CEBPE pThr74 antibody Ab
- Known as:
- CEBPE pThr74 (anti-) Antibody
- Catalog number:
- 1488059
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- CEBPE pThr74 antibody
Related genes to: CEBPE pThr74 antibody Ab
- Gene:
- CEBPE NIH gene
- Name:
- CCAAT enhancer binding protein epsilon
- Previous symbol:
- -
- Synonyms:
- CRP1
- Chromosome:
- 14q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-06-24
- Date modifiied:
- 2019-04-23
Related products to: CEBPE pThr74 antibody Ab
Related articles to: CEBPE pThr74 antibody Ab
- We previously showed that deficiency in myeloid cells promotes proliferation, impairs differentiation and inhibits apoptosis, but its role and underlying mechanism in acute myeloid leukemia (AML) are unknown. Here, in NB-4 cells, an M3 subtype of AML, overexpression suppressed proliferation ( < 0.001), induced S-phase arrest (from 35.35% to 19.47%, < 0.001), increased apoptosis (from 10.37% to 23.5%, < 0.001), and promoted differentiation. Mechanistically, overexpression upregulated and at the mRNA and protein levels; conversely, knockdown downregulated both. Rescue experiments in knockdown 32Dcl3 cells showed that ectopic or reversed the uncontrolled proliferation, blocked apoptosis, and impaired differentiation. In xenograft mouse models, overexpression reduced leukemic infiltration in the bone marrow, spleen, and liver; extended overall survival; and elevated and expression in vivo. Analysis of public APL datasets revealed that high expression is associated with a favorable prognosis (HR = 0.43, 95% CI: 0.2-0.93, logrank = 0.028). Collectively, our findings demonstrate that suppresses proliferation, promotes apoptosis and differentiation, and attenuates disease progression by upregulating and , positioning this regulatory mechanism as a potential therapeutic target and prognostic biomarker for this disease. - Source: PubMed
Publication date: 2026/06/15
Yang TaomeiWan YonghuChu ChunweiChen Xiangyun - 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 - IDH1 and IDH2 are frequently mutated in various cancers, including acute leukemias. However, the distinct mechanisms by which mutant IDH1 or IDH2 drive hematopoietic neoplasms remain poorly understood. Here, we analyzed DNA methylation in IDH1- and IDH2-mutant AML and found neutrophil lineage-specific epigenetic alterations in IDH1-mutant cases that went along with severely impaired neutrophil differentiation. Transcriptional analysis of normal hematopoiesis in humans and mice revealed a strong physiological upregulation of IDH1/Idh1 in myeloid progenitors. To study the functional effects of Idh1 mutations on hematopoiesis in a pre-leukemic setting, we used a genetically engineered inducible mouse model expressing a heterozygous Idh1 mutation under control of the endogenous promotor. Our study revealed a cell-intrinsic block in neutrophil differentiation caused by repression of myeloid transcription programs in neutrophil progenitors. This included impaired expression of Cebpe, which encodes a key transcription factor regulating neutrophil differentiation. Reactivation of Cebpe expression, by overexpression of its upstream regulator Cebpa or following treatment with hypomethylating agents restored differentiation, indicating that the differentiation block is reversible.In summary, we found a reversible, pre-leukemic impairment of neutrophil differentiation in IDH1-mutant hematopoiesis that correlates with elevated IDH1 expression in myeloid progenitors and likely explains the strong association of IDH1 mutations with myeloid neoplasms. - Source: PubMed
Publication date: 2026/05/26
Hakobyan MariamLangstein JensRamos Medina María JoséKleinert EmelySchönung MaximilianHartmann MarkRohdjess HannahWojtarowicz JessicaStaeble SinaTüre MelissaPobiedonoscew YasmineClaus RainerBullinger LarsOakes Christopher CZoldan KatharinaCross MichaelPlatzbecker UweKneisel NiclasRaffel SimonGerming UlrichHoermann GregorHaas SimonRippe KarstenFröhling StefanPusch StefanPlass ChristophMilsom Michael DLipka Daniel B - Neutrophils are short-lived cells of the innate immune system that play numerous roles in defense against infection, regulation of immune responses, tissue damage and repair, autoimmunity, and other non-communicable diseases. Understanding neutrophil function at a mechanistic level has been hampered by the difficulty of working with primary neutrophils, which die rapidly upon isolation, and the relative paucity of neutrophil cell lines. Here, we report the creation of a Cas9 +ER-Hoxb8 neutrophil progenitor cell line that enables both forward and reverse genetic analysis of neutrophils. By editing progenitors via transduction with sgRNAs and then withdrawing estrogen, Cas9-edited neutrophils are produced with high efficiency. Importantly, neutrophil differentiation of edited progenitors occurs both in vitro in cell culture and when transferred into murine recipients. To demonstrate the utility of Cas9 +ER-Hoxb8 progenitors for forward genetics, we performed a pooled CRISPR screen to identify factors required for survival during neutrophil differentiation. This screen identified hundreds of genes, including , a transcription factor known to be required for neutrophil differentiation from pre-neutrophils to immature neutrophils. Using this progenitor cell line, we confirmed that is required for neutrophil differentiation in vivo, validating the utility of this line for studying in vivo phenotypes. The screen also identified all components of the WASH complex as being required for neutrophil differentiation, extending its known role in hematopoietic stem cell differentiation to later stages of neutrophil development. Taken together, this resource enables the analysis of the role of neutrophils in numerous disease states using genetics for the first time. - Source: PubMed
Publication date: 2026/05/18
Jong Robyn MChing Krystal LGarelis Nicholas EZilinskas AlexWrynla Xammy HuuRawal SagarHill Bianca CLuckie Bridget AShallow LillianCox Jeffery SBarton Gregory MStanley Sarah A - Chemotherapy-induced neutropenia (CIN) remains a major dose-limiting toxicity associated with myelosuppressive chemotherapy regimens. The development of therapeutic strategies capable of effectively restoring neutrophil production and function could address a critical unmet clinical issue. ZGSII, a bioactive compound derived from , has shown potential in ameliorating leukopenia. To further evaluate its therapeutic applicability for CIN, a comprehensive understanding of its underlying mechanisms is essential. This study aims to assess the efficacy of ZGSII in mitigating cyclophosphamide-induced neutropenia and myelosuppression and to elucidate the underlying mechanism involved through transcriptome sequencing, protein-protein interaction network construction, and functional validation assays. - Source: PubMed
Publication date: 2026/02/26
Li LingdiLei HuanChen LuqiCao ChunyeHe HaolinZhang YanfengZhang LinPeng LiangYang YuxiuFeng YulinFang Haihong