Evidence map›Paper›PMID 30400005›Full record

ReviewEndocrine-related cancer2019

Otubain 1: a non-canonical deubiquitinase with an emerging role in cancer.

Matthew Saldana, Kacey VanderVorst, Anastasia L Berg, Hyun Lee, Kermit L Carraway

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrine-related cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

63 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
  2. Selective Modulation of OTUB1 Noncanonical Function via a bioPhosTAC Strategy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Research progress of DUB enzyme in breast cancer.Clinical and experimental medicine · 2025
    Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Review

3 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

5 authors at 2 institutions in 1 country.

Matthew SaldanaDepartment of Biochemistry and Molecular Medicine, UC Davis School of Medicine, UC Davis Comprehensive Cancer Center, Sacramento, California, USA.
Kacey VanderVorstDepartment of Biochemistry and Molecular Medicine, UC Davis School of Medicine, UC Davis Comprehensive Cancer Center, Sacramento, California, USA.
Anastasia L BergDepartment of Biochemistry and Molecular Medicine, UC Davis School of Medicine, UC Davis Comprehensive Cancer Center, Sacramento, California, USA.
Hyun LeeDepartment of Biochemistry and Molecular Medicine, UC Davis School of Medicine, UC Davis Comprehensive Cancer Center, Sacramento, California, USA.
Kermit L CarrawayDepartment of Biochemistry and Molecular Medicine, UC Davis School of Medicine, UC Davis Comprehensive Cancer Center, Sacramento, California, USA.
University of California, Davis · USUC Davis Comprehensive Cancer Center

Funding

Predoctoral Training in the Pharmacological SciencesT32GM067795 · NIGMS · UNIVERSITY OF IOWA · PI STRACK, STEFAN · 2004 to 2021
$3.4M
NRDP1 PROTEIN DEGRADATION PATHWAY IN MAMMARY TUMOR PROGRESSIONR01CA123541 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CARRAWAY, KERMIT L · 2006 to 2016
$2.5M
Predoctoral Training in Pharmacological SciencesT32GM099608 · NIGMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HELL, JOHANNES W · 2012 to 2021
$2.2M
Muc4 Involvement in Mammary Tumor ProgressionR01CA166412 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CARRAWAY, KERMIT L · 2013 to 2017
$1.5M
Vangl Dependent PCP Signaling Mediates EMT Induced Cell InvasivenessF31CA210467 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI VANDERVORST, KACEY · 2016 to 2018
$116k
NCI NIH HHS F31 CA210467NCI NIH HHS R01 CA123541NCI NIH HHS R01 CA166412NIGMS NIH HHS T32 GM067795NIGMS NIH HHS T32 GM099608
6 · The paper itself

Abstract

The ubiquitin system regulates diverse biological processes, many involved in cancer pathogenesis, by altering the ubiquitination state of protein substrates. This is accomplished by ubiquitin ligases and deubiquitinases (DUBs), which respectively add or remove ubiquitin from substrates to alter their stability, activity, localization and interactions. While lack of catalytic activity makes therapeutic targeting of ubiquitin ligases difficult, DUB inhibitors represent an active area of research and the identification of cancer-associated DUBs may lead to the development of novel therapeutics. A growing body of literature demonstrates that the DUB Otubain 1 (OTUB1) regulates many cancer-associated signaling pathways including MAPK, ERa, epithelial-mesenchymal transition (EMT), RHOa, mTORC1, FOXM1 and P53 to promote tumor cell survival, proliferation, invasiveness and therapeutic resistance. In addition, clinical studies have associated elevated OTUB1 expression with high grade, invasiveness and metastasis in several tumor types including lung, breast, ovarian, glioma, colon and gastric. Interestingly, in addition to catalytic DUB activity, OTUB1 displays a catalytic-independent, non-canonical activity where it inhibits the transfer of ubiquitin onto protein substrates by sequestration of E2 ubiquitin-conjugating enzymes. The aim of this review is to describe the canonical and non-canonical activities of OTUB1, summarize roles for OTUB1 in cancer-associated pathways and discuss its potential therapeutic targeting.

Indexed as

AnimalsCysteine EndopeptidasesDeubiquitinating EnzymesHumansNeoplasmsCysteine EndopeptidasesDeubiquitinating EnzymesOTUB1 protein, humanDUB inhibitorE2 enzymemetastasisOTUB1ubiquitin ligase

Identifiers

PMID30400005
PMCPMC6226034
OpenAlexW2891607360

What OpenQuestion holds

Textmetadata
LicenceTDM
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.