ArticleCell research2017
Cancer: a new role for non-canonical Hippo signaling.
Article in Cell research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Neutrophil extracellular traps mediate TLR9/Merlin axis to resist ferroptosis and promote triple negative breast cancer progression.Apoptosis : an international journal on programmed cell death · 2023Article
- ARSD, a novel ERα downstream target gene, inhibits proliferation and migration of breast cancer cells via activating Hippo/YAP pathway.Cell death & disease · 2021Article
- The role of Hippo signal pathway in breast cancer metastasis.OncoTargets and therapy · 2018Review
Corrections and comments
- Comment on
Authors and funding
2 authors.
Funding
Abstract
The molecular mechanisms governing self-renewal and differentiation of the mammary epithelium are incompletely defined; a better understanding of the events implicated in the specification and expansion of luminal progenitors is of particular importance as many breast cancers originate from their transformation. Britschgi et al. found that, in addition to phosphorylating and inactivating YAP, LATS functions as a scaffold to facilitate estrogen receptor-α ubiquitylation by the E3 ligase CRL4 and consequently suppresses luminal progenitor specification and expansion.
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.