Evidence map›Paper›PMID 26032413›Full record

ArticleThe Journal of biological chemistry2015

SPSB1, a Novel Negative Regulator of the Transforming Growth Factor-β Signaling Pathway Targeting the Type II Receptor.

Sheng Liu, Thao Nheu, Rodney Luwor, Sandra E Nicholson, Hong-Jian Zhu

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 41 citations in OpenAlex.

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  7. Testis-enrichedAmerican journal of translational research · 2025
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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 1 country.

Sheng LiuDepartments of Surgery (the Royal Melbourne Hospital), University of Melbourne, Parkville, Victoria 3050, Australia; Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3050, Australia.
Thao NheuDepartments of Surgery (the Royal Melbourne Hospital), University of Melbourne, Parkville, Victoria 3050, Australia.
Rodney LuworDepartments of Surgery (the Royal Melbourne Hospital), University of Melbourne, Parkville, Victoria 3050, Australia.
Sandra E NicholsonWalter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3050, Australia; Departments of Medical Biology, University of Melbourne, Parkville, Victoria 3050, Australia.
Hong-Jian ZhuDepartments of Surgery (the Royal Melbourne Hospital), University of Melbourne, Parkville, Victoria 3050, Australia. Electronic address: hongjian@unimelb.edu.au.
The Royal Melbourne Hospital · AUUniversity of Melbourne · AUWalter and Eliza Hall Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Appropriate cellular signaling is essential to control cell proliferation, differentiation, and cell death. Aberrant signaling can have devastating consequences and lead to disease states, including cancer. The transforming growth factor-β (TGF-β) signaling pathway is a prominent signaling pathway that has been tightly regulated in normal cells, whereas its deregulation strongly correlates with the progression of human cancers. The regulation of the TGF-β signaling pathway involves a variety of physiological regulators. Many of these molecules act to alter the activity of Smad proteins. In contrast, the number of molecules known to affect the TGF-β signaling pathway at the receptor level is relatively low, and there are no known direct modulators for the TGF-β type II receptor (TβRII). Here we identify SPSB1 (a Spry domain-containing Socs box protein) as a novel regulator of the TGF-β signaling pathway. SPSB1 negatively regulates the TGF-β signaling pathway through its interaction with both endogenous and overexpressed TβRII (and not TβRI) via its Spry domain. As such, TβRII and SPSB1 co-localize on the cell membrane. SPSB1 maintains TβRII at a low level by enhancing the ubiquitination levels and degradation rates of TβRII through its Socs box. More importantly, silencing SPSB1 by siRNA results in enhanced TGF-β signaling and migration and invasion of tumor cells.

Indexed as

Signal TransductionAnimalsCell LineCell Line, TumorCell MovementGene SilencingHEK293 CellsHumansMiceNeoplasm InvasivenessNeoplasmsNIH 3T3 CellsProtein Interaction MapsProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IIProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IISPSB1 protein, humanSSB-1 protein, mouseSuppressor of Cytokine Signaling ProteinsTransforming Growth Factor betaprotein degradationreceptor modificationreceptor regulationsignal transductionSPSBtransforming growth factor beta (TGF-B)

Identifiers

PMID26032413
PMCPMC4505038
OpenAlexW1869688000

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.