CNPY2

Last update 08 May 2025

Basic Info

Synonyms

canopy FGF signaling regulator 2, CNPY2, HP10390

+ [7]

Introduction

Positive regulator of neurite outgrowth by stabilizing myosin regulatory light chain (MRLC). It prevents MIR-mediated MRLC ubiquitination and its subsequent proteasomal degradation.

100 Clinical Results associated with CNPY2

100 Translational Medicine associated with CNPY2

0 Patents (Medical) associated with CNPY2

Literatures (Medical) associated with CNPY2

01 Dec 2025·Molecular Biology Reports

The role of canopy family proteins: biological mechanism and disease function

Review

Author: Zhang, Shu-Tian ; Xie, Si-An ; Yin, Min-Yue ; Li, Xue

Canopy family proteins are highly sequence-conserved proteins with an N-terminal hydrophobic signal sequence, a unique pattern of six cysteine residues characteristic of the saposin-like proteins, and a C-terminal putative endoplasmic reticulum retention signal sequence. At present, the known canopy family proteins are canopy fibroblast growth factor signaling regulator 1 (CNPY1), CNPY2, CNPY3, and CNPY4. Despite similar structures, canopy family proteins regulate complex signal networks to participate in various biological processes. They are involved in a wide range of diseases, including angiogenesis, abnormal immune responses, neurodevelopmental disorders, and the development of tumors. Here, we summarized the biological processes and influence on the disease of every CNPY family protein to elucidate potential biomarkