Evidence map›Paper›PMID 26270036›Full record

ArticlePloS one2015

Identification of MiR-205 As a MicroRNA That Is Highly Expressed in Medullary Thymic Epithelial Cells.

Imran S Khan, Chong Y Park, Anastasia Mavropoulos, Nikki Shariat, Joshua L Pollack, Andrea J Barczak, David J Erle, Michael T McManus, Mark S Anderson, Lukas T Jeker

Abstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Review
  2. Article
  3. The polysaccharide ofRSC advances · 2018
    Article
  4. A Fine-Tune Role of Mir-125a-5p onAging and disease · 2017
    Article
  5. Review
  6. Article
  7. 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

10 authors.

Imran S KhanUCSF Diabetes Center, University of California San Francisco, San Francisco, California, United States of America.
Chong Y ParkUCSF Diabetes Center, University of California San Francisco, San Francisco, California, United States of America; WM Keck Center for Noncoding RNAs, University of California San Francisco, San Francisco, California, United States of America.
Anastasia MavropoulosUCSF Diabetes Center, University of California San Francisco, San Francisco, California, United States of America; Department of Medicine, University of California San Francisco, San Francisco, California, United States of America.
Nikki ShariatUCSF Diabetes Center, University of California San Francisco, San Francisco, California, United States of America; WM Keck Center for Noncoding RNAs, University of California San Francisco, San Francisco, California, United States of America; Department of Microbiology and Immunology, University of California San Francisco, San Francisco, California, United States of America.
Joshua L PollackDepartment of Medicine, University of California San Francisco, San Francisco, California, United States of America.
Andrea J BarczakDepartment of Medicine, University of California San Francisco, San Francisco, California, United States of America.
David J ErleDepartment of Medicine, University of California San Francisco, San Francisco, California, United States of America.
Michael T McManusUCSF Diabetes Center, University of California San Francisco, San Francisco, California, United States of America; WM Keck Center for Noncoding RNAs, University of California San Francisco, San Francisco, California, United States of America; Department of Microbiology and Immunology, University of California San Francisco, San Francisco, California, United States of America.
Mark S AndersonUCSF Diabetes Center, University of California San Francisco, San Francisco, California, United States of America.
Lukas T JekerUCSF Diabetes Center, University of California San Francisco, San Francisco, California, United States of America; Department of Medicine, University of California San Francisco, San Francisco, California, United States of America; Department of Pathology, University of California San Francisco, San Francisco, California, United States of America.

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007618 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ANDERSON, MARK S · 1985 to 2020
$29.6M
Research BaseP30DK063720 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KRUMMEL, MATTHEW F · 2003 to 2019
$21.8M
Thymic medullary epithelial cell turnover and control of immune toleranceR37AI097457 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Mark S Anderson · 2017 to 2026
$4.0M
Thymic medullary epithelial cell turnover and control of immune toleranceR01AI097457 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ANDERSON, MARK S · 2012 to 2016
$1.9M
The Role of microRNAs in autoimmune diseaseR01AI106923 · NIAID · UNIVERSITY HOSPITAL BASEL · PI JEKER, LUKAS T. · 2014 to 2018
$1.3M
The Role of microRNAs in autoimmune diseaseR56AI106923 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JEKER, LUKAS T. · 2013 to 2013
$369k
NIAID NIH HHS AI097457NIAID NIH HHS R01 AI097457NIAID NIH HHS R01 AI106923NIAID NIH HHS R37 AI097457NIAID NIH HHS R56 AI106923NIAID NIH HHS R56AI106923NIDDK NIH HHS P30 DK063720NIGMS NIH HHS T32 GM007618
6 · The paper itself

Abstract

Thymic epithelial cells (TECs) support T cell development in the thymus. Cortical thymic epithelial cells (cTECs) facilitate positive selection of developing thymocytes whereas medullary thymic epithelial cells (mTECs) facilitate the deletion of self-reactive thymocytes in order to prevent autoimmunity. The mTEC compartment is highly dynamic with continuous maturation and turnover, but the genetic regulation of these processes remains poorly understood. MicroRNAs (miRNAs) are important regulators of TEC genetic programs since miRNA-deficient TECs are severely defective. However, the individual miRNAs important for TEC maintenance and function and their mechanisms of action remain unknown. Here, we demonstrate that miR-205 is highly and preferentially expressed in mTECs during both thymic ontogeny and in the postnatal thymus. This distinct expression is suggestive of functional importance for TEC biology. Genetic ablation of miR-205 in TECs, however, neither revealed a role for miR-205 in TEC function during homeostatic conditions nor during recovery from thymic stress conditions. Thus, despite its distinct expression, miR-205 on its own is largely dispensable for mTEC biology.

Indexed as

AnimalsEpithelial CellsGene Expression RegulationMiceMice, TransgenicMicroRNAsThymocytesThymus GlandMicroRNAsMIRN205 microRNA, mouse

Identifiers

PMID26270036
PMCPMC4535774

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.