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人 TNR 抗体对
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人 TNR 抗体对

01AB01858

Tenascin R (TNR) is a neural extracellular matrix glycoprotein predominantly expressed in the central nervous system, where it plays a key role in neural development and function. Structurally, TNR is the smallest member of the tenascin family, comprising an N-terminal cysteine-rich segment, 4.5 EGF-like repeats, nine fibronectin type III domains, and a C-terminal fibrinogen-like domain, allowing it to form oligomeric structures such as trimers and dimers. TNR localizes to perineuronal nets and nodes of Ranvier, interacting with other extracellular matrix components and cell adhesion molecules, and modulates neural cell adhesion, axon guidance, and neurite outgrowth, often providing only weak adhesion or even repelling axons. Functionally, TNR is essential for the normal development of perineuronal nets and proper conduction velocity in optic nerves, as evidenced by TNR-deficient mice showing disrupted perineuronal net structure and reduced nerve conduction speed. Clinically, mutations in the TNR gene are associated with neurodevelopmental disorders characterized by nonprogressive spasticity and transient motor deficits, highlighting its importance in neural integrity and signaling.

Human
规格起售价
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技术参数

靶点基因名
TNR
蛋白别名
tenascin R; TNR
UniProt
Q92752
物种
Human

产品详情

靶点名称
TNR
蛋白名称
tenascin R
蛋白别名
Tenascin-R; TN-R; Janusin; Restrictin
靶点基因名
TNR
UniProt
Q92752
来源物种
Homo sapiens (Human)
物种反应性
Human

背景介绍

Tenascin R (TNR) is a neural extracellular matrix glycoprotein predominantly expressed in the central nervous system, where it plays a key role in neural development and function. Structurally, TNR is the smallest member of the tenascin family, comprising an N-terminal cysteine-rich segment, 4.5 EGF-like repeats, nine fibronectin type III domains, and a C-terminal fibrinogen-like domain, allowing it to form oligomeric structures such as trimers and dimers. TNR localizes to perineuronal nets and nodes of Ranvier, interacting with other extracellular matrix components and cell adhesion molecules, and modulates neural cell adhesion, axon guidance, and neurite outgrowth, often providing only weak adhesion or even repelling axons. Functionally, TNR is essential for the normal development of perineuronal nets and proper conduction velocity in optic nerves, as evidenced by TNR-deficient mice showing disrupted perineuronal net structure and reduced nerve conduction speed. Clinically, mutations in the TNR gene are associated with neurodevelopmental disorders characterized by nonprogressive spasticity and transient motor deficits, highlighting its importance in neural integrity and signaling.