Evidence map›Paper›PMID 28348210›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Myosin-1E interacts with FAK proline-rich region 1 to induce fibronectin-type matrix.

Joel B Heim, Edwin J Squirewell, Ancilla Neu, Georg Zocher, Sindhuja Sominidi-Damodaran, Saranya P Wyles, Ekaterina Nikolova, Nille Behrendt, Ditte M Saunte, Jorgen Lock-Andersen and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

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  13. Long-Tailed Unconventional Class I Myosins in Health and Disease.International journal of molecular sciences · 2020
    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

21 authors at 8 institutions in 3 countries.

Joel B HeimDepartment of Dermatology, Mayo Clinic, Rochester, MN 55905.
Edwin J SquirewellDepartment of Dermatology, Mayo Clinic, Rochester, MN 55905.
Ancilla NeuMax Planck Institute for Developmental Biology, 72076 Tuebingen, Germany.
Georg ZocherInterfaculty Institute of Biochemistry, University of Tuebingen, 72076 Tuebingen, Germany.
Sindhuja Sominidi-DamodaranDepartment of Dermatology, Mayo Clinic, Rochester, MN 55905.
Saranya P WylesDepartment of Dermatology, Mayo Clinic, Rochester, MN 55905.
Ekaterina NikolovaDepartment of Dermatology, Mayo Clinic, Rochester, MN 55905.
Nille BehrendtDepartment of Pathology, University of Copenhagen, Roskilde Hospital, DK-4000 Roskilde, Denmark.
Ditte M SaunteDepartment of Dermatology, University of Copenhagen, Roskilde Hospital, DK-4000 Roskilde, Denmark.
Jorgen Lock-AndersenDepartment of Plastic Surgery, University of Copenhagen, Roskilde Hospital, DK-4000 Roskilde, Denmark.
Krutika S GaonkarDivision of Biostatistics and Informatics, Department of Health Science Research, Mayo Clinic, Rochester, MN 55905.
Huihuang YanDivision of Biostatistics and Informatics, Department of Health Science Research, Mayo Clinic, Rochester, MN 55905.
Jann N SarkariaDepartment of Radiation Oncology, Mayo Clinic, Rochester, MN 55905.
Mira KrendelCell and Developmental Biology, SUNY Upstate Medical University, Syracuse, NY 13210.
Jan van DeursenDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN 55905.
Remco SprangersMax Planck Institute for Developmental Biology, 72076 Tuebingen, Germany.
Thilo StehleInterfaculty Institute of Biochemistry, University of Tuebingen, 72076 Tuebingen, Germany.
Ralph T BöttcherDepartment of Molecular Medicine, Max Planck Institute for Biochemistry, 82152 Martinsried, Germany.
Jeong-Heon LeeEpigenomics Program, Center for Individualized Medicine, Mayo Clinic, Rochester, MN 55905.
Tamas OrdogEpigenomics Program, Center for Individualized Medicine, Mayo Clinic, Rochester, MN 55905.
Alexander MevesDepartment of Dermatology, Mayo Clinic, Rochester, MN 55905; meves.alexander@mayo.edu.ORCID 0000-0001-7462-8288
Mayo Clinic · USUniversity of Copenhagen · DKMax Planck Institute for Developmental Biology · DEGerman Centre for Cardiovascular Research · DEMayo Clinic in Arizona · USSUNY Upstate Medical University · USUniversity of Tübingen · DEVanderbilt University · US

Funding

Women's Cancer ProgramP30CA015083 · NCI · MAYO CLINIC ROCHESTER · PI Felicity Enders · 1985 to 2026
$151.3M
Targeted MV-CEA as a Potent Antitumor Agent against GBMP50CA108961 · NCI · MAYO CLINIC ROCHESTER · PI O'NEILL, BRIAN PATRICK · 2004 to 2015
$22.5M
Role of myosin 1e in podocyte biology and renal filtrationR01DK083345 · NIDDK · UPSTATE MEDICAL UNIVERSITY · PI Mira Krendel · 2011 to 2026
$6.8M
NCI NIH HHS P30 CA015083NCI NIH HHS P50 CA108961NIDDK NIH HHS R01 DK083345
6 · The paper itself

Abstract

Focal adhesion kinase (FAK) is a nonreceptor tyrosine kinase involved in development and human disease, including cancer. It is currently thought that the four-point one, ezrin, radixin, moesin (FERM)-kinase domain linker, which contains autophosphorylation site tyrosine (Y) 397, is not required for in vivo FAK function until late midgestation. Here, we directly tested this hypothesis by generating mice with FAK Y397-to-phenylalanine (F) mutations in the germline. We found that Y397F embryos exhibited reduced mesodermal fibronectin (FN) and osteopontin expression and died during mesoderm development akin to FAK kinase-dead mice. We identified myosin-1E (MYO1E), an actin-dependent molecular motor, to interact directly with the FAK FERM-kinase linker and induce FAK kinase activity and Y397 phosphorylation. Active FAK in turn accumulated in the nucleus where it led to the expression of osteopontin and other FN-type matrix in both mouse embryonic fibroblasts and human melanoma. Our data support a model in which FAK Y397 autophosphorylation is required for FAK function in vivo and is positively regulated by MYO1E.

Indexed as

AnimalsEmbryo LossExtracellular MatrixFemaleFibroblastsFibronectinsFocal Adhesion Kinase 1HumansMelanomaMesodermMice, Mutant StrainsMyosinsMyosin Type IOsteopontinPhosphorylationPregnancyFibronectinsFocal Adhesion Kinase 1Myo1e protein, mouseMyosinsMyosin Type IOsteopontinPTK2 protein, humanPtk2 protein, mouseSpp1 protein, mouseTyrosinecancerfibronectinfocal adhesionmelanomamyosin

Identifiers

PMID28348210
PMCPMC5393228
OpenAlexW2602988718

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.