ArticleChemistry & biology2014
RETRACTED: An ATP-competitive inhibitor modulates the allosteric function of the HER3 pseudokinase.
Article in Chemistry & biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 10 papers.
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.
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.
Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Targeting HER2 by Combination Therapies.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2018Article
- Structure of Fam20A reveals a pseudokinase featuring a unique disulfide pattern and inverted ATP-binding.eLife · 2017Article
- Effective treatment of HER2-amplified breast cancer by targeting HER3 and β1 integrin.Breast cancer research and treatment · 2016Article
- Nucleotide-binding mechanisms in pseudokinases.Bioscience reports · 2015Review
- Targeting HER3 by interfering with its Sec61-mediated cotranslational insertion into the endoplasmic reticulum.Oncogene · 2015Article
- ATP binding to the pseudokinase domain of JAK2 is critical for pathogenic activation.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- The Tribbles 2 (TRB2) pseudokinase binds to ATP and autophosphorylates in a metal-independent manner.The Biochemical journal · 2015Article
- Navigating into the binding pockets of the HER family protein kinases: discovery of novel EGFR inhibitor as antitumor agent.Drug design, development and therapy · 2015Article
- Pharmacological targeting of the pseudokinase Her3.Nature chemical biology · 2014Article
- Flicking the molecular switch underlying MLKL-mediated necroptosis.Molecular & cellular oncologyArticle
Corrections and comments
- Retraction · 2017-07-20Falsification/Fabrication of Data · Investigation by Company/Institution · Investigation by ORI · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author · · NIH finding of Misconduct for Peter Littlefield: https://ori.hhs.gov/content/case-summary-littlefield-peter
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- Retracted
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Human epidermal growth factor receptor 3 (HER3) is a receptor tyrosine kinase that lacks catalytic activity but is essential for cellular homeostasis due to its ability to allosterically activate EGFR and HER2. Although catalytically inactive, HER3 binds ATP tightly, hinting at a possible role of the nucleotide-binding pocket in modulating HER3 function. We report a structure of the HER3 pseudokinase bound to the ATP-competitive inhibitor bosutinib. Previously solved structures show that bosutinib can potently interact with multiple kinase domain conformations. In complex with HER3, bosutinib binds to yet another conformation, which is nearly identical to that observed in the HER3-ATP complex. Interestingly, occupation of the ATP-binding site by bosutinib improves the ability of HER3 to act as an allosteric activator of EGFR in vitro by increasing the affinity of the HER3-EGFR heterodimer in a membrane-dependent manner.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.