CREB3L4
- Known as:
- CREB3L4
- Catalog number:
- 000408A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CREB3L4
Related genes to: CREB3L4
- Gene:
- CREB3L4 NIH gene
- Name:
- cAMP responsive element binding protein 3 like 4
- Previous symbol:
- -
- Synonyms:
- AIbZIP, CREB4, CREB3, hJAL, ATCE1
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-09
- Date modifiied:
- 2016-10-05
Related products to: CREB3L4
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- Calorie restriction (CR) is a well-established non-genetic intervention for lifespan extension in multiple model organisms. Seasonal food shortage in cold and temperate seas may mimic CR, inducing in bivalves a response similar to that in vertebrates and thereby prolonging life expectancy. However, the relationship and the mechanism underlying the food availability and lifespan in bivalves remain largely unexplored. Two closely related scallop species the short-lived warm-water Argopecten irradians (lifespan <2 years) and the longer-lived cold-water Argopecten purpuratus (7-10 years) provide an ideal comparative system to investigate species-specific adaptive strategies. In this study, we subjected both species to CR for 30 and 56 days and performed comparative transcriptomic profiling, weighted gene co-expression network analysis (WGCNA), and physiological assays to elucidate their distinct molecular responses. Transcriptomic analysis revealed that A. purpuratus exhibited substantially more DEGs than A. irradians at both time points under CR, with both species showing downregulation of metabolic pathways but to different extents. A. irradians mounted an early nutrient-sensing response at 30 days (IGF1R, PIK3R3, INSR suppression), indicating acute sensitivity to limitation; by contrast, A. purpuratus displayed delayed FoxO activation at 56 days, along with its downstream effectors NFKBIA, CREB3L4, and SMAD4, suggesting a gradual adaptive program may link to its extended lifespan. WGCNA identified three negatively correlated modules in each species, with coral2 being the most prominent in A. irradians and darkolivegreen in A. purpuratus. The former was dominated by ciliary motility genes, whereas the latter featured coordinated repression of oxidative phosphorylation. Additionally, both species exhibited conserved suppression of mTOR/S6K growth signaling and activation of cellular maintenance programs. Collectively, these findings expand the understanding of CR-mediated longevity regulation in bivalves and provide candidate gene resources for future functional studies and breeding programs. - Source: PubMed
Publication date: 2026/08/10
Zhao YangZhang JilinLiu ChangdaWang ChunyeShao XiangXu XinWang Chunde - Cisplatin resistance remains a major obstacle in the treatment of gastric cancer (GC), and autophagy has been increasingly recognized as a key cytoprotective mechanism contributing to chemoresistance. CREB3L4 is an endoplasmic reticulum membrane-bound transcription factor that has been shown to regulate the expression of Bcl-2 associated athanogene 3 (BAG3), a co-chaperone protein involved in autophagy and survival signaling in various cancers. However, whether the CREB3L4/BAG3 axis regulates autophagy and contributes to cisplatin resistance in gastric cancer cells remains unclear. In the present study, we investigated the roles of CREB3L4 and BAG3 in cisplatin-resistant GC cell lines and found that CREB3L4 and BAG3 were overexpressed. Furthermore, BAG3 expression was inhibited following CREB3L4 knockdown in gastric cancer cells. Notably, knockdown of CREB3L4 inhibited autophagy and alleviated cisplatin resistance in gastric cancer cells by down-regulating BAG3. In addition, silencing of CREB3L4 promoted apoptosis and inhibited cell proliferation, which was also associated with decreased BAG3 expression. Taken together, these findings indicate that depletion of CREB3L4 suppressed autophagy and reduced cisplatin resistance in GC cells by downregulating BAG3. - Source: PubMed
Publication date: 2026/05/07
