ArticleScientific reports2015
Stability of HIB-Cul3 E3 ligase adaptor HIB Is Regulated by Self-degradation and Availability of Its Substrates.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 23 citations in OpenAlex.
- High-throughput screening identifies a critical role of the SPOP-PABPC1 axis in lung adenocarcinoma progression.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Reversible acetylation of Hpo regulates the Hippo pathway.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- SPOP and HAUSP bidirectionally regulate LZTS2 ubiquitination to modulate the Wnt pathway.Cell death & disease · 2025Article
- Article
- Rapid increase of C/EBPα p42 induces growth arrest of acute myeloid leukemia (AML) cells by Cop1 deletion in Trib1-expressing AML.Leukemia · 2024Article
- Tai/NCOA2 suppresses the Hedgehog pathway by directly targeting the transcription factor Ci/GLI.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- SPOP point mutations regulate substrate preference and affect its function.Cell death & disease · 2024Article
- Kelch-like proteins in the gastrointestinal tumors.Acta pharmacologica Sinica · 2023Review
- Inhibition of the transcription factor ZNF281 by SUFU to suppress tumor cell migration.Cell death and differentiation · 2023Article
- Primary bilateral macronodular adrenal hyperplasia: definitely a genetic disease.Nature reviews. Endocrinology · 2022Review
- Hippo signaling suppresses tumor cell metastasis via a Yki-Src42A positive feedback loop.Cell death & disease · 2021Article
- The Hh pathway promotes cell apoptosis through Ci-Rdx-Diap1 axis.Cell death discovery · 2021Article
- Dual functions of Rack1 in regulating Hedgehog pathway.Cell death and differentiation · 2020Article
- CUL3Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Usp7 regulates Hippo pathway through deubiquitinating the transcriptional coactivator Yorkie.Nature communications · 2019Article
- Apontic directly activates hedgehog and cyclin E for proper organ growth and patterning.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The HIB-Cul3 complex E3 ligase regulates physiological homeostasis through regulating its substrate stability and its activity can be modulated by changing HIB abundance. However, regulation of HIB remains elusive. Here we provide evidence that HIB is degraded through the proteasome by Cul3-mediated polyubiquitination in K48 manner in Drosophila. Strikingly, HIB is targeted for degradation by itself. We further identify that three degrons ((52)LKSS(56)T, (76)LDEE(80)S and (117)MESQ(121)R) and K185 and K198 of HIB are essential for its auto-degradation. Finally, we demonstrate that HIB-Cul3 substrates, Ci and Puc, can effectively protect HIB from HIB-Cul3-mediated degradation. Taken together, our study indicates that there is an exquisite equilibrium between the adaptor and targets to achieve the tight control of the HIB, which is essential for maintaining suitable Hh and JNK signaling. And the mechanism of adaptor self-degradation and reciprocal control of the abundance between adaptor and its substrates is also applied to BTB-Cul3 E3 ligase adaptor dKeap1, dDiablo and dKLHL18.
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.