Evidence map›Paper›PMID 24829397›Full record

ArticleMolecular cancer research : MCR2014

Convergent and divergent cellular responses by ErbB4 isoforms in mammary epithelial cells.

Vikram B Wali, Jonathan W Haskins, Maureen Gilmore-Hebert, James T Platt, Zongzhi Liu, David F Stern

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

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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.

Vikram B WaliDepartment of Pathology, Yale School of Medicine, New Haven, Connecticut vikram.wali@yale.edu.
Jonathan W HaskinsDepartment of Pathology, Yale School of Medicine, New Haven, Connecticut.
Maureen Gilmore-HebertDepartment of Pathology, Yale School of Medicine, New Haven, Connecticut.
James T PlattDepartment of Pathology, Yale School of Medicine, New Haven, Connecticut.
Zongzhi LiuDepartment of Pathology, Yale School of Medicine, New Haven, Connecticut.
David F SternDepartment of Pathology, Yale School of Medicine, New Haven, Connecticut.
Yale University · US

Funding

Yale Pathology Tissue Services Shared ResourceP30CA016359 · NCI · YALE UNIVERSITY · PI MEGAN C KING · 1985 to 2026
$85.0M
Skill Development for Diverse Scientific Careers: A New Course Predoctoral Program in Cellular and Molecular BiologyT32GM007223 · NIGMS · YALE UNIVERSITY · PI BASERGA, SUSAN J · 1985 to 2019
$31.0M
SIGNALING BY NEUREGULINS AND ERBB4 IN BREAST CANCERR01CA080065 · NCI · YALE UNIVERSITY · PI STERN, DAVID F · 1999 to 2013
$4.4M
NCI NIH HHS R01 CA080065NCI NIH HHS R01 CA80065NIGMS NIH HHS T32 GM007223NIGMS NIH HHS T32GM07223
6 · The paper itself

Abstract

unlabelledAssociations of ErbB4 (ERBB4/HER4), the fourth member of the EGFR family, with cancer are variable, possibly as a result of structural diversity of this receptor. There are multiple structural isoforms of ERBB4 arising by alternative mRNA splicing, and a subset undergo proteolysis that releases membrane-anchored and soluble isoforms that associate with transcription factors and coregulators to modulate transcription. To compare the differential and common signaling activities of full-length (FL) and soluble intracellular isoforms of ERBB4, four JM-a isoforms (FL and soluble intracellular domain (ICD) CYT-1 and CYT-2) were expressed in isogenic MCF10A cells and their biologic activities were analyzed. Both FL and ICD CYT-2 promoted cell proliferation and invasion, and CYT-1 suppressed cell growth. Transcriptional profiling revealed several new and underexplored ERBB4-regulated transcripts, including: proteases/protease inhibitors (MMP3 and SERPINE2), the YAP/Hippo pathway (CTGF, CYR61, and SPARC), the mevalonate/cholesterol pathway (HMGCR, HMGCS1, LDLR, and DHCR7), and cytokines (IL8, CCL20, and CXCL1). Many of these transcripts were subsequently validated in a luminal breast cancer cell line that normally expresses ERBB4. Furthermore, ChIP-seq experiments identified ADAP1, APOE, SPARC, STMN1, and MXD1 as novel molecular targets of ERBB4. These findings clarify the diverse biologic activities of ERBB4 isoforms, and reveal new and divergent functions. IMPLICATIONS: ErbB4 as a regulator of Hippo and mevalonate pathways provides new insight into milk production and anabolic processes in normal mammary epithelia and cancer.

Indexed as

Breast NeoplasmsCell Line, TumorCell ProliferationCells, CulturedEpithelial CellsFemaleHumansMammary Glands, HumanProtein IsoformsReceptor, ErbB-4Signal TransductionTranscription FactorsTranscription, GeneticERBB4 protein, humanProtein IsoformsReceptor, ErbB-4Transcription Factors

Identifiers

PMID24829397
PMCPMC4728083
OpenAlexW2141525353

What OpenQuestion holds

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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.