Evidence map›Paper›PMID 26269592›Full record

ArticleThe Journal of biological chemistry2015

Signal Transduction and Intracellular Trafficking by the Interleukin 36 Receptor.

Siddhartha S Saha, Divyendu Singh, Ernest L Raymond, Rajkumar Ganesan, Gary Caviness, Christine Grimaldi, Joseph R Woska, Detlev Mennerich, Su-Ellen Brown, M Lamine Mbow and 1 more

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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 29 citations in OpenAlex.

  1. Generalized Pustular Psoriasis and Systemic Organ Dysfunctions.International journal of molecular sciences · 2024
    Review
  2. Article
  3. Review
  4. Interleukin-36: Structure, Signaling and Function.Advances in experimental medicine and biology · 2021
    Review
  5. The Significance of IL-36 Hyperactivation and IL-36R Targeting in Psoriasis.International journal of molecular sciences · 2019
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. 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

11 authors at 2 institutions in 1 country.

Siddhartha S SahaFrom the Department of Molecular and Cellular Biochemistry, Indiana University, Bloomington, Indiana 47401 and.
Divyendu SinghFrom the Department of Molecular and Cellular Biochemistry, Indiana University, Bloomington, Indiana 47401 and.
Ernest L RaymondBoehringer Ingelheim Pharmaceuticals, Ridgefield, Connecticut 06877.
Rajkumar GanesanBoehringer Ingelheim Pharmaceuticals, Ridgefield, Connecticut 06877.
Gary CavinessBoehringer Ingelheim Pharmaceuticals, Ridgefield, Connecticut 06877.
Christine GrimaldiBoehringer Ingelheim Pharmaceuticals, Ridgefield, Connecticut 06877.
Joseph R WoskaBoehringer Ingelheim Pharmaceuticals, Ridgefield, Connecticut 06877.
Detlev MennerichBoehringer Ingelheim Pharmaceuticals, Ridgefield, Connecticut 06877.
Su-Ellen BrownBoehringer Ingelheim Pharmaceuticals, Ridgefield, Connecticut 06877.
M Lamine MbowBoehringer Ingelheim Pharmaceuticals, Ridgefield, Connecticut 06877 lamine.mbow@boehringer-ingelheim.com.
C Cheng KaoFrom the Department of Molecular and Cellular Biochemistry, Indiana University, Bloomington, Indiana 47401 and ckao@indiana.edu.
Boehringer Ingelheim (United States) · USIndiana University Bloomington · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Improper signaling of the IL-36 receptor (IL-36R), a member of the IL-1 receptor family, has been associated with various inflammation-associated diseases. However, the requirements for IL-36R signal transduction remain poorly characterized. This work seeks to define the requirements for IL-36R signaling and intracellular trafficking. In the absence of cognate agonists, IL-36R was endocytosed and recycled to the plasma membrane. In the presence of IL-36, IL-36R increased accumulation in LAMP1+ lysosomes. Endocytosis predominantly used a clathrin-mediated pathway, and the accumulation of the IL-36R in lysosomes did not result in increased receptor turnover. The ubiquitin-binding Tollip protein contributed to IL-36R signaling and increased the accumulation of both subunits of the IL-36R.

Indexed as

Cell LineEndocytosisHumansInterleukin-1Intracellular Signaling Peptides and ProteinsLysosomesProtein TransportReceptors, InterleukinSignal TransductionInterleukin-1interleukin 36, humaninterleukin-36 receptor, humanIntracellular Signaling Peptides and ProteinsReceptors, InterleukinTOLLIP protein, humanendocytosisIL-1immunologyinterleukin 36 receptorsignal transductionTolliptrafficking

Identifiers

PMID26269592
PMCPMC4583048
OpenAlexW2434498632

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.