CEBPG antibody - middle region (ARP35644_P050)
- Known as:
- CEBPG (anti-) - middle region (ARP35644_P050)
- Catalog number:
- arp35644_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CEBPG antibody - middle region (ARP35644_P050)
Related genes to: CEBPG antibody - middle region (ARP35644_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 - middle region (ARP35644_P050)
Related articles to: CEBPG antibody - middle region (ARP35644_P050)
- The integrated stress response (ISR) coordinates cellular adaptation to diverse stress conditions. In Drosophila, two bZIP transcription factors, Xrp1 and crc (ATF4 homolog), are induced during ISR. Crc protein can dimerize with two CEBP factors in vitro, but the in vivo relevance of those interactions remained unknown. Here, we report that the CEBPG homolog, Irbp18, is an essential partner of crc during ISR. Specifically, Irbp18 is broadly required for the transcriptional induction of ISR target genes in the photoreceptors of ninaE, a Drosophila model of retinitis pigmentosa. Moreover, CUT&RUN analysis indicates that Irbp18 loss reduces or abolishes crc binding to target DNAs in photoreceptors and impairs crc's ability to induce target transcripts upon overexpression. Functionally, Irbp18 loss causes retinal degeneration and suppresses ISR signaling in parkin mutants, a model of Parkinson's disease. Together, these findings identify Irbp18 as a cofactor for crc, impacting pathological outcomes in Drosophila models of degeneration. - Source: PubMed
Publication date: 2026/07/27
Mitra SahanaHuang Huai-WeiFaruk RhihabLow ArissaYeo Adam IRyoo Hyung Don - This study focused on developing a novel nanodelivery system, BP-PEG-S2P@H, with hesperetin-loaded black phosphorus nanosheets to target tumor-associated macrophages (TAMs) in triple-negative breast cancer (TNBC). Through RNA sequencing and proteomic analyses, CEBPG upregulation was observed in TAMs, potentially controlling the SLC7A11-mediated ferroptosis pathway. and experiments, including FerroOrange and malondialdehyde assays, demonstrated the induction of ferroptosis by BP-PEG-S2P@H. The nanoplatform facilitated the transition of TAMs from the M2 to the M1 subtype, enhancing IL-12 secretion while reducing IL-10 levels. Functional analyses confirmed the reversal of the pro-migratory TAM phenotype and inhibition of tumor cell invasion. imaging validated efficient tumor targeting, with immunohistochemical staining revealing decreased CEBPG/SLC7A11 expression in tumors, reduced macrophage infiltration, and enhanced CD8 T cell activation, promoting the efficacy of PD-L1 immunotherapy. Biosafety assessments indicated no apparent toxicity, supporting the potential of the BP-PEG-S2P@H nanoplatform for TAM-targeted nano-immunotherapy in TNBC. - Source: PubMed
Publication date: 2026/05/29
Feng LiangWang HuanLiang ZuodiTian YingGuo YangLi Zhuo - Fatty acids (FAs) create a pro-metastatic niche in multiple cancers, but how the tumor microenvironment (TME) counteracts FA stress remains unclear. Here, we found that the FA transporter CD36 was upregulated in myofibroblastic cancer-associated fibroblasts (myoCAFs), where it correlated with the metastasis of oral squamous cell carcinoma (OSCC). Among five predominant FA species enriched in OSCC tissues, palmitic acid (PA) potently activated myoCAF phenotypes across 2D, 3D, and organoid co-culture models. In vivo, PA promoted lymph node metastasis in orthotopic tumors comprising OSCC cells and CAFs, an effect abolished by CD36 knockdown in cancer-associated fibroblasts (CAFs). Mechanistically, PA remodeled the chromatin landscape to enhance H3K27ac occupancy at multiple genes including ERN1 and TMBIM6, two stress-adaptive regulators. Transcription of ERN1 and TMBIM6 in CAFs was regulated by CCAAT/enhancer-binding protein γ (CEBPG) in an enhancer-associated manner. Disruption of the CEBPG-IRE1α/TMBIM6 axis attenuated myoCAFs properties and abrogated PA-driven metastasis. Our results unveil a stromal metabolic checkpoint and establish CEBPG-mediated stress resilience as a therapeutic target to curtail metastasis. Significance: Palmitic acid promotes metastasis via a stromal CEBPG-IRE1α/TMBIM6 axis, uncovering a metabolic vulnerability that offers novel therapeutic targets to inhibit oral squamous cell carcinoma. - Source: PubMed
Publication date: 2026/06/02
Duan YilingLi YitongWu YufeiYang XiaoLi RuiZhao HuiShang Zhengjun - 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