Elk1 (Phospho_Ser389) Antibody
- Known as:
- Elk1 (Phospho_Ser389) Antibody
- Catalog number:
- E011037-1
- Product Quantity:
- 50ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- Elk1 (Phospho_Ser389) Antibody
Related genes to: Elk1 (Phospho_Ser389) Antibody
- 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 (Phospho_Ser389) Antibody
Related articles to: Elk1 (Phospho_Ser389) Antibody
- (1) Different classes of antidepressant drugs have been shown to activate lysophosphatidic acid (LPA) receptors, but their effects on the receptor signaling stimulated by LPA have not been fully investigated. In the present study, we examined the effect of the tricyclic antidepressant amitriptyline on the LPA-induced activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) and Rho signaling in C6 glioma cells and cultured rat astrocytes. (2) LPA receptor signaling was investigated by using Western blot and microscopic immunofluorescence assays. Rho activation was determined by a pull-down assay. (3) Amitriptyline potentiated the LPA-induced activation of ERK1/2 signaling, as indicated by the more than additive increases in the phosphorylation/activation of key components of this pathway including fibroblast growth factor 1 receptor, MEK1/2, ERK1/2, Elk-1, and cyclic AMP response element binding protein (CREB). Amitriptyline also enhanced the expression of brain-derived neurotrophic factor (BDNF) elicited by LPA. In contrast, the antidepressant failed to mimic the LPA-induced activation of Rho and Rho-dependent responses, such as the reversal of astrocyte stellation, accumulation of stress fibers, and the phosphorylation of focal adhesion kinase and myosin target subunit of myosin phosphatase isoform 1. Moreover, when combined with LPA, amitriptyline curtailed Rho activation and the Rho-mediated cellular responses. (4) These results demonstrate that in astroglial cells, amitriptyline exerts a balanced action on LPA-activated receptors by enhancing the neuroprotective ERK1/2-CREB-BDNF signaling and dampening the potentially detrimental Rho-ROCK pathway, and suggest that this unique property may contribute to the antidepressant activity of the drug. - Source: PubMed
Publication date: 2026/04/20
Olianas Maria CDedoni SimonaOnali Pierluigi - 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