Evidence map›Paper›PMID 29665313›Full record

ArticlePigment cell & melanoma research2018

Refinement of the endogenous epitope tagging technology allows the identification of a novel NRAS binding partner in melanoma.

Michal Alon, Rafi Emmanuel, Nouar Qutob, Anna Bakhman, Victoria Peshti, Alexandra Brodezki, David Bassan, Mickey Kosloff, Yardena Samuels

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In one paragraph

Article in Pigment cell & melanoma research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 97% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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

9 authors at 2 institutions in 1 country.

Michal AlonDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Rafi EmmanuelDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Nouar QutobDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Anna BakhmanDepartment of Human Biology, Faculty of Natural Science, University of Haifa, Haifa, Israel.
Victoria PeshtiDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Alexandra BrodezkiDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
David BassanDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Mickey KosloffDepartment of Human Biology, Faculty of Natural Science, University of Haifa, Haifa, Israel.
Yardena SamuelsDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.ORCID 0000-0002-3349-7266
Weizmann Institute of Science · ILUniversity of Haifa · IL

Funding

ERC StG-335377Estate of Alice Schwarz-GardosEstate of John HunterEU-H2020-ERC-POC 712730Henry Chanoch Krenter Institute for Biomedical Imaging and GenomicsIsrael Science Foundation 712811Melanoma Research AlliancePeter and Patricia Gruber AwardThe Hamburger FamilyThe Knell Family
6 · The paper itself

Abstract

The NRAS oncoprotein is highly mutated in melanoma. However, to date, no comprehensive proteomic study has been reported for NRAS. Here, we utilized the endogenous epitope tagging (EET) approach for the identification of novel NRAS binding partners. Using EET, an epitope tag is added to the endogenously expressed protein, via modification of its genomic coding sequence. Existing EET systems are not robust, suffer from high background, and are labor-intensive. To this end, we present a polyadenylation signal-trap construct for N'-tagging that generates a polycistronic mRNA with the gene of interest. This system requires the integration of the tagging cassette in frame with the target gene to be expressed. Using this design, we demonstrate, for the first time, endogenous tagging of NRAS in melanoma cells allowing the identification of the E3 ubiquitin ligase c-CBL as a novel NRAS binding partner. Thus, our developed EET technology allows the characterization of new RAS effectors, which could be beneficial for the design of future drugs that inhibit constitutive signaling of RAS oncogenic mutants.

Indexed as

Epitope MappingEpitopesGTP PhosphohydrolasesHumansMelanomaMembrane ProteinsMutationProtein Interaction Domains and MotifsProteomicsProto-Oncogene Proteins c-cblTumor Cells, CulturedCBL protein, humanEpitopesGTP PhosphohydrolasesMembrane ProteinsNRAS protein, humanProto-Oncogene Proteins c-cblendogenous epitope taggingmelanomaNRAS

Identifiers

PMID29665313
PMCPMC6438458
OpenAlexW2800892455

What OpenQuestion holds

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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.