ELK1 TAD in vivo Kinase Assay Kit
- Known as:
- ELK1 TAD vivo Kinase Assay Kit
- Catalog number:
- LK0009
- Product Quantity:
- 10ug
- Category:
- Peptides
- Supplier:
- Panomics
- Gene target:
- ELK1 TAD vivo Kinase Assay Kit
Related genes to: ELK1 TAD in vivo Kinase Assay Kit
- 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
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- 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 - Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by Amyloid-β plaques and neurofibrillary tangles. Disrupted circadian rhythms are common in AD and may worsen cognitive decline and psychological symptoms. The link between sleep deprivation and Alzheimer's risk remains unclear. This study aimed to identify potential diagnostic markers for Alzheimer's and sleep deprivation, focusing on the role of immune cell infiltration in disease progression. - Source: PubMed
Publication date: 2026/03/10
Yanchao LiangYuchen LiHuan XiangYuyan GaiJunfei ZhaoRoumiantsev SergeyMashkin AndreyBeylerli OzalGareev IlgizSibin ZhangYang Guang - To investigate the effects of ELK1 on hippocampal cells and its related mechanisms in the progression of vascular dementia (VD). Twenty-seven SD rats were divided into three groups: sham group (n = 9), Model group (n = 9), and Model+ELK1-OE group (n = 9). The VD animal model was established in the Model group by bilateral common carotid artery occlusion (BCCAO). The Morris water maze test was performed to observe the learning and memory abilities of the rats in the three groups. HE staining was used to examine the morphological changes in the hippocampal region, and immunohistochemical staining was conducted to observe the expression levels of ELK1. In the in vitro experiments, hippocampal tissues were isolated from rats in the sham group to prepare hippocampal single-cell suspensions. After different stimuli, Western blot was performed to observe protein expression, flow cytometry for apoptosis was used to assess hippocampal cell apoptosis, and a colorimetric assay kit was employed to detect the Fe2 + levels in the hippocampal cells of each group. In the in vivo experiments, the levels of ELK1 in VD rats were significantly lower than those in the sham group. ELK1 improved the learning and memory abilities of VD rats. After ELK1 intervention, the arrangement of neural cells in the hippocampal region of the rats was more regular, the nucleoli were clearer, the number of glial cells decreased, and the number of inflammatory cells was reduced. In the in vitro experiments, ELK1 promoted the expression of P-mTOR, P-CREB, and nuclear YAP, inhibited the expression of NOX4 and nuclear TFEB, and reduced hippocampal cell apoptosis and Fe2 + content. ELK1 inhibits the progression of vascular dementia by regulating mTOR/CREB/YAP/TFEB signaling-induced ferroptosis in hippocampal cells. - Source: PubMed
Publication date: 2026/02/26
Xu JingLiu MiaomiaoQi QianqianAn JinXiao YiningGuan TianyuanTeng ZhenjieChen WeihongLi RuiDong YanhongChang YanzhongLu Peiyuan