CEBPG antibody - N-terminal region (ARP35645_P050)
- Known as:
- CEBPG (anti-) - N-terminal region (ARP35645_P050)
- Catalog number:
- arp35645_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CEBPG antibody - N-terminal region (ARP35645_P050)
Related genes to: CEBPG antibody - N-terminal region (ARP35645_P050)
- Gene:
- CEBPG NIH gene
- Name:
- CCAAT enhancer binding protein gamma
- Previous symbol:
- -
- Synonyms:
- GPE1BP, IG/EBP-1
- Chromosome:
- 19q13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1992-07-08
- Date modifiied:
- 2018-02-23
Related products to: CEBPG antibody - N-terminal region (ARP35645_P050)
Related articles to: CEBPG antibody - N-terminal region (ARP35645_P050)
- CD8 T cells need to function in complex environments with varied nutrient availability, including the tumor microenvironment and inflamed tissues. The mechanisms that allow CD8 T cells to maintain immune function in these perturbed settings are poorly understood. Here, we show that CD8 T cells adapt to nutrient stresses over time, reconfiguring gene-regulatory and metabolic networks to license functional recovery. Under acute stress, T cells reoriented translational programming, which limited nutrient demand and prioritized stress-sensitive metabolic and transcriptional responses. Within these responses, the transcription factors activating transcription factor 4 (ATF4) and CCAAT/enhancer-binding protein gamma (CEBPG) jointly established an adaptive metabolic program, promoting amino acid synthesis and uptake while maintaining mitochondrial metabolism. Despite diminished energetic capacity under environmental stress, this program sustained central carbon metabolism. This subsequently mitigated cellular dysfunction and potentiated anti-tumor immunity. Altogether, we demonstrate that biosynthetic plasticity via translational and metabolic reprioritization confers T cell resilience in unfavorable environments, offering potential strategies to enhance immunotherapies. - Source: PubMed
Publication date: 2026/04/29
Scaglione MichaelKnight MontanaTrihemasava KrittinRome KellyArchambault Anne-SophieOh JuheeTanaka ErinHall EliseVan Le Tran NgocLines Caleb LGoldspiel BrianFazelinia HosseinQueriault ClemenceTurner LucienParnaik TanayXu JimmyBrown MorganBardhan OishiAxsom JessieBennett Frederick CSpruce Lynn ABartman CarolineMesaros ClementinaKlein Geltink Ramon IConn Crystal SBailis Will - Colorectal cancer (CRC) ranks among the most prevalent gastrointestinal malignancies with liver metastasis being the primary cause of CRC-related death. Although surgical and chemotherapeutic interventions continue to improve, patients with hepatic metastases frequently experience recurrence and limited treatment benefits. Liver metastasis is driven by tumor heterogeneity and immune evasion. Therefore, defining the cellular composition of CRC liver metastases may help identify new therapeutic targets. - Source: PubMed
Publication date: 2026/03/25
Zhu GuangshengLiu YaShi YunxuanQian NuanSong ChengchengLiu XuXiahou ZhikaiXiong ZhiguoHu Junjie - Dysregulation of phospholipid metabolism has been increasingly recognized as a critical contributor to colorectal cancer (CRC) progression; however, the key molecular determinants governing this process remain incompletely defined. In this study, we identify CDP-diacylglycerol synthetase 1 (CDS1) as a central player in CRC pathogenesis and systematically elucidate its functional mechanism. Through an integrated approach combining bioinformatic analysis of TCGA datasets with extensive experimental validation using in vitro cellular models and in vivo tumor systems, we demonstrate that CDS1 expression is significantly downregulated in CRC tissues. Functional studies reveal that loss of CDS1 promotes tumor growth in an immune microenvironment-dependent manner. Mechanistically, CDS1 catalyzes the synthesis and secretion of CDP-diacylglycerol (CDP-DAG), which binds to transcription factor CEBPG and induces ferroptosis in myeloid-derived suppressor cells (MDSCs). This process effectively alleviates MDSC-mediated immunosuppression, leading to enhanced infiltration and activation of cytotoxic T lymphocytes within the tumor microenvironment. Furthermore, we show that CDP-DAG exhibits synergistic effects with anti-PDL1 therapy, significantly enhancing antitumor immune responses. These findings establish the CDS1/CDP-DAG signaling axis as a novel immunometabolic checkpoint in CRC, providing important insights into the interplay between phospholipid metabolism and antitumor immunity. The study highlights the potential of targeting this pathway for both diagnostic and therapeutic applications in CRC immunotherapy. - Source: PubMed
Publication date: 2025/10/27
Li ChongLiu WeiZhang YanyanYu ShaohongLi Dejia - The regulatory mechanisms governing transcriptional programs in the cancer genome remain elusive, particularly those concerning cell-type specificity. We carefully curated single-cell assay for transposase-accessible chromatin sequencing (scATAC-seq) and single-cell RNA sequencing (scRNA-seq) data from eight distinct carcinoma tissues, including breast, skin, colon, endometrium, lung, ovary, liver, and kidney. Using single-cell multi-omics analysis, we identified extensive open chromatin regions and constructed peak-gene link networks, which can reveal distinct cancer gene regulation and genetic risks. We further explored conserved epigenetic regulation across cell types within cancer and elucidated their functional implications. Moreover, we identified cell-type-associated transcription factors (TFs) that regulate key cellular functions, such as the TEAD family of TFs, which widely control cancer-related signaling pathways in tumor cells. In colon cancer, we further identified tumor-specific TFs that are more highly activated in tumor cells than in normal epithelial cells, including CEBPG, LEF1, SOX4, TCF7, and TEAD4, which are pivotal in driving malignant transcriptional programs and represent potential therapeutic targets, as corroborated by single-cell sequencing data from multiple sources and in vitro experiments. Our findings provide a comprehensive understanding of the regulatory dynamics underlying carcinomas and offer valuable insights into potential therapeutic interventions. - Source: PubMed
Publication date: 2025/10/21
Tang XiaoweiZhang QiaolingShen ZichuXiao JianLi MinghaoMeng XiangyanWang ChenyiZhang GuangzeLiu AnhangYin Yuxin - Pancreas fat deposition, measured by pancreatic proton density fat fraction (PDFF) in the MRI, has emerged as a critical area of research within the metabolic field. However, its genetic basis and how genetic predisposition impacts the pancreatic disorders remain poorly understood. - Source: PubMed
Publication date: 2025/07/26
Chen HaotianBai XiaoyinLiu ZhengyeDu HanzeChen XiaoliWu DongMi Jiarui