Evidence map›Paper›PMID 28765528›Full record

ArticleScientific reports2017

Pdx1-Cre-driven conditional gene depletion suggests PAK4 as dispensable for mouse pancreas development.

Miao Zhao, Parisa Rabieifar, Tânia D F Costa, Ting Zhuang, Audrey Minden, Matthias Löhr, Rainer Heuchel, Staffan Strömblad

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
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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

8 authors at 3 institutions in 2 countries.

Miao ZhaoDepartment of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-4895-1177
Parisa RabieifarDepartment of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden.
Tânia D F CostaDepartment of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden.
Ting ZhuangDepartment of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden.
Audrey MindenSusan Lehman Cullman Laboratory for Cancer Research, Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey, USA.
Matthias LöhrDivision of Surgery, CLINTEC, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-7647-198X
Rainer HeuchelDivision of Surgery, CLINTEC, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-2782-585X
Staffan StrömbladDepartment of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden. Staffan.Stromblad@ki.se.
Karolinska Institutet · SEKarolinska University Hospital · SERutgers, The State University of New Jersey · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Constitutive depletion of p21-activated kinase 4 (PAK4) in the mouse causes embryonic lethality associated with heart and brain defects. Given that conventional gene depletion of PAK1 or PAK3 caused functional deficits in the mouse pancreas, while gene depletion of PAK5 or PAK6 did not, we asked if PAK4 might have a functional role in pancreas development. We therefore introduced conditional, Pdx1-Cre-mediated, pancreatic PAK4 gene depletion in the mouse, verified by loss of PAK4 protein expression in the pancreas. PAK4 knock-out (KO) mice were born at Mendelian ratios in both genders. Further, morphological and immunohistochemical examinations and quantifications indicated that exocrine, endocrine and ductal compartments retained the normal proportions and distributions upon PAK4 gene depletion. In addition, body weight records and a glucose tolerance test revealed no differences between WT and PAK4 KO mice. Together, this suggests that PAK4 is dispensable for mouse pancreas development. This will facilitate future use of our Pdx1-Cre-driven conditional PAK4 KO mouse model for testing in vivo potential functions of PAK4 in pancreatic disease models such as for pancreatitis and different pancreatic cancer forms.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsGene Knockout TechniquesHomeodomain ProteinsIntegrasesMicep21-Activated KinasesPancreasTrans-ActivatorsCre recombinaseHomeodomain ProteinsIntegrasesp21-Activated KinasesPak4 protein, mousepancreatic and duodenal homeobox 1 proteinTrans-Activators

Identifiers

PMID28765528
PMCPMC5539201
OpenAlexW2737428896

What OpenQuestion holds

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Registered trials

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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.