Evidence map›Paper›PMID 31246957›Full record

ArticlePLoS genetics2019

Loss of ASAP1 in mice impairs adipogenic and osteogenic differentiation of mesenchymal progenitor cells through dysregulation of FAK/Src and AKT signaling.

Caroline Schreiber, Supriya Saraswati, Shannon Harkins, Annette Gruber, Natascha Cremers, Wilko Thiele, Melanie Rothley, Diana Plaumann, Claudia Korn, Olivier Armant and 2 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2019. 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
1.5field-weighted citation impact, top 18% 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, 48 citations in OpenAlex.

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  9. Role of the GRP78-c-Src signaling pathway on osteoblast differentiation of periodontal ligament fibroblasts induced by cyclic mechanical stretch.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 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

12 authors at 2 institutions in 1 country.

Caroline SchreiberEuropean Center for Angioscience (ECAS), Medical Faculty of Mannheim, University of Heidelberg, Mannheim, Germany.ORCID 0000-0001-7919-4597
Supriya SaraswatiEuropean Center for Angioscience (ECAS), Medical Faculty of Mannheim, University of Heidelberg, Mannheim, Germany.
Shannon HarkinsEuropean Center for Angioscience (ECAS), Medical Faculty of Mannheim, University of Heidelberg, Mannheim, Germany.ORCID 0000-0002-7272-9197
Annette GruberEuropean Center for Angioscience (ECAS), Medical Faculty of Mannheim, University of Heidelberg, Mannheim, Germany.
Natascha CremersEuropean Center for Angioscience (ECAS), Medical Faculty of Mannheim, University of Heidelberg, Mannheim, Germany.
Wilko ThieleEuropean Center for Angioscience (ECAS), Medical Faculty of Mannheim, University of Heidelberg, Mannheim, Germany.ORCID 0000-0002-8978-4192
Melanie RothleyEuropean Center for Angioscience (ECAS), Medical Faculty of Mannheim, University of Heidelberg, Mannheim, Germany.
Diana PlaumannEuropean Center for Angioscience (ECAS), Medical Faculty of Mannheim, University of Heidelberg, Mannheim, Germany.
Claudia KornGerman Cancer Research Center (DKFZ-ZMBH-Alliance), Heidelberg, Germany.
Olivier ArmantInstitute for Toxicology and Genetics, KIT Campus Nord, Karlsruhe, Germany.
Hellmut G AugustinEuropean Center for Angioscience (ECAS), Medical Faculty of Mannheim, University of Heidelberg, Mannheim, Germany.
Jonathan P SleemanEuropean Center for Angioscience (ECAS), Medical Faculty of Mannheim, University of Heidelberg, Mannheim, Germany.
Heidelberg University · DEGerman Cancer Research Center · DE

Funding

Worldwide Cancer Research 08-0015
6 · The paper itself

Abstract

ASAP1 is a multi-domain adaptor protein that regulates cytoskeletal dynamics, receptor recycling and intracellular vesicle trafficking. Its expression is associated with poor prognosis for a variety of cancers, and promotes cell migration, invasion and metastasis. Little is known about its physiological role. In this study, we used mice with a gene-trap inactivated ASAP1 locus to study the functional role of ASAP1 in vivo, and found defects in tissues derived from mesenchymal progenitor cells. Loss of ASAP1 led to growth retardation and delayed ossification typified by enlarged hypertrophic zones in growth plates and disorganized chondro-osseous junctions. Furthermore, loss of ASAP1 led to delayed adipocyte development and reduced fat depot formation. Consistently, deletion of ASAP1 resulted in accelerated chondrogenic differentiation of mesenchymal cells in vitro, but suppressed osteo- and adipogenic differentiation. Mechanistically, we found that FAK/Src and PI3K/AKT signaling is compromised in Asap1GT/GT MEFs, leading to impaired adipogenic differentiation. Dysregulated FAK/Src and PI3K/AKT signaling is also associated with attenuated osteogenic differentiation. Together these observations suggest that ASAP1 plays a decisive role during the differentiation of mesenchymal progenitor cells.

Indexed as

Adaptor Proteins, Signal TransducingAdipogenesisAnimalsCell DifferentiationChondrogenesisFocal Adhesion Kinase 1Gene Expression Regulation, DevelopmentalGrowth PlateHumansMesenchymal Stem CellsMiceOncogene Protein v-aktOsteogenesisPhosphatidylinositol 3-Kinasessrc-Family KinasesAdaptor Proteins, Signal TransducingAsap1 protein, mouseFocal Adhesion Kinase 1Oncogene Protein v-aktPhosphatidylinositol 3-KinasesPtk2 protein, mousesrc-Family Kinases

Identifiers

PMID31246957
PMCPMC6619832
OpenAlexW2954856809

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.