Yin Wen-KeXie Xue-MeiSong Xiao-YanXiang Yue - Alzheimer's disease (AD) is characterized by progressive neurodegeneration driven by tau and amyloid-β (Aβ) pathology, although the underlying molecular mechanisms remain incompletely understood. Emerging evidence implicates altered DNA methylation (DNAm) in AD but comprehensive analyses in experimental models are limited. Here, we profile DNAm dynamics in two widely used transgenic mouse models of tau (rTg4510) and Aβ (J20) neuropathology, focusing on the entorhinal cortex and hippocampus. Using reduced representation bisulfite sequencing (RRBS) and methylation arrays across multiple disease stages, we identified widespread pathology-associated DNAm alterations in both models. Tau pathology in rTg4510 mice was associated with extensive DNAm remodeling at genes involved in neuronal plasticity, apoptosis, and lipid metabolism, including , , and . In contrast, J20 mice exhibited more modest changes, primarily at immune-related loci such as , , and . Tau-associated DNAm changes were more consistent across brain areas than those associated with Aβ pathology. Comparison with human AD DNAm datasets revealed overlapping DNAm differences, including hypermethylation at and in rTg4510 mice. These findings provide robust evidence for early, pathology-associated epigenetic alterations in AD and highlight the utility of epigenomic profiling in transgenic models for identifying novel targets for early intervention in AD. - Source: PubMed
Publication date: 2026/04/07
Leung Szi KayWalker Emma MPolicicchio StefaniaDahir AishaVellame Dorothea SeilerSmith Adam RSwarbrick RhianLunnon KatieDempster Emma LAhmed ZeshanHannon EilisCastanho IsabelMill Jonathan - Uterine corpus endometrial carcinoma (UCEC) is a common gynecologic malignancy characterized by metabolic reprogramming and immune dysregulation. This study aimed to investigate the prognostic and diagnostic value of lipid metabolism- and oxidative stress-related genes (LMOSGs) in UCEC. - Source: PubMed
Publication date: 2026/04/06
Li HongfengBian JiaZhang QinweiDu QiaoWang YijieShang YapingLi Xuehe - The porcine endometrium undergoes dynamic cellular remodeling across the estrous cycle, yet epithelial heterogeneity and differentiation trajectories remain incompletely characterized. In this study, a single-cell transcriptomic atlas of the endometrial epithelium during the follicular and luteal phases in Meishan pigs was generated using high-resolution single-cell RNA sequencing. Canonical epithelial cell types were identified, including glandular epithelium (GE), secretory glandular epithelium (secretory GE), luminal epithelium (LE), ciliated epithelium, as well as an epithelial stem cell subpopulation marked by ALDH1A3 and LGR5 and a progenitor subpopulation marked by ALDH1A1. During the follicular phase, the epithelium was primarily composed of ALDH1A3+LGR5+ stem cells and ALDH1A1+ progenitor cells, whereas GE, secretory GE, and LE predominated during the luteal phase. Integrated trajectory inference and RNA velocity analyses suggested a continuous differentiation trajectory from ALDH1A3+LGR5+ stem cells through ALDH1A1+ progenitors toward GE. Gene expression patterns indicated that glandular epithelial formation was associated with activation of transcriptional regulatory programs and increased mitochondrial respiratory activity. In contrast, differentiation toward the secretory glandular epithelial lineage was characterized by early activation of stress-response pathways, secretion-related genes, and specific metabolic programs. Several transcription factors, including ZFP36L1, TRPS1, and KLF6, were associated with glandular differentiation, whereas MBD4, CREB3L4, ZNF524, SPDEF, USF1, XBP1, and MLX were predicted to contribute to glandular secretory function. These genes showed significant associations with sow reproductive traits in a phenome-wide association study. Overall, this study provides a single-cell framework for understanding epithelial dynamics in the porcine endometrium across the estrous cycle. - Source: PubMed
Jiang NengjingChen YuejiaYin YanzhenXiao WeiXiao XuemeiMa JinfengLiao XingLiu QianJin XuexiaXu BinBinWang JingZhou TengbinZhao QingboLi PinghuaHuang Ruihua