Evidence map›Paper›PMID 9334332›Full record

ArticleGenes & development1997

Mammalian homologs of seven in absentia regulate DCC via the ubiquitin-proteasome pathway.

G Hu, S Zhang, M Vidal, J L Baer, T Xu, E R Fearon

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
–field-weighted citation impact
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

80 citing papers in PubMed, 190 citations in OpenAlex.

  1. Article
  2. Parallel Selection for Longevity in Mammals and Birds.bioRxiv : the preprint server for biology · 2025
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  7. The Ubiquitinated Axon: Local Control of Axon Development and Function by Ubiquitin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
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  15. Che-1 sustains hypoxic response of colorectal cancer cells by affecting Hif-1α stabilization.Journal of experimental & clinical cancer research : CR · 2017
    Article
  16. Review
  17. Molecular Pharmacology of δ-Opioid Receptors.Pharmacological reviews · 2016
    Review
  18. Central role of SIAH inhibition in DCC-dependent cardioprotection provoked by netrin-1/NO.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  19. Article
  20. Article

20 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 1 country.

G HuDivision of Molecular Medicine and Genetics, University of Michigan Medical Center, Ann Arbor, Michigan 48109-0638 USA.
S Zhang
M Vidal
J L Baer
T Xu
E R Fearon
Cancer Genetics (United States) · USMassachusetts General Hospital · USUniversity of Michigan–Ann Arbor · US

Funding

FUNCTIONAL STUDIES OF THE DCC TUMOR SUPPRESSOR GENER01CA070097 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FEARON, ERIC R. · 1995 to 1999
–
NCI NIH HHS CA70097
6 · The paper itself

Abstract

DCC (deleted in colorectal cancer) is postulated to function as transmembrane receptor for the axon and cell guidance factor netrin-1. We report here that the DCC cytoplasmic domain binds to proteins encoded by mammalian homologs of the Drosophila seven in absentia (sina) gene, as well as Drosophila Sina. Sina has a critical role in R7 photoreceptor development and shows upward of 85% amino acid identity with its mammalian homologs (termed Siahs), but the function of the Sina/Siah proteins has not been defined. We sought, therefore, to characterize further their interaction with DCC. Immunofluorescence studies suggested the Sina/Siah proteins localized predominantly in the cytoplasm and in association with DCC. DCC was found to be ubiquitinated and the Sina/Siah proteins regulated its expression. Proteasome inhibitors blocked the effects of Sina/Siah on DCC, and the Sina/Siah proteins interacted with ubiquitin-conjugating enzymes (Ubcs). A mutant Siah protein lacking the amino-terminal Ubc-binding sequences complexed with DCC, but did not degrade it. The in vivo interaction between Sina/Siah and DCC was confirmed through studies of transgenic Drosophila lines in which DCC and Sina were ectopically expressed in the eye. Taken together, the data imply that the Sina/Siah proteins regulate DCC and perhaps other proteins via the ubiquitin-proteasome pathway.

Indexed as

Genes, DCCTumor Suppressor ProteinsAnimalsAnimals, Genetically ModifiedCell Adhesion MoleculesCell LineCHO CellsCOS CellsCricetinaeDCC ReceptorDrosophilaGene LibraryGlioblastomaHumansMammalsNuclear ProteinsCell Adhesion MoleculesDCC protein, humanDCC ReceptorNuclear ProteinsReceptors, Cell SurfaceRecombinant Fusion ProteinsSeven in Absentia ProteinsTumor Suppressor ProteinsUbiquitin-Protein Ligases

Identifiers

PMID9334332
PMCPMC316613
OpenAlexW2014519647

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.