ReviewExpert reviews in molecular medicine2009
CCAAT/enhancer-binding protein beta: its role in breast cancer and associations with receptor tyrosine kinases.
Review in Expert reviews in molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.
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
107 citing papers in PubMed, 1 synthesis or guideline pooled it, 180 citations in OpenAlex.
- C/EBPβ as a master regulator of inflammasome signaling in neurodegenerative diseases: mechanisms and therapeutic implications.Frontiers in immunology · 2025Pooled it
- Article
- Expression of RUNX1::RUNX1T1 deregulates the proteome, induces C/EBPβ suppression, and blocks myeloid differentiation.Blood neoplasia · 2026Article
- The adipogenesis-related gene CEBPD as a prognostic biomarker and functional tumor suppressor in breast cancer.Cell division · 2026Article
- CEBPB emerges as a key regulatory factor in human cancers through diverse molecular mechanisms and clinical implications.Discover oncology · 2025Review
- Anoikis resistance and cancer.BMC cancer · 2025Review
- Sox9 regulates Papss2 mRNA expression through derepression of the transcriptional repressor, C/EBPβ, in chondrogenic cells.Gene reports · 2025Article
- Interleukin-10 augments human endogenous retroviral E1B variant of cd5 in aged T cells.Blood research · 2025Article
- CEBPB regulates ERK1/2 activity through SOS1 and contributes to ovarian cancer progression.Medical oncology (Northwood, London, England) · 2025Article
- C/EBPβ increases tumor aggressiveness by enhancing KIFC1 expression in androgen receptor negative triple negative breast cancer.Cell communication and signaling : CCS · 2025Article
- Role of Non-Coding RNAs in White and Brown Adipose Tissue Differentiation and Development.Non-coding RNA · 2025Review
- Design and Evaluation of RNA Aptamer-Mediated Delivery of C/EBPJournal of nucleic acids · 2025Article
- Conditional knockout of C/EBPβ in epidermis results in dysregulated lipid biosynthesis and a defect in skin barrier function.PloS one · 2025Article
- Proteomic insights into breast cancer response to brain cell-secreted factors.Scientific reports · 2024Article
- Genetic disruption of ATAT1 causes RhoA downregulation through abnormal truncation of C/EBPβ.BMB reports · 2024Article
- Article
- Proteomic Assessment of SKBR3/HER2+ Breast Cancer Cellular Response to Lapatinib and Investigational Ipatasertib Kinase Inhibitors.bioRxiv : the preprint server for biology · 2024Article
- Interplay of p62-mTORC1 and EGFR signaling promotes cisplatin resistance in oral cancer.Heliyon · 2024Article
- Transcription Factors in the Pathogenesis of Lupus Nephritis and Their Targeted Therapy.International journal of molecular sciences · 2024Review
- Proteomic assessment of SKBR3/HER2+ breast cancer cellular response to Lapatinib and investigational Ipatasertib kinase inhibitors.Frontiers in pharmacology · 2024Article
47 more citing papers are in PubMed but not listed here.
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
The CCAAT/enhancer-binding proteins (C/EBPs) are a family of leucine-zipper transcription factors that regulate gene expression to control cellular proliferation, differentiation, inflammation and metabolism. Encoded by an intronless gene, C/EBPbeta is expressed as several distinct protein isoforms (LAP1, LAP2, LIP) whose expression is regulated by the differential use of several in-frame translation start sites. LAP1 and LAP2 are transcriptional activators and are associated with differentiation, whereas LIP is frequently elevated in proliferative tissue and acts as a dominant-negative inhibitor of transcription. However, emerging evidence suggests that LIP can serve as a transcriptional activator in some cellular contexts, and that LAP1 and LAP2 might also have unique actions. The LIP:LAP ratio is crucial for the maintenance of normal growth and development, and increases in this ratio lead to aggressive forms of breast cancer. This review discusses the regulation of C/EBPbeta activity by post-translational modification, the individual actions of LAP1, LAP2 and LIP, and the functions and downstream targets that are unique to each isoform. The role of the C/EBPbeta isoforms in breast cancer is discussed and emphasis is placed on their interactions with receptor tyrosine kinases.
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.