Active IKKβ promotes the stability of GLI1 oncogene in diffuse large B-cell lymphoma
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Key Points: IKKβ, independently of NF-κB, regulates the stability and transcriptional activity of GLI1 oncogene. Combined inhibition of IKKβ and GLI1 activities synergistically decreases DLBCL cell viability in vivo and in vitro.
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Gli1 has three main functional domains including SUFU binding sites, DNA binding domain, and C-terminal transcriptional activation domain.
“Gli1 has three main functional domains including SUFU binding sites, DNA binding domain, and C‐terminal transcriptional activation domain [36].”
From Saikosaponin b1 Attenuates Liver Fibrosis by Blocking STAT3/Gli1 Interaction and Inducing Gli1 Degradation (2025) · cites this paper as [36]
The Introduction (page not provided) says GLI1 has zinc-finger domains that bind DNA and a C-terminal transcriptional activation domain. It does not identify SUFU-binding sites or describe these as GLI1’s three main functional domains. (LLM, conf=0.86)
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- Authors
- Agarwal, N. K., Kim, C. H., Kunkalla, K., Konno, H., Tjendra, Y., Kwon, D., Blonska, M., Kozloski, G. A., Moy, V. T., Verdun, R. E., Barber, G. N., Lossos, I. S., & Vega, F.
- Affiliations
- Division of Hematopathology, Department of Pathology,
- Department of Cell Biology,
- Biostatistics and Bioinformatics Core,
- Division of Hematology-Oncology, Department of Medicine,
- University of Miami (US)
- Division of Gerontology and Geriatric Medicine, Department of Medicine, University of Miami Miller School of Medicine, Miami, FL; and
- ORCID
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2016-02-04
- Volume
- 127
- Issue
- 5
- Pages
- 605-615
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- PMC
- PMC4742548
- OpenAlex
- W2175693901
- Cited by
- 23
- References
- 44
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 1 · 2023: 2 · 2022: 1 · 2021: 2 · 2020: 1 · 2019: 3 · 2018: 2 · 2017: 4 · 2016: 1
- FWCI
- 0.77
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Miami (1UL1TR000460)
- European Hematology Association (TRTH78)
- National Institutes of Health (KL2TR000461, UL1TR000460, 1k08ca143151-01)
- National Cancer Institute (K08 CA143151, 1 K08 CA143151-01)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Health Sciences › Medicine › Pathology and Forensic Medicine › Lymphoma Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Hedgehog Signaling Pathway Studies
- Keywords
- Gli1, IKKβ, diffuse large B-cell lymphoma, protein stability, phosphorylation sites, Itch E3 ubiquitin ligase, K48-linked ubiquitination, TNF-α, NF-κB signaling, Hedgehog signaling, protein degradation, therapeutic synergy
- MeSH terms
- Zinc Finger Protein GLI1, Cell Survival, Humans, Phosphorylation, Repressor Proteins, Transcription Factors, NF-kappa B, Lymphoma, Large B-Cell, Diffuse, Ubiquitin-Protein Ligases, Cell Line, Tumor, I-kappa B Kinase, Ubiquitination, Protein Stability
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