ELK1 Luciferase Reporter Vector
- Known as:
- ELK1 Luciferase Reporter Vector
- Catalog number:
- LR0019
- Product Quantity:
- 10 ug
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- ELK1 Luciferase Reporter Vector
Related genes to: ELK1 Luciferase Reporter Vector
- Gene:
- ELK1 NIH gene
- Name:
- ETS transcription factor ELK1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- Xp11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2019-01-21
Related products to: ELK1 Luciferase Reporter Vector
Related articles to: ELK1 Luciferase Reporter Vector
- Numerous neurological deficiency disorders are caused by the thyroid hormones' early-life modulatory actions, which persist throughout adulthood. Pairing-pulse facilitation is used to assess hippocampal short-term plasticity, while long-term potentiation (LTP) is used to assess long-term plasticity. Thyroid hormones target the genes that cause synaptic plasticity to occur. This study focused on the non-genomic effects of T4 hormone in the hippocampus. - Source: PubMed
Publication date: 2026/02/11
Bitiktaş SonerSüer CemAltuntaş Hamiyet Dönmez - Myofiber type determines meat quality by governing postmortem glycolytic potential and lactate-driven pH decline. However, whether endogenous lactate actively regulates myofiber type through epigenetic signaling remains unknown. Here, we found that histone H3 lysine 27 lactylation (H3K27la), a modification driven by lactate, is a critical regulator of myoblast differentiation. Elevating lactate enhanced differentiation and H3K27la levels in myoblasts. Multi-omics analyses revealed that H3K27la enrichment is associated with transcriptional repression of the member of RAS oncogene family (RAP2C) during goat myoblast differentiation. This inactivation of the RAP2C-ERK-ELK1 signaling axis subsequently upregulates myosin light chain, phosphorylatable, fast skeletal muscle (MYLPF), thereby promoting glycolytic myofiber specification. Our study uncovers a lactate-H3K27la regulatory axis that translates the metabolic state of developing muscle into an epigenetic signal that orchestrates myofiber type, providing profound insights into the early-life programming of myofiber determination and meat quality. - Source: PubMed
Publication date: 2026/04/20
Zhang ZhenZhou XiaohuaHuang XinaiYang YueDeng KaipingZhou JunLiu ZhipengLi JingzhengLi DongxuEl-Samahy M AZhang GuominFan YixuanWang Feng - Dual-specificity phosphatase 5 (DUSP5) is a key regulator of the mitogen-activated protein kinase (MAPK) pathway, with established roles in various types of cancer. However, its function in esophageal squamous cell carcinoma (ESCC) remains unclear. This study combines single-cell transcriptomics with in vitro and in vivo models to investigate the role of DUSP5 in ESCC. Single-cell RNA sequencing revealed tumor-infiltrating myeloid populations, including apolipoprotein C-positive (APOC⁺) macrophages, which interact with tumor cells via the amphiregulin-epidermal growth factor receptor (AREG-EGFR) axis, activating MAPK/extracellular signal-regulated kinase (ERK) signaling to promote tumor growth and immune modulation. We identified a prognostic gene signature linked to these macrophages. DUSP5 expression was downregulated in ESCC tissues, and its overexpression inhibited cell proliferation, induced senescence and apoptosis, and suppressed migration and invasion. In mouse xenografts, overexpression of DUSP5 reduced tumor growth and metastasis. Mechanistically, DUSP5 inhibited ERK1/2 activation, and its tumor-suppressive effects were reversed by ERK1/2 activation. Moreover, ETS Like-1 protein (ELK1), an ERK1/2 downstream transcription factor, was identified as a negative regulator of DUSP5. In a carcinogen-induced model, DUSP5 knockout increased tumor burden, effects reversed by ERK1/2 inhibition. Our findings indicate that the DUSP5-ERK1/2-ELK1 signaling axis, modulated by tumor-infiltrating myeloid cells, contributes to ESCC progression and represents a promising source of biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/04/10
Huang XuXu WenyiYou RunzeKuang JunjieZhu KaiLi JunLi JingzhangErtas Yavuz NuriMa QiuhongTian MaojinLin Miao - Colon cancer harboring TP53 mutations is highly aggressive and associated with short survival. Adaptive, rather than apoptotic, endoplasmic reticulum (ER) stress endows TP53-mutant tumor cells with enhanced protein-folding capacity, metabolic plasticity, and chemoresistance. However, the upstream regulators that selectively drive this cytoprotective program within the cancer stem cell compartment remain elusive. - Source: PubMed
Publication date: 2026/03/19
Zhang LifenGao YangXu JingjingYe JiahaoWen YouleLi TianHe Weiling - Ferroptosis, an iron-dependent form of programmed cell death driven by toxic lipid peroxide accumulation, plays a critical role in various diseases, making its modulation a promising therapeutic strategy. In this study, we identified defactinib, a specific inhibitor of FAK as a novel ferroptosis suppressors. We demonstrate that FAK/SRC-JNK signaling positively regulates ferroptosis by upregulating ACSL4, a critical mediator of ferroptosis. We reveal that a subset of JNK downstream transcription factors, including ATF2, NFATC1, NFATC3, and SMAD4, promote ferroptosis through direct binding to the ACSL4 promoter and activation of its expression. In contrast, another subset of JNK-associated transcription factors, including c-Jun, STAT3, ELK1, and HSF1, inhibit ferroptosis by binding to the ACSL4 promoter and repressing its expression. The net effect of FAK/SRC-JNK signaling in our models is a significant upregulation of ACSL4 and promotion of ferroptosis. Notably, elevated FAK/SRC-JNK signaling sensitizes cancer cells to ferroptosis-inducing therapies, while inhibition of the FAK/SRC-JNK signaling pathway protects against acute pancreatitis by suppressing ferroptosis. These findings highlight the central role of FAK/ SRC-JNK signaling in controlling ferroptotic cell death and underscore the therapeutic potential of targeting FAK/ SRC-JNK mediated ferroptosis, offering new avenues for the treatment of cancer and acute pancreatitis. - Source: PubMed
Publication date: 2026/03/20
Qin JianhuaMa ShuangWang JunyangHuang SiyuanLuan JingHe JiyuanHou GuoyuanSun NaZhang WeiGao Minghui