Evidence map›Paper›PMID 27402838›Full record

ArticleThe Journal of biological chemistry2016

Integrator of Stress Responses Calmodulin Binding Transcription Activator 1 (Camta1) Regulates miR-212/miR-132 Expression and Insulin Secretion.

Inês Guerra Mollet, Helena Anna Malm, Anna Wendt, Marju Orho-Melander, Lena Eliasson

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

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  20. Simulated Cholinergic Reinnervation ofInternational journal of endocrinology · 2018
    Article
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 1 institution in 1 country.

Inês Guerra MolletFrom the Department of Clinical Sciences, Clinical Research Centre, Lund University, Jan Waldenströms Gata 35, SE-20502 Malmö, Sweden inesmollet@gmail.com.ORCID 0000-0002-1422-1336
Helena Anna MalmFrom the Department of Clinical Sciences, Clinical Research Centre, Lund University, Jan Waldenströms Gata 35, SE-20502 Malmö, Sweden.
Anna WendtFrom the Department of Clinical Sciences, Clinical Research Centre, Lund University, Jan Waldenströms Gata 35, SE-20502 Malmö, Sweden.ORCID 0000-0001-8807-5979
Marju Orho-MelanderFrom the Department of Clinical Sciences, Clinical Research Centre, Lund University, Jan Waldenströms Gata 35, SE-20502 Malmö, Sweden.ORCID 0000-0002-3578-2503
Lena EliassonFrom the Department of Clinical Sciences, Clinical Research Centre, Lund University, Jan Waldenströms Gata 35, SE-20502 Malmö, Sweden.ORCID 0000-0002-6467-5029
Lund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Altered microRNA profiles have been demonstrated in experimental models of type 2 diabetes, including in islets of the diabetic Goto-Kakizaki (GK) rat. Our bioinformatic analysis of conserved sequences in promoters of microRNAs, previously observed to be up-regulated in GK rat islets, revealed putative CGCG-core motifs on the promoter of the miR-212/miR-132 cluster, overexpression of which has been shown to increase insulin secretion. These motifs are possible targets of calmodulin binding transcription activators Camta1 and Camta2 that have been recognized as integrators of stress responses. We also identified putative NKE elements, possible targets of NK2 homeobox proteins like the essential islet transcription factor Nkx2-2. As Camtas can function as co-activators with NK2 proteins in other tissues, we explored the role of Camta1, Camta2, and Nkx2-2 in the regulation of the miR-212/miR-132 cluster and insulin secretion. We demonstrate that exposure of control Wistar or GK rat islets to 16.7 mm glucose increases miR-212/miR-132 expression but significantly less so in the GK rat. In addition, Camta1, Camta2, and Nkx2-2 were down-regulated in GK rat islets, and knockdown of Camta1 reduced miR-212/miR-132 promoter activity and miR-212/miR-132 expression, even under cAMP elevation. Knockdown of Camta1 decreased insulin secretion in INS-1 832/13 cells and Wistar rat islets but increased insulin content. Furthermore, knockdown of Camta1 reduced K(+)-induced insulin secretion and voltage-dependent Ca(2+) currents. We also demonstrate Camta1 and Nkx2-2 protein interaction. These results indicate that Camta1 is required not only for expression of the miR-212/miR-132 cluster but at multiple levels for regulating beta cell insulin content and secretion.

Indexed as

Calcium SignalingGene Expression RegulationAnimalsCalcium-Binding ProteinsHomeobox Protein Nkx-2.2Homeodomain ProteinsInsulinInsulin-Secreting CellsMaleMiceMicroRNAsNuclear ProteinsRatsRats, WistarTrans-ActivatorsTranscription FactorsCalcium-Binding ProteinsCAMTA1 protein, humanCAMTA1 protein, mouseHomeobox Protein Nkx-2.2Homeodomain ProteinsInsulinMicroRNAsMIRN132 microRNA, humanMIRN132 microRNA, mouseMIRN132 microRNA, ratMIRN212 microRNA, humanMIRN212 microRNA, mouseMIRN212 microRNA, ratnkx2.2b protein, zebrafishNKX2-2 protein, humanNkx2-2 protein, mouseNkx2-2 protein, ratNuclear ProteinsTrans-ActivatorsTranscription FactorsZebrafish Proteinsbeta cell (B-cell)calmodulin binding transcription activator 1 (Camta1)cyclic AMP (cAMP)insulin secretionmicroRNA (miRNA)NK2 homeobox 2 (Nkx2-2)pancreatic islettranscription coactivatortranscription promotertype 2 diabetes

Identifiers

PMID27402838
PMCPMC5000089
OpenAlexW2471849573

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.