Ask about this productRelated genes to: CEBPD Blocking Peptide
- Gene:
- CEBPD NIH gene
- Name:
- CCAAT enhancer binding protein delta
- Previous symbol:
- -
- Synonyms:
- CRP3, CELF, C/EBP-delta, NF-IL6-beta
- Chromosome:
- 8q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1992-06-24
- Date modifiied:
- 2018-02-23
Related products to: CEBPD Blocking Peptide
Related articles to: CEBPD Blocking Peptide
- B-cell acute lymphoblastic leukemia (B-ALL) is a heterogeneous malignancy driven by diverse genetic alterations. Among these, family genes and are recurrently involved, yet the spectrum of genomic mechanisms and their clinical impact remain incompletely defined. Integrated genomic analyses of a cohort of 992 Philadelphia-negative adult B-ALL patients revealed multiple mechanisms of enhancer hijacking-mediated deregulation of , , , and , including and several non- fusions, as well as noncoding mutations in regulatory regions. Combined with gene expression analysis, we identified three distinct subtypes, defined by co-occurring and p.H1038R alterations (CEBP/ZEB2, = 18 cases); isolated alterations (CEBPalt, = 43), associated with frequent deletions and deregulation; and isolated p.H1038R mutation (ZEB2alt, = 15), associated with various additional genomic hits targeting and enhancing mutant expression. The three subtypes exhibited distinct clinical features, including age distribution (patients with CEBP/ZEB2 and ZEB2alt B-ALL were younger) and sex bias (female and male predominance in CEBPalt and ZEB2alt, respectively). Early treatment responses and outcomes also differed: patients with CEBP/ZEB2 B-ALL had a favorable early response, in contrast to patients with ZEB2alt B-ALL, who had high levels of minimal residual disease and a dismal prognosis. Collectively, our findings define and alterations as drivers of genetically and clinically distinct subtypes of adult B-ALL and provide a rationale for subtype-specific risk stratification. Preclinical experiments in CEBPalt B-ALL patient-derived xenografts demonstrated sensitivity to FLT3 inhibition, highlighting a potential therapeutic vulnerability. - Source: PubMed
Publication date: 2026/06/15
Kim RathanaPasset MarieBergugnat HugoVasseur LoïcLeguay ThibautHuguet FrançoiseHunault MathildeSexton TomBenlebna MelhaRenard JulieRaffoux EmmanuelPastoret CédricErb CathieChat LaureenDelabesse EricGachet StéphanieBonmati CarolineBalsat MarieBraun ThorstenBidet AudreyDuployez NicolasGraux CarlosChalandon YvesRousselot PhilippeChevallier PatriceSoulier JeanLhéritier VéroniqueDombret HervéBoissel NicolasClappier Emmanuelle - Ischemia-reperfusion injury (IRI) significantly impacts post-kidney transplantation (KTx), leading to delayed graft function (DGF) and potential graft loss. Current biomarkers and therapies for DGF and graft survival are inadequate. Immune cell infiltration after renal IRI is crucial in driving inflammation and injury. - Source: PubMed
Zhang YifeiLi YuqingQiu XuemengWu JiyueBi QingCao PengZhang JiandongWang Wei - Triple-negative breast cancer is marked by extensive cellular heterogeneity and limited availability of actionable targeted treatments, which contributes to an unfavorable prognosis. In this work, single-cell and spatial transcriptomic profiling was integrated with network-based analyses and machine-learning approaches to characterize malignant epithelial programs in TNBC and to pinpoint prognostic biomarkers.Single-cell RNA sequencing identified a malignant epithelial subpopulation, Luminal_inflam, characterized by elevated inferred copy number variation, a terminal pseudotime state, and enrichment of cell cycle-associated transcriptional programs. Cell-cell communication analysis indicated microenvironmental remodeling in TNBC and prioritized a fibroblast-associated S100A4-EGFR axis that may regulate Luminal_inflam-associated gene expression. Gene regulatory network analysis further revealed increased activities of transcription factors including MYBL2, TFDP1, CEBPD, and MBD2. A 12-gene risk signature constructed from Luminal_inflam-associated modules and survival cohorts effectively stratified overall survival and captured differences in immune features and potential drug sensitivities. In our MDA-MB-231 model, RPN1 knockdown was associated with