Evidence map›Paper›PMID 26070564›Full record

ArticleThe Journal of biological chemistry2015

Lipopolysaccharides Promote S-Nitrosylation and Proteasomal Degradation of Liver Kinase B1 (LKB1) in Macrophages in Vivo.

Zhaoyu Liu, Xiaoyan Dai, Huaiping Zhu, Miao Zhang, Ming-Hui Zou

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. LKB1 biology: assessing the therapeutic relevancy of LKB1 inhibitors.Cell communication and signaling : CCS · 2024
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. A novel role for myeloid cell-specific neuropilin 1 in mitigating sepsis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  15. [Role of interleukin-17 in alveolar fluid clearance in mice with acute lung injury].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2016
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Zhaoyu LiuFrom the Section of Molecular Medicine, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104.
Xiaoyan DaiFrom the Section of Molecular Medicine, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104.
Huaiping ZhuFrom the Section of Molecular Medicine, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104.
Miao ZhangFrom the Section of Molecular Medicine, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104.
Ming-Hui ZouFrom the Section of Molecular Medicine, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104 ming-hui-zou@ouhsc.edu.
University of Oklahoma Health Sciences Center · US

Funding

Reactive Nitrogen species and Diabetic Endothelial DysfunctionR01HL079584 · NHLBI · UNIVERSITY OF TENNESSEE KNOXVILLE · PI ZOU, MING-HUI · 2004 to 2021
$7.3M
Inflammasome and unstable atherosclerotic plaquesR01HL089920 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2008 to 2022
$6.9M
AMP-Activated Protein Kinase in DiabetesR01HL080499 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2006 to 2019
$5.8M
Controlling VSMC Proliferation and MigrationR01HL110488 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2011 to 2020
$3.9M
Oxidant stress and diabetic endothelial dysfunctionR01HL074399 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2005 to 2013
$3.2M
Suppression of Autophagy-Dependent Clearance Mitochondria in Type 2 DiabetesR01HL128014 · NHLBI · GEORGIA STATE UNIVERSITY · PI XIE, ZHONGLIN, ZOU, MING-HUI · 2015 to 2018
$2.4M
Prevention of High Fat Diet-Induced Vascular InjuryR01HL105157 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2010 to 2014
$1.8M
Angiotensin-II, GTPCH1 and 26S ProtesomesR01HL096032 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2009 to 2013
$1.8M
Sirt1, Vascular Aging, and Aortic AneurysmR01AG047776 · NIA · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2014 to 2018
$1.5M
NHLBI NIH HHS HL074399NHLBI NIH HHS HL079584NHLBI NIH HHS HL080499NHLBI NIH HHS HL089920NHLBI NIH HHS HL096032NHLBI NIH HHS HL105157NHLBI NIH HHS HL110488NHLBI NIH HHS HL128014NHLBI NIH HHS R01 HL074399NHLBI NIH HHS R01 HL079584NHLBI NIH HHS R01 HL080499NHLBI NIH HHS R01 HL089920NHLBI NIH HHS R01 HL096032NHLBI NIH HHS R01 HL105157NHLBI NIH HHS R01 HL110488NHLBI NIH HHS R01 HL128014NIA NIH HHS AG047776NIA NIH HHS R01 AG047776
6 · The paper itself

Abstract

LKB1 (liver kinase B1) plays important roles in tumor suppression, energy metabolism, and, recently, in innate immune responses. However, how LKB1 is regulated under physiological or pathological conditions is still unclear. Here, we report that LKB1 protein (but not mRNA) was decreased in both LPS-treated RAW 264.7 cells and peritoneal macrophages isolated from LPS-challenged mice. Additional LPS treatment promoted protein ubiquitination and degradation of LKB1. Pharmacological inhibition or gene silencing of inducible NOS abrogated LPS-induced LKB1 degradation, whereas exposure of RAW 264.7 cells to S-nitroso-l-glutathione, a NO donor, triggered LKB1 S-nitrosylation. Consistently, mutation of one cysteine (C430S) in LKB1 prevented LPS-induced S-nitrosylation, ubiquitination, and degradation. Moreover, S-nitrosylation and ubiquitination of LKB1 were confirmed in macrophages from LPS-challenged mice in vivo. Co-administration of the inducible NOS inhibitor S-methylisothiourea or the proteasome inhibitor MG132 prevented LPS-induced LKB1 degradation and improved the survival rate. Finally, mice lacking LKB1 in macrophages had significantly lower survival rates in response to LPS challenge compared with wild-type mice. Thus, we concluded that LKB1 is degraded by LPS treatment via S-nitrosylation-dependent proteasome pathways, and this had a protective role in LPS-induced septic shock.

Indexed as

UbiquitinationAMP-Activated Protein KinasesAnimalsCell LineCysteineLipopolysaccharidesMacrophagesMice, KnockoutNitric OxideProteasome Endopeptidase ComplexProtein Serine-Threonine KinasesProteolysisS-NitrosothiolsAMP-Activated Protein KinasesCysteineLipopolysaccharidesNitric OxideProteasome Endopeptidase ComplexProtein Serine-Threonine KinasesS-nitrosocysteineS-NitrosothiolsStk11 protein, mouseliver kinase B1 (LKB1)macrophagenitric oxideproteasomeshockS-nitrosylation

Identifiers

PMID26070564
PMCPMC4521026
OpenAlexW2035381219

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.