ReviewPediatric research2010
Protacs for treatment of cancer.
Review in Pediatric research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 57 citations in OpenAlex.
- Advancing PROTAC therapeutics through chemistry-guided design of smart delivery systems.Acta pharmacologica Sinica · 2026Review
- Advantages of PROTACs in achieving selective degradation of homologous protein families.Beilstein journal of organic chemistry · 2026Review
- The Role of Reactive Oxygen Species in Lung Cancer Development: Nanomedicine as a Therapeutic Strategy.Biomolecules · 2025Review
- Emerging Concepts of Targeted Protein Degrader Technologies via Lysosomal Pathways.International journal of molecular sciences · 2025Review
- A Review of Novel Cancer Therapeutics and Current Research Trends.TheScientificWorldJournal · 2025Review
- Recent Advances in Optically Controlled PROTAC.Bioengineering (Basel, Switzerland) · 2023Review
- Emerging degrader technologies engaging lysosomal pathways.Chemical Society reviews · 2022Review
- Recent Advances in PROTACs for Drug Targeted Protein Research.International journal of molecular sciences · 2022Review
- PROTACs: The Future of Leukemia Therapeutics.Frontiers in cell and developmental biology · 2022Review
- Is PROTAC technology really a game changer for central nervous system drug discovery?Expert opinion on drug discovery · 2021Article
- Light-Controllable PROTACs for Temporospatial Control of Protein Degradation.Frontiers in cell and developmental biology · 2021Review
- Bromodomain and BET family proteins as epigenetic targets in cancer therapy: their degradation, present drugs, and possible PROTACs.RSC advances · 2020Review
- Ubiquitination and deubiquitination of MCL1 in cancer: deciphering chemoresistance mechanisms and providing potential therapeutic options.Cell death & disease · 2020Review
- Proteolysis-targeting chimera (PROTAC) for targeted protein degradation and cancer therapy.Journal of hematology & oncology · 2020Review
- Targeting the Chromosomal Passenger Complex Subunit INCENP Induces Polyploidization, Apoptosis, and Senescence in Neuroblastoma.Cancer research · 2019Article
- Degrading proteins in animals: "PROTAC"tion goes in vivo.Cell research · 2019Article
- The emerging role for Cullin 4 family of E3 ligases in tumorigenesis.Biochimica et biophysica acta. Reviews on cancer · 2019Review
- The PROTAC technology in drug development.Cell biochemistry and function · 2019Review
- Ligand-mediated protein degradation reveals functional conservation among sequence variants of the CUL4-type E3 ligase substrate receptor cereblon.The Journal of biological chemistry · 2018Article
- The chimeric ubiquitin ligase SH2-U-box inhibits the growth of imatinib-sensitive and resistant CML by targeting the native and T315I-mutant BCR-ABL.Scientific reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Protein degradation is the cell's mechanism of eliminating misfolded or unwanted proteins. The pathway by which proteins are degraded occurs through the ubiquitin-proteasome system. Ubiquitin is a small 9-kD (kDa) protein that is attached to proteins. A minimum of four ubiquitins are required for proteins to be recognized by the degradation machinery, known as the 26S proteasome. Defects in ubiquitination have been identified in a number of diseases, including cancer, neurodegenerative diseases, and metabolic disorders. We sought to exploit the delicate balance between protein synthesis and degradation to treat cancer by designing a chimeric molecule, known as Protac (Proteolysis Targeting Chimeric molecule). Protacs are heterobifunctional nanomolecules that are approximately 10 nm in size and can recruit proteins that cause cancer to the ubiquitin-proteasome machinery for degradation. In this review, we discuss the development of this novel technology for the treatment of cancer.
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.