Evidence map›Paper›PMID 17310991›Full record

ArticleOncogene2007

Uncovering residues that regulate cyclin D1 proteasomal degradation.

Q Feng, D Sekula, R Müller, S J Freemantle, E Dmitrovsky

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. E3 ligase MG53 suppresses tumor growth by degrading cyclin D1.Signal transduction and targeted therapy · 2023
    Article
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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

5 authors at 3 institutions in 2 countries.

Q FengDepartment of Pharmacology and Toxicology, Dartmouth Medical School, Hanover, NH 03755, USA.
D Sekula
R Müller
S J Freemantle
E Dmitrovsky
Dartmouth College · USDartmouth–Hitchcock Medical Center · USPhilipps University of Marburg · DE

Funding

RETINOID CANCER PREVENTION MECHANISMSR01CA087546 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DMITROVSKY, ETHAN · 2000 to 2015
$4.1M
Cyclin D as a Retinoid Molecular TargetR01CA111422 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DMITROVSKY, ETHAN · 2005 to 2014
$2.7M
NCI NIH HHS R01 CA087546NCI NIH HHS R01 CA111422
6 · The paper itself

Abstract

Cyclin D1 regulates G1 cell-cycle progression and is aberrantly expressed in carcinogenesis. Proteasomal degradation of cyclin D1 was highlighted as a cancer chemopreventive mechanism. To understand this mechanism better, residues responsible for degradation and ubiquitination of cyclin D1 were investigated. Eighteen lysines in cyclin D1 had single, double or multiple mutations engineered before transfection into BEAS-2B human bronchial epithelial (HBE) cells to evaluate stabilities after all-trans-retinoic acid (RA) or cycloheximide treatments. Specific mutations stabilized cyclin D1, including substitutions of lysines surrounding the cyclin box domain that inhibited RA-mediated degradation and extended the cyclin D1 half-life. Mutation of all cyclin D1 lysines blocked polyubiquitination. N-terminus (but not C-terminus) modification stabilized cyclin D1. Ubiquitination-resistant mutants preferentially localized cyclin D1 to the nucleus, directly implicating subcellular localization in regulating cyclin D1 degradation. Taken together, these findings uncover specific residues conferring ubiquitination of cyclin D1. These provide a mechanistic basis for proteasomal degradation of cyclin D1.

Indexed as

Cell NucleusCyclin D1CycloheximideHumansLysineMutationProteasome Endopeptidase ComplexProtein Structure, TertiaryTretinoinUbiquitinCyclin D1CycloheximideLysineProteasome Endopeptidase ComplexTretinoinUbiquitin

Identifiers

PMID17310991
OpenAlexW2162370807

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.