reduced cell viability, which could be partially rescued by 4-PBA. We further found that RPN1 depletion was accompanied by increased intracellular ROS and Ca levels, altered cell-cycle distribution, and elevated apoptosis, and that these changes were also partially reversible upon 4-PBA treatment. These data support the view that loss of RPN1 perturbs ER homeostasis and is linked to stress-associated cell fate changes in TNBC cells. At the same time, these findings should be interpreted in the context of prior work showing that RPN1 depletion can induce ER-stress-dependent apoptosis in breast cancer models. Thus, rather than establishing an entirely new mechanism, our study extends previous observations by connecting this stress-related phenotype to a specific malignant epithelial program and a clinically derived risk framework.Collectively, this study delineates a key malignant epithelial state in TNBC and suggests that RPN1-associated proteostasis vulnerability may represent a potential therapeutic opportunity. - Source: PubMed
Publication date: 2026/06/11
Wu JinpengFan JingjingSha TongLi Hongtao - Radiofrequency ablation (RFA) is becoming a standard treatment for early-stage hepatocellular carcinoma (HCC). However, high rates of postoperative recurrence, particularly following insufficient RFA (iRFA), remains a clinical obstacle. iRFA contributes to the formation of an immunosuppressive tumor microenvironment and facilitates tumor progression, though the molecular mechanisms driving these processes are not fully elucidated. This study seeks to comprehensively characterize the spatial architecture and cellular interactions within iRFA HCC, and to identify key transcriptional mechanisms through which sublethal heat stress promotes immune evasion and recurrence. - Source: PubMed
Publication date: 2026/06/08
Lin KeZhang NanZhang ZongxuZhou XinweiQiao BinDaopeng YangGuo JianpingZeng ZexianXie XiaoyanBowen Zhuang - Rising temperatures driven by global warming and industrial thermal pollution are threatening the survival of both wild and farmed fish, which has emerged as one of the central concerns in international aquaculture. Understanding the physiological and behavioral responses of fish to heat exposure is critical for enhancing their survival. However, most studies rely on bulk-omic analyses at the tissue level which fail to reveal cellular heterogeneity. In the present study, ultrastructural observation and single-nuclei RNA sequencing (snRNA-seq) were applied to systematically study the physiological changes and the mechanisms of the Hucho bleekeri under acute heat stress. Histological analysis showed focal hemorrhage and lamellae broken in gill after heat stress. Ultrastructural observation revealed that after heat exposure, gill epithelial cells shed and the morphology of cell organelle damaged in pavement and mitochondria-rich cells. SnRNA-seq of gill generated 28 clusters, with the number of cells in each cluster ranging from 129 to 5590. After heat stress, epithelial (GobC) and endothelial cell proportion decreased significantly while neutrophil increased. Specifically, the change of cell proportion and pseudotime analysis indicated the occurrence of endothelial-to-mesenchymal transition during heat stress, and the expression of inflammation-related genes increased along the pseudotime axis. Differentially expressed genes (DEGs) analysis revealed that genes in heat shock protein and haemoglobin families were up-regulated in most cell type, whereas each cell also displayed specific DEGs profiles. Transcription factors analysis revealed increased activity of CEBPD, JUNB and CEBPA in most of the cell type after heat stress. Cell communication analysis showed interactions of CXCL12A-CXCR4B as well as CLDN11A-CLDN11A after heat stress. In addition, the results of snRNA-seq were validated through real-time PCR and fluorescence in situ hybridization analysis. Our study provides insights into cellular heterogeneity and physiological changes of H. bleekeri in response to heat stress, and lay a foundation for future studies on the mechanism of environmental stress on salmonid fish. - Source: PubMed
Publication date: 2026/06/06
Chen YeyuWei QinyaoWu XiaoyunYang HuanchaoLiu ZhaoChen YanlingYu YiTu QuanyuLiu GuiliangLi Hua