Evidence map›Paper›PMID 23135355›Full record

ReviewLeukemia2013

Parental imprinting regulates insulin-like growth factor signaling: a Rosetta Stone for understanding the biology of pluripotent stem cells, aging and cancerogenesis.

M Z Ratajczak, D-M Shin, G Schneider, J Ratajczak, M Kucia

Open access · bronzeAbstract readReview
In one paragraph

Review in Leukemia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
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  5. Frontiers in cell and developmental biology · 2024
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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 3 countries.

M Z RatajczakStem Cell Biology Program at the James Graham Brown Cancer Center, University of Louisville, Louisville, KY, USA.
D-M Shin
G Schneider
J Ratajczak
M Kucia
University of Louisville · USPomeranian Medical University · PLUniversity of Ulsan · KR

Funding

Novel mechanisms involving complement cascade in stem cell traffickingR01DK074720 · NIDDK · UNIVERSITY OF LOUISVILLE · PI RATAJCZAK, MARIUSZ Z · 2007 to 2020
$4.1M
BIOACTIVE LIPIDS IN STEM CELL HOMING AND MOBILIZATIONR01HL112788 · NHLBI · UNIVERSITY OF LOUISVILLE · PI RATAJCZAK, MARIUSZ Z · 2013 to 2016
$1.5M
NHLBI NIH HHS R01 HL112788NIDDK NIH HHS 2R01 DK074720NIDDK NIH HHS R01 DK074720
6 · The paper itself

Abstract

In recent years, solid evidence has accumulated that insulin-like growth factor-1 (IGF-1) and 2 (IGF-2) regulate many biological processes in normal and malignant cells. Recently, more light has been shed on the epigenetic mechanisms regulating expression of genes involved in IGF signaling (IFS) and it has become evident that these mechanisms are crucial for initiation of embryogenesis, maintaining the quiescence of pluripotent stem cells deposited in adult tissues (for example, very-small embryonic-like stem cells), the aging process, and the malignant transformation of cells. The expression of several genes involved in IFS is regulated at the epigenetic level by imprinting/methylation within differentially methylated regions (DMRs), which regulate their expression from paternal or maternal chromosomes. The most important role in the regulation of IFS gene expression is played by the Igf-2-H19 locus, which encodes the autocrine/paracrine mitogen IGF-2 and the H19 gene, which gives rise to a non-coding RNA precursor of several microRNAs that negatively affect cell proliferation. Among these, miR-675 has recently been demonstrated to downregulate expression of the IGF-1 receptor. The proper imprinting of DMRs at the Igf-2-H19 locus, with methylation of the paternal chromosome and a lack of methylation on the maternal chromosome, regulates expression of these genes so that Igf-2 is transcribed only from the paternal chromosome and H19 (including miR-675) only from the maternal chromosome. In this review, we will discuss the relevance of (i) proper somatic imprinting, (ii) erasure of imprinting and (iii) loss of imprinting within the DMRs at the Igf-2-H19 locus to the expression of genes involved in IFS, and the consequences of these alternative patterns of imprinting for stem cell biology.

Indexed as

Cell Transformation, NeoplasticGenomic ImprintingSignal TransductionAgingDNA MethylationEpigenesis, GeneticFemaleHumansInsulin-Like Growth Factor IIMalePluripotent Stem CellsRNA, Long NoncodingH19 long non-coding RNAInsulin-Like Growth Factor IIRNA, Long Noncoding

Identifiers

PMID23135355
PMCPMC5538807
OpenAlexW1964583702

What OpenQuestion holds

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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.