Evidence map›Paper›PMID 27077812›Full record

ArticleCell death & disease2016

TAK1 regulates Paneth cell integrity partly through blocking necroptosis.

A N Simmons, R Kajino-Sakamoto, J Ninomiya-Tsuji

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Intercalated cell function, kidney innate immunity, and urinary tract infections.Pflugers Archiv : European journal of physiology · 2024
    Review
  4. Review
  5. Article
  6. Article
  7. TAK1 inhibition elicits mitochondrial ROS to block intracellular bacterial colonization.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  8. Cell death in the gut epithelium and implications for chronic inflammation.Nature reviews. Gastroenterology & hepatology · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Activation of TGF-Physiological reports · 2017
    Article
  14. 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

3 authors at 1 institution in 1 country.

A N SimmonsDepartment of Biological Sciences, North Carolina State University, Raleigh, NC 27695-7633, USA.
R Kajino-SakamotoDepartment of Biological Sciences, North Carolina State University, Raleigh, NC 27695-7633, USA.
J Ninomiya-TsujiDepartment of Biological Sciences, North Carolina State University, Raleigh, NC 27695-7633, USA.
North Carolina State University · US

Funding

TAK1 signaling network in tissue homeostasisR01GM068812 · NIGMS · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI NINOMIYA-TSUJI, JUN · 2004 to 2013
$2.4M
TAK1 regulation of metabolismR01GM112986 · NIGMS · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI NINOMIYA-TSUJI, JUN · 2015 to 2018
$1.4M
NIGMS NIH HHS GM068812NIGMS NIH HHS GM112986NIGMS NIH HHS R01 GM068812NIGMS NIH HHS R01 GM112986
6 · The paper itself

Abstract

Paneth cells reside at the base of crypts of the small intestine and secrete antimicrobial factors to control gut microbiota. Paneth cell loss is observed in the chronically inflamed intestine, which is often associated with increased reactive oxygen species (ROS). However, the relationship between Paneth cell loss and ROS is not yet clear. Intestinal epithelial-specific deletion of a protein kinase Tak1 depletes Paneth cells and highly upregulates ROS in the mouse model. We found that depletion of gut bacteria or myeloid differentiation factor 88 (Myd88), a mediator of bacteria-derived cell signaling, reduced ROS but did not block Paneth cell loss, suggesting that gut bacteria are the cause of ROS accumulation but bacteria-induced ROS are not the cause of Paneth cell loss. In contrast, deletion of the necroptotic cell death signaling intermediate, receptor-interacting protein kinase 3 (Ripk3), partially blocked Paneth cell loss. Thus, Tak1 deletion causes Paneth cell loss in part through necroptotic cell death. These results suggest that TAK1 participates in intestinal integrity through separately modulating bacteria-derived ROS and RIPK3-dependent Paneth cell loss.

Indexed as

ApoptosisAnimalsAnti-Bacterial AgentsBacteriaDNA, BacterialIntestinal MucosaIntestinesMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMiceMice, Inbred C57BLMice, KnockoutMyeloid Differentiation Factor 88NecrosisPaneth CellsReactive Oxygen SpeciesAnti-Bacterial AgentsDNA, BacterialMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMyd88 protein, mouseMyeloid Differentiation Factor 88Reactive Oxygen SpeciesReceptor-Interacting Protein Serine-Threonine KinasesRipk3 protein, mouseRNA, MessengerToll-Like Receptors

Identifiers

PMID27077812
PMCPMC4855677
OpenAlexW2341401866

What OpenQuestion holds

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LicenceCC BY
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.