Ask about this productRelated genes to: SREBF1 antibody
- Gene:
- SREBF1 NIH gene
- Name:
- sterol regulatory element binding transcription factor 1
- Previous symbol:
- -
- Synonyms:
- SREBP1, bHLHd1, SREBP-1c, SREBP1a
- Chromosome:
- 17p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-23
- Date modifiied:
- 2016-02-03
Related products to: SREBF1 antibody
Related articles to: SREBF1 antibody
- Bladder cancer progression is frequently accompanied by metabolic reprogramming and immune escape, yet how these processes are coupled remains unclear. Sterol regulatory element-binding transcription factor 1 (SREBF1) governs lipid homeostasis and is often deregulated in cancer. We find that SREBF1 is upregulated in human bladder tumours and associates with invasion, metastasis and poor patient outcome, critically, it sustains tumor growth by driving immune evasion. Mechanistically, SREBF1 directly interacts with the SUMO E3 ligase TRIM28, which catalyses SUMO2 conjugation of SREBF1 at K470, antagonizes K48-linked ubiquitination and stabilizes SREBF1. TRIM28 further enhances SREBF1 occupancy at the MGAT4A promoter and upregulates MGAT4A, thereby promoting N-linked glycosylation of PD-L1, which stabilizes PD-L1 and increases its plasma-membrane localization, dampening CD8 + T-cell cytotoxicity. In immunocompetent mice, TRIM28 knockdown reduces tumor growth, lowers PD-L1 and increases CD8 + T-cell infiltration-effects reversed by SREBF1 overexpression; in an immune-augmented human PDX model, SREBF1 targeting synergizes with anti-PD-1 without overt toxicity. These findings identify a TRIM28-SREBF1-MGAT4A axis that couples lipid metabolic rewiring to immune-checkpoint regulation via PD-L1 N-glycosylation, positioning SREBF1 as a biomarker for BCa progression and risk stratification and as a druggable node to potentiate PD-1 blockade. - Source: PubMed
Publication date: 2026/05/18
Chen RuSu YuzheChen JianhuiZhu ShaoxingChen XiaobaoSu Yiming - Fatty liver is a common metabolic disease in dairy cows during early postpartum period, which is characterized by excessive hepatic triacylglycerol (TAG) accumulation. However, the mechanisms of bile acid (BA) metabolism in dairy cows experiencing fatty liver remain poorly elucidated. The farnesoid X receptor () plays a critical role in the regulation of BA homeostasis. Consequently, the aim of this study was to investigate the effect of -mediated BA metabolism following stimulation with high concentrations of free fatty acids (FFA). - Source: PubMed
Publication date: 2026/04/30
Jia BinTian YanGao ChanghongChang YaqiZhang ZexinSong YuxiXia ChengQu YongliYang Wei - Aneurysm progression is associated with complex molecular alterations that are insufficiently studied at transcriptomics level. An aneurysm is characterized as a bulge or a weak spot in a blood artery's wall that causes the vessel to abnormally enlarge or balloon, exceeding 50% of its normal diameter. In the present study aneurysm RNA sequencing (RNA-Seq) dataset involving 14 samples, which include 7 controls and 7 treatments was selected for the analysis. Pathway analysis showed the involvement of key genes in major shifts within lipid metabolism pathways. The protein-protein interaction (PPI) network analysis using the STRING database identified key hub genes that were significantly differentially expressed, including LIPE, SREBF1, SCARB2, LPL, PNPLA2, UCP1, CIDEC, DGAT2, CIDEA and FABP4. These key gene-encoded proteins may be prominent drug targets for future interventions aimed at treating aneurysms. - Source: PubMed
Publication date: 2026/03/31
Lois G ShirleyMurugan ShanmugapriyaJaganathan Mohana ShanmugamS Dhanush KumarJ Jino Blessy - Postmenopausal Osteoporosis (PMOP) is an age-related disease prevalent among elderly women, characterized by decreased bone density and increased fracture risk. This study investigates the mechanisms of traditional Chinese medicine (TCM) in treating PMOP. - Source: PubMed
Publication date: 2026/05/08
Xiao HefangWang YaobinChen YiGeng BinXia Yayi - Malignant melanoma remains a formidable clinical challenge due to its propensity for metastasis and therapeutic resistance. Identifying molecular targets that regulate malignant melanoma progression is critical for developing effective therapies. In this study, we investigated the role of cysteine-rich intestinal protein 1 (CRIP1), a novel oncogene, in melanoma progression. CRIP1 expression was analyzed using public datasets, and functional roles of CRIP1 in proliferation, colony formation, migration, and invasion were assessed via overexpression cell models. Mechanistic insights were gained through RNA sequencing, bioinformatics, 4-phenylbutyric acid (4-PBA) or N-acetylcysteine (NAC) treatment, Western blot, dual-luciferase reporter, and chromatin immunoprecipitation (ChIP). Xenograft models were used to confirm in vivo effects. CRIP1 was significantly upregulated in melanoma tissues, particularly in metastases, and correlated with an endoplasmic reticulum (ER) stress gene signature. CRIP1 overexpression promoted malignant phenotypes in vitro and tumor growth in vivo, which was dependent on the activation of ER stress. Integrative analysis identified SREBF1 (Sterol Regulatory Element Binding Transcription Factor 1) as a downstream target. CRIP1 increased intracellular ROS levels by promoting SREBF1 expression, thereby activating ER stress and promoting malignant phenotypes in melanoma cells. Mechanistically, CRIP1 promoted NFATC2 (nuclear factor of activated T cells 2) binding to the SREBF1 promoter to drive transcription of SREBF1. These findings indicate that CRIP1 serves as a critical driver of melanoma progression through ER stress activation and identify a novel CRIP1/NFATC2/SREBF1 axis, providing insights into the role of CRIP1 in melanoma biology and presenting new potential therapeutic targets for this aggressive malignancy. - Source: PubMed
Publication date: 2026/05/13
Yu TingSu YongfengZou Ping'anJian YanWang Yaqi