Evidence map›Paper›PMID 22290424›Full record

ArticleCell research2012

Modulation of microRNA processing by mismatch repair protein MutLα.

Guogen Mao, Sanghee Lee, Janice Ortega, Liya Gu, Guo-Min Li

Open access · bronzeAbstract read
In one paragraph

Article in Cell research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.0field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. MiR-6511b-5p suppresses metastasis of pMMR colorectal cancer through methylation of CD44 by directly targeting BRG1.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Article
  5. The Effect of Tobacco SmokeCurrent oncology (Toronto, Ont.) · 2022
    Article
  6. Article
  7. Article
  8. Role of mismatch repair in aging.International journal of biological sciences · 2021
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. A NovelBioMed research international · 2018
    Article
  15. Novel Implications in Molecular Diagnosis of Lynch Syndrome.Gastroenterology research and practice · 2017
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Small molecules targeting c-Myc oncogene: promising anti-cancer therapeutics.International journal of biological sciences · 2014
    Review
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 3 institutions in 1 country.

Guogen MaoGraduate Center for Toxicology, University of Kentucky College of Medicine, Lexington, KY 40536, USA.
Sanghee Lee
Janice Ortega
Liya Gu
Guo-Min Li
University of Kentucky · USMarkey Cancer Center · USThe Graduate Center, CUNY · US

Funding

DNA Mismatch Repair Deficiency and Leukemia RelapseR01CA104333 · NCI · UNIVERSITY OF KENTUCKY · PI GU, LIYA · 2005 to 2010
$1.3M
Mechanism of PCNA-dependent 5'->3' Mismatch ExcisionR01CA115942 · NCI · UNIVERSITY OF KENTUCKY · PI LI, GUO-MIN · 2006 to 2010
$1.2M
Dissection and Reconstitution of Human Mismatch RepairR01GM072756 · NIGMS · UNIVERSITY OF KENTUCKY · PI LI, GUO-MIN · 2006 to 2009
$1.0M
NCI NIH HHS CA104333NCI NIH HHS CA115942NCI NIH HHS R01 CA104333NCI NIH HHS R01 CA115942NIGMS NIH HHS GM072756NIGMS NIH HHS R01 GM072756
6 · The paper itself

Abstract

MicroRNAs (miRNAs) are critical post-transcriptional regulators and are derived from hairpin-shaped primary transcripts via a series of processing steps. However, how the production of individual miRNAs is regulated remains largely unknown. Similarly, loss or overexpression of the key mismatch repair protein MutLα (MLH1-PMS2 heterodimer) leads to genome instability and tumorigenesis, but the mechanisms controlling MutLα expression are unknown. Here we demonstrate in vitro and in vivo that MLH1 and miR-422a participate in a feedback loop that regulates the level of both molecules. Using a defined in-vitro miRNA processing system, we show that MutLα stimulates the conversion of pri-miR-422a to pre-miR-422a, as well as the processing of other miRNAs tested, implicating MutLα as a general stimulating factor for miRNA biogenesis. This newly identified MutLα function requires its ATPase and pri-miRNA binding activities. In contrast, miR-422a downregulates MutLα levels by suppressing MLH1 expression through base pairing with the MLH1 3'-untranslated region. A model depicting this feedback mechanism is discussed.

Indexed as

DNA Mismatch Repair3' Untranslated RegionsAdaptor Proteins, Signal TransducingAdenosine TriphosphatasesDimerizationDNA-Binding ProteinsDNA Repair EnzymesHCT116 CellsHEK293 CellsHeLa CellsHumansMicroRNAsMismatch Repair Endonuclease PMS2MutL Protein Homolog 1MutL ProteinsNuclear Proteins3' Untranslated RegionsAdaptor Proteins, Signal TransducingAdenosine TriphosphatasesDNA-Binding ProteinsDNA Repair EnzymesMicroRNAsMIRN422 microRNA, humanMismatch Repair Endonuclease PMS2MLH1 protein, humanMutLalpha protein, humanMutL Protein Homolog 1MutL ProteinsNuclear ProteinsPMS2 protein, humanRNA, Small Interfering

Identifiers

PMID22290424
PMCPMC3367530
OpenAlexW1975152594

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.