Evidence map›Paper›PMID 10930472›Full record

ArticleMolecular biology of the cell2000

Cell cycle-dependent expression of mammalian E2-C regulated by the anaphase-promoting complex/cyclosome.

A Yamanaka, S Hatakeyama, K Kominami, M Kitagawa, M Matsumoto, K Nakayama

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In one paragraph

Article in Molecular biology of the cell, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

25 citing papers in PubMed, 53 citations in OpenAlex.

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  17. Processive ubiquitin chain formation by the anaphase-promoting complex.Seminars in cell & developmental biology · 2011
    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

6 authors at 1 institution in 1 country.

A YamanakaDepartment of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
S Hatakeyama
K Kominami
M Kitagawa
M Matsumoto
K Nakayama
Kyushu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Progression through mitosis requires the precisely timed ubiquitin-dependent degradation of specific substrates. E2-C is a ubiquitin-conjugating enzyme that plays a critical role with anaphase-promoting complex/cyclosome (APC/C) in progression of and exit from M phase. Here we report that mammalian E2-C is expressed in late G(2)/M phase and is degraded as cells exit from M phase. The mammalian E2-C shows an autoubiquitinating activity leading to covalent conjugation to itself with several ubiquitins. The ubiquitination of E2-C is strongly enhanced by APC/C, resulting in the formation of a polyubiquitin chain. The polyubiquitination of mammalian E2-C occurs only when cells exit from M phase. Furthermore, mammalian E2-C contains two putative destruction boxes that are believed to act as recognition motifs for APC/C. The mutation of this motif reduced the polyubiquitination of mammalian E2-C, resulting in its stabilization. These results suggest that mammalian E2-C is itself a substrate of the APC/C-dependent proteolysis machinery, and that the periodic expression of mammalian E2-C may be a novel autoregulatory system for the control of the APC/C activity and its substrate specificity.

Indexed as

Cell CycleUbiquitin-Protein Ligase Complexes3T3 CellsAmino Acid MotifsAnaphase-Promoting Complex-CyclosomeAnimalsHeLa CellsHumansLigasesMiceMutagenesisRecombinant Fusion ProteinsSequence AlignmentTransfectionUbiquitin-Conjugating EnzymesUbiquitin-Protein LigasesAnaphase-Promoting Complex-CyclosomeLigasesRecombinant Fusion Proteinsubiquitin carrier proteinsUbiquitin-Conjugating EnzymesUbiquitin-Protein Ligase ComplexesUbiquitin-Protein LigasesUbiquitins

Identifiers

PMID10930472
PMCPMC14958
OpenAlexW2120744441

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.