Evidence map›Paper›PMID 18515495›Full record

ArticleThe Journal of endocrinology2008

MafA is a dedicated activator of the insulin gene in vivo.

Isabella Artner, Yan Hang, Min Guo, Guoqiang Gu, Roland Stein

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of endocrinology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.6field-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

29 citing papers in PubMed, 50 citations in OpenAlex.

  1. CaBiomedicines · 2023
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  20. MafA and MafB activity in pancreatic β cells.Trends in endocrinology and metabolism: TEM · 2011
    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 2 institutions in 2 countries.

Isabella ArtnerDepartments of, Molecular Physiology and Biophysics Cell and Developmental Biology, Vanderbilt University Medical Center, Nashville, Tennessee 37205, USA. isabella.artner@med.lu.se
Yan Hang
Min Guo
Guoqiang Gu
Roland Stein
Vanderbilt University Medical Center · USInstitute of Molecular Biology and Biophysics · RU

Funding

Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI ALVIN C POWERS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI POWERS, ALVIN C · 1986 to 2011
$28.1M
The Mechanisms of Islet Cell Specification and DifferentiationR01DK065949 · NIDDK · VANDERBILT UNIVERSITY · PI GU, GUOQIANG · 2004 to 2017
$4.4M
TRANSGENIC MICE COREP01DK042502 · NIDDK · VANDERBILT UNIVERSITY · PI STEIN, ROLAND W · 1990 to 2000
$994k
NIDDK NIH HHS 1R01 DK065949-01A1NIDDK NIH HHS P01 DK042502NIDDK NIH HHS P01 DK42502NIDDK NIH HHS P30 DK020593NIDDK NIH HHS P60 DK020593NIDDK NIH HHS R01 DK065949
6 · The paper itself

Abstract

As successful generation of insulin-producing cells could be used for diabetes treatment, a concerted effort is being made to understand the molecular programs underlying islet beta-cell formation and function. The closely related MafA and MafB transcription factors are both key mammalian beta-cell regulators. MafA and MafB are co-expressed in insulin+beta-cells during embryogenesis, while in the adult pancreas only MafA is produced in beta-cells and MafB in glucagon+alpha-cells. MafB-/- animals are also deficient in insulin+ and glucagon+ cell production during embryogenesis. However, only MafA over-expression selectively induced endogenous Insulin mRNA production in cell line-based assays, while MafB specifically promoted Glucagon expression. Here, we analyzed whether these factors were sufficient to induce insulin+ and/or glucagon+ cell formation within embryonic endoderm using the chick in ovo electroporation assay. Ectopic expression of MafA, but not MafB, promoted Insulin production; however, neither MafA nor MafB were capable of inducing Glucagon. Co-electroporation of MafA with the Ngn3 transcription factor resulted in the development of more organized cell clusters containing both insulin- and glucagon-producing cells. Analysis of chimeric proteins of MafA and MafB demonstrated that chick Insulin activation depended on sequences within the MafA C-terminal DNA-binding domain. MafA was also bound to Insulin and Glucagon transcriptional control sequences in mouse embryonic pancreas and beta-cell lines. Collectively, these results demonstrate a unique ability for MafA to independently activate Insulin transcription.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsChick EmbryoDNAElectroporationEndodermGlucagonHeLa CellsHumansImmunohistochemistryInsulinIslets of LangerhansMafB Transcription FactorMaf Transcription FactorsMiceNerve Tissue ProteinsBasic Helix-Loop-Helix ProteinsDNAGlucagonInsulinMafB Transcription FactorMaf Transcription FactorsNerve Tissue ProteinsNeurog3 protein, mouse

Identifiers

PMID18515495
PMCPMC3787904
OpenAlexW2012154903

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.