Evidence map›Paper›PMID 35401699›Full record

ArticleFrontiers in genetics2022

DOT1L Mediated Gene Repression in Extensively Self-Renewing Erythroblasts.

Shaon Borosha, Anamika Ratri, Subhra Ghosh, Carrie A Malcom, V Praveen Chakravarthi, Jay L Vivian, Timothy A Fields, M A Karim Rumi, Patrick E Fields

Open access · goldAbstract read
In one paragraph

Article in Frontiers in genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Connecting the DOTs on Cell Identity.Frontiers in cell and developmental biology · 2022
    Review
  11. The Role of DOT1L in Normal and Malignant Hematopoiesis.Frontiers in cell and developmental biology · 2022
    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

9 authors at 1 institution in 1 country.

Shaon BoroshaDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, United States.
Anamika RatriDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, United States.
Subhra GhoshDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, United States.
Carrie A MalcomDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, United States.
V Praveen ChakravarthiDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, United States.
Jay L VivianDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, United States.
Timothy A FieldsDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, United States.
M A Karim RumiDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, United States.
Patrick E FieldsDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, United States.
University of Kansas Medical Center · US

Funding

The Role of the Histone Methyltransferase DOT1L in ErythropoiesisR01DK091277 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI FIELDS, PATRICK E · 2012 to 2016
$1.6M
High Throughput Sequencing System for KUMC Genomics CoreS10OD021743 · OD · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SMITH, PETER G · 2017 to 2017
$493k
NIDDK NIH HHS R01 DK091277
6 · The paper itself

Abstract

DOT1L is essential for embryonic hematopoiesis but the precise mechanisms of its action remain unclear. The only recognized function of DOT1L is histone H3 lysine 79 (H3K79) methylation, which has been implicated in both transcriptional activation and repression. We observed that deletion of the mouse

Indexed as

DOT1L methyltransferaseDot1l methyltransferase mutant mouseerythroid-myeloid differentiationerythroid-myeloid progenitorsmutant mouse models

Identifiers

PMID35401699
PMCPMC8984088
OpenAlexW4220652433

What OpenQuestion holds

Textmetadata
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.