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人 ELK3 抗体对
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人 ELK3 抗体对

01AB02173

ETS transcription factor ELK3 (ELK3) is a nuclear transcription factor belonging to the ternary complex factor subfamily of the ETS domain family. It primarily functions as a transcriptional repressor that binds to serum response elements in cooperation with serum response factor to regulate immediate-early gene expression. Upon signal-induced phosphorylation by the Ras/ERK and related kinase cascades, ELK3 can switch from a repressor to a transcriptional activator. It plays a central role in controlling genes involved in cell proliferation, migration, angiogenesis, and neural crest development. Clinically, ELK3 is strongly implicated in tumor progression, epithelial-mesenchymal transition, and metastasis across several cancers. Its dysregulation is specifically linked to prostate cancer progression and the development of chemoresistance, making it a key factor in oncogenic signaling.

Human
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技术参数

靶点基因名
ELK3
基因别名
NET; SAP2
蛋白别名
ETS transcription factor ELK3; ELK3
UniProt
P41970
物种
Human

产品详情

靶点名称
ELK3
蛋白名称
ETS transcription factor ELK3
蛋白别名
ETS domain-containing protein Elk-3; ETS-related protein ERP; ETS-related protein NET; Serum response factor accessory protein 2; SAP-2; SRF accessory protein 2
靶点基因名
ELK3
基因别名
NET; SAP2
UniProt
P41970
来源物种
Homo sapiens (Human)
物种反应性
Human

背景介绍

ETS transcription factor ELK3 (ELK3) is a nuclear transcription factor belonging to the ternary complex factor subfamily of the ETS domain family. It primarily functions as a transcriptional repressor that binds to serum response elements in cooperation with serum response factor to regulate immediate-early gene expression. Upon signal-induced phosphorylation by the Ras/ERK and related kinase cascades, ELK3 can switch from a repressor to a transcriptional activator. It plays a central role in controlling genes involved in cell proliferation, migration, angiogenesis, and neural crest development. Clinically, ELK3 is strongly implicated in tumor progression, epithelial-mesenchymal transition, and metastasis across several cancers. Its dysregulation is specifically linked to prostate cancer progression and the development of chemoresistance, making it a key factor in oncogenic signaling.