Target intelligence / Profile preview

Nitric oxide synthase traffic inducer (NOSTRIN)

Target
NOSTRIN
Molecular classification
Adaptor protein (PCH family), Cytoskeletal-associated protein, eNOS-interacting protein
01

Overview

NOSTRIN (Nitric oxide synthase traffic inducer) is an adaptor protein of the Pombe cdc15 homology (PCH) family, containing a cdc15 domain and a C-terminal SH3 domain. NOSTRIN is highly expressed in vascular endothelial cells and tissues with active nitric oxide (NO) signaling such as placenta, kidney, lung, and heart. It binds specifically to endothelial nitric oxide synthase (eNOS) and other partners (including caveolin-1 and dynamin-2), facilitating eNOS trafficking from the plasma membrane to intracellular vesicular structures. Overexpression of NOSTRIN induces a reduction in Ca(2+)-stimulated NO release by redistributing eNOS, thus negatively regulating NO bioavailability in endothelial cells. This mechanism affects vascular function, with implications in diseases involving endothelial dysfunction and inflammation. NOSTRIN is not a receptor, enzyme, or transporter, but serves as an adaptor modulating the subcellular localization and activity of eNOS, acting within a larger protein network governing vascular NO signaling. No specific drugs directly target NOSTRIN, and it is not currently used as a biomarker.

Other names
Nitric oxide synthase traffic inducerNitric oxide synthase traffickereNOS traffic inducereNOS-trafficking inducerBM247 homologDaIP2NOSTRINnostrinendothelial nitric oxide synthase traffic inducerortholog of mouse disabled 2 interacting protein 2MGC20702
02

Mechanism of action

Indirect: Modulation of nitric oxide release via its effect on eNOS, with drugs affecting eNOS (such as nitric oxide synthase inhibitors/activators), but no direct drug acting on NOSTRIN known

03

Biological functions

Regulation of nitric oxide synthesisTrafficking and subcellular localization of endothelial nitric oxide synthase (eNOS)Modulation of eNOS activity
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Disease associations

Cardiovascular disease (e.g., endothelial dysfunction)Inflammation (via regulation of NO production)
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Safety considerations

Overexpression leads to attenuation of nitric oxide release, which can impair endothelial function and vascular toneExcessive redistribution of eNOS may potentially disrupt vascular homeostasis

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