Evidence map›Paper›PMID 35663262›Full record

ArticleCurrent pharmacology reports2016

Bioinformatic and Genomic Analyses of Cellular Reprogramming and Direct Lineage Conversion.

Michael S Kareta

Open access · bronzeAbstract read
In one paragraph

Article in Current pharmacology reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 99% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

1 author at 1 institution in 1 country.

Michael S KaretaDepartment of Pediatrics, Stanford University, Stanford, CA 94305, USA.
California Institute for Regenerative Medicine · US

Funding

Oncogenic mechanism of Sox2 in Rb-deficient tumorsR01CA233661 · NCI · SANFORD RESEARCH/USD · PI KARETA, MICHAEL S. · 2019 to 2023
$1.9M
NCI NIH HHS R01 CA233661
6 · The paper itself

Abstract

Cellular reprogramming, whereby cell fate can be changed by the expression of a few defined factors, is a remarkable process that harnesses the innate ability of a cell's own genome to rework its expressional networks and function. Since cell lineages are defined by global regulation of gene expression, transcriptional regulators, and coupled to the epigenetic markings of the chromatin, changing the cell fate necessitates broad changes to these central cellular features. To properly characterize these changes, and the mechanisms that drive them, computational and genomic approaches are perfectly suited to provide a holistic picture of the reprogramming mechanisms. In particular, the use of bioinformatic analysis has been a major driver in the study of cellular reprogramming, both as it relates to induced pluripotency or direct lineage conversion. This review will summarize many of the bioinformatic studies that have advanced our knowledge of reprogramming and address future directions for these investigations.

Indexed as

bioinformaticsdirect lineage conversiongenomicsinduced pluripotencyReprogramming

Identifiers

PMID35663262
PMCPMC9165525
OpenAlexW2289425880

What OpenQuestion holds

Textmetadata
LicenceTDM
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.