mouse (EC 2.7.11.30) ; Bone Morphogenetic Protein Receptors, Type I (EC 2.7.11.30)
Language	English
Publishing date	2018-02-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2004544-X
ISSN	1526-968X ; 1526-954X
ISSN (online)	1526-968X
ISSN	1526-954X
DOI	10.1002/dvg.23093
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2772: 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)

Order via subito

Details ▾

Article ; Online: TAK1 regulates resident macrophages by protecting lysosomal integrity.

Sakamachi, Yosuke / Morioka, Sho / Mihaly, September R / Takaesu, Giichi / Foley, Julie F / Fessler, Michael B / Ninomiya-Tsuji, Jun

Cell death & disease

2017 Volume 8, Issue 2, Page(s) e2598

Abstract: Hematopoietic cell survival and death is critical for development of a functional immune system. Here, we report that a protein kinase, TAK1, is selectively required for resident macrophage integrity during embryogenesis. Hematopoietic lineage-specific ... ...

Abstract	Hematopoietic cell survival and death is critical for development of a functional immune system. Here, we report that a protein kinase, TAK1, is selectively required for resident macrophage integrity during embryogenesis. Hematopoietic lineage-specific deletion of Tak1 gene (Tak1
MeSH term(s)	Animals ; Cell Death/physiology ; Cell Survival/physiology ; Embryonic Development/physiology ; Lung/metabolism ; Lysosomes/metabolism ; MAP Kinase Kinase Kinases/metabolism ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL ; Protective Agents/metabolism ; Receptors, Tumor Necrosis Factor, Type I/metabolism ; Signal Transduction/physiology ; Thymocytes/physiology ; Thymus Gland/metabolism ; Toll-Like Receptors/metabolism
Chemical Substances	Protective Agents ; Receptors, Tumor Necrosis Factor, Type I ; Toll-Like Receptors ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; MAP kinase kinase kinase 7 (EC 2.7.11.25)
Language	English
Publishing date	2017-02-09
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/cddis.2017.23
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito