What is it about?

In this study, we identify Cnpy1 as an endoplasmic reticulum (ER) chaperone essential for the function and survival of a subset of vomeronasal sensory neurons.

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Why is it important?

In our recent work () we uncovered a striking divergence in ER organisation associated with sensory neuron development and differentiation. Basal VNO neurons arise from a stem cell population and differentiate to express V2R type GPCRs and a hypertrophic gyroid ER along with elevated levels of ER chaperones. How do these neurons sustain what appears to be an elevated ER-stress-like state as part of their normal biology? Our findings suggest that specialised, cell-type-specific proteostatic factors—such as Cnpy1—may help; enabling stable GPCR expression, function and neuronal survival. Understanding these mechanisms may offer insights not only into sensory systems, but also into pathological contexts where ER stress and proteostasis are interlinked.

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This page is a summary of: Cnpy1 is a candidate endoplasmic reticulum chaperone of vomeronasal type 2 GPCRs, Proceedings of the National Academy of Sciences, March 2026, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2528466123.
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