Evidence map›Paper›PMID 28034848›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2017

Regulated intramembrane proteolysis of the AXL receptor kinase generates an intracellular domain that localizes in the nucleus of cancer cells.

Yinzhong Lu, Jun Wan, Zhifeng Yang, Xiling Lei, Qi Niu, Lanxin Jiang, Willemijn M Passtoors, Aiping Zang, Patrick C Fraering, Fang Wu

Open access · hybridAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

28 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. MERTK Inhibition as a Targeted Novel Cancer Therapy.International journal of molecular sciences · 2024
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. WNK1 collaborates with TGF-β in endothelial cell junction turnover and angiogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. 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

10 authors at 3 institutions in 4 countries.

Yinzhong LuKey Laboratory of Systems Biomedicine, Ministry of Education, Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China.
Jun WanKey Laboratory of Systems Biomedicine, Ministry of Education, Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China.
Zhifeng YangSchool of Life Science and Biotechnology, Shanghai Jiao Tong University, Shanghai, China.
Xiling LeiKey Laboratory of Systems Biomedicine, Ministry of Education, Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China.
Qi NiuKey Laboratory of Systems Biomedicine, Ministry of Education, Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China.
Lanxin JiangSchool of Life Science and Biotechnology, Shanghai Jiao Tong University, Shanghai, China.
Willemijn M PasstoorsKey Laboratory of Systems Biomedicine, Ministry of Education, Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China.
Aiping ZangKey Laboratory of Systems Biomedicine, Ministry of Education, Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China.
Patrick C FraeringBrain Mind Institute-School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.
Fang WuKey Laboratory of Systems Biomedicine, Ministry of Education, Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China; fang.wu@sjtu.edu.cn.
Institute for Biomedicine · ITShanghai Jiao Tong University · CNBiotech Park · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deregulation of the TAM (TYRO3, AXL, and MERTK) family of receptor tyrosine kinases (RTKs) has recently been demonstrated to predominately promote survival and chemoresistance of cancer cells. Intramembrane proteolysis mediated by presenilin/γ-secretase is known to regulate the homeostasis of some RTKs. In the present study, we demonstrate that AXL, but not TYRO3 or MERTK, is efficiently and sequentially cleaved by α- and γ-secretases in various types of cancer cell lines. Proteolytic processing of AXL redirected signaling toward a secretase-mediated pathway, away from the classic, well-known, ligand-dependent canonical RTK signaling pathway. The AXL intracellular domain cleavage product, but not full-length AXL, was further shown to translocate into the nucleus

Indexed as

ProteolysisActive Transport, Cell NucleusAmyloid Precursor Protein SecretasesAxl Receptor Tyrosine KinaseCell Nucleusc-Mer Tyrosine KinaseDrug Resistance, NeoplasmHCT116 CellsHEK293 CellsHeLa CellsHumansMutationNuclear Localization SignalsProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesAmyloid Precursor Protein SecretasesAXL protein, humanAxl Receptor Tyrosine Kinasec-Mer Tyrosine KinaseMERTK protein, humanNuclear Localization SignalsProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesTYRO3 protein, humannuclear translocationpresenilinprotein processingreceptor tyrosine kinaseγ-secretase

Identifiers

PMID28034848
PMCPMC5349800
OpenAlexW2563570608

What OpenQuestion holds

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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.