人 LMO4 抗体对
01AB01754
LIM domain only 4 (LMO4) is a cysteine-rich nuclear protein that functions as a transcription cofactor. Characterized by two LIM zinc-binding domains and the absence of a DNA-binding homeodomain, it regulates gene expression by forming multiprotein complexes with partners such as LDB1. LMO4 plays a critical role in neuronal development, specifically in establishing motor neuron identity through the modulation of LDB1–LHX3 complexes. It is widely expressed in embryonic and adult tissues, where it promotes proliferation and inhibits differentiation in various epithelia, including the mammary epithelium. Clinically, LMO4 is implicated in oncogenesis and is frequently overexpressed in breast cancers, where it drives tumor cell proliferation and invasion. It has also been linked to T-cell acute lymphoblastic leukemia and cochlear disease. Mouse models demonstrate its essential role in neural tube closure, as its loss leads to exencephaly and increased neuroepithelial apoptosis.
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技术参数
- 靶点基因名
- LMO4
- 蛋白别名
- LIM domain only 4; LMO4
- UniProt
- P61968
- 物种
- Human
产品详情
- 靶点名称
- LMO4
- 蛋白名称
- LIM domain only 4
- 蛋白别名
- LIM domain transcription factor LMO4; Breast tumor autoantigen; LIM domain only protein 4; LMO-4
- 靶点基因名
- LMO4
- UniProt
- P61968
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
LIM domain only 4 (LMO4) is a cysteine-rich nuclear protein that functions as a transcription cofactor. Characterized by two LIM zinc-binding domains and the absence of a DNA-binding homeodomain, it regulates gene expression by forming multiprotein complexes with partners such as LDB1. LMO4 plays a critical role in neuronal development, specifically in establishing motor neuron identity through the modulation of LDB1–LHX3 complexes. It is widely expressed in embryonic and adult tissues, where it promotes proliferation and inhibits differentiation in various epithelia, including the mammary epithelium. Clinically, LMO4 is implicated in oncogenesis and is frequently overexpressed in breast cancers, where it drives tumor cell proliferation and invasion. It has also been linked to T-cell acute lymphoblastic leukemia and cochlear disease. Mouse models demonstrate its essential role in neural tube closure, as its loss leads to exencephaly and increased neuroepithelial apoptosis.