ArticleCell research2011
Notch-induced Asb2 expression promotes protein ubiquitination by forming non-canonical E3 ligase complexes.
Article in Cell research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 45 citations in OpenAlex.
- Notch-hedgehog antagonism regulates stem cell niche formation through an E2-E3-E3 ubiquitin module.EMBO reports · 2026Article
- JAK1/2 inhibitor ruxolitinib reduces aggregates in cardiac proteinopathy.EMBO molecular medicine · 2026Article
- ASB5 is a specific marker for muscle satellite cells but dispensable for skeletal muscle development and regeneration.Skeletal muscle · 2026Article
- CUL5-mediated ubiquitination in cancer cell therapy: context-dependent roles, molecular networks, and emerging therapeutic avenues.Frontiers in medicine · 2026Review
- Urinary exosomal lnc-TAF12-2:1 promotes bladder cancer progression through the miR-7847-3p/ASB12 regulatory axis.Genes & diseases · 2025Article
- T Cell Development: From T-Lineage Specification to Intrathymic Maturation.Advances in experimental medicine and biology · 2025Review
- Novel targets and their functions in the prognosis of uterine corpus endometrial cancer patients.Journal of applied genetics · 2024Article
- Whole exome sequencing of patients with varicella-zoster virus and herpes simplex virus induced acute retinal necrosis reveals rare disease-associated genetic variants.Frontiers in molecular neuroscience · 2023Article
- Advances in the potential roles of Cullin-RING ligases in regulating autoimmune diseases.Frontiers in immunology · 2023Review
- An unconventional role of an ASB family protein in NF-κB activation and inflammatory response during microbial infection and colitis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Role of Cullin-RING Ligases in Striated Muscle Development, Function, and Disease.International journal of molecular sciences · 2020Review
- Epigenetic alterations in skin homing CD4Scientific reports · 2020Article
- TCF-1 and HEB cooperate to establish the epigenetic and transcription profiles of CD4Nature immunology · 2018Article
- ASB1 differential methylation in ischaemic cardiomyopathy: relationship with left ventricular performance in end-stage heart failure patients.ESC heart failure · 2018Article
- The notch pathway promotes NF-κB activation through Asb2 in T cell acute lymphoblastic leukemia cells.Cellular & molecular biology letters · 2018Article
- CBL family E3 ubiquitin ligases control JAK2 ubiquitination and stability in hematopoietic stem cells and myeloid malignancies.Genes & development · 2017Article
- Proteolysis regulates cardiomyocyte maturation and tissue integration.Nature communications · 2017Article
- The role of cullin 5-containing ubiquitin ligases.Cell division · 2016Review
- Substrates of the ASB2α E3 ubiquitin ligase in dendritic cells.Scientific reports · 2015Article
- Families of microRNAs Expressed in Clusters Regulate Cell Signaling in Cervical Cancer.International journal of molecular sciences · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Notch signaling controls multiple developmental processes, thus demanding versatile functions. We have previously shown that this may be partly achieved by accelerating ubiquitin-mediated degradation of important regulators of differentiation. However, the underlying mechanism was unknown. We now find that Notch signaling transcriptionally activates the gene encoding ankyrin-repeat SOCS box-containing protein 2 (Asb2). Asb2 promotes the ubiquitination of Notch targets such as E2A and Janus kinase (Jak) 2, and a dominant-negative (DN) mutant of Asb2 blocks Notch-induced degradation of these proteins. Asb2 likely binds Jak2 directly but associates with E2A through Skp2. We next provide evidence to suggest that Asb2 bridges the formation of non-canonical cullin-based complexes through interaction with not only ElonginB/C and Cullin (Cul) 5, but also the F-box-containing protein, Skp2, which is known to associate with Skp1 and Cul1. Consistently, ablating the function of Cul1 or Cul5 using DN mutants or siRNAs protected both E2A and Jak2 from Asb2-mediated or Notch-induced degradation. By shifting monomeric E3 ligase complexes to dimeric forms through activation of Asb2 transcription, Notch could effectively control the turnover of a variety of substrates and it exerts diverse effects on cell proliferation and differentiation.
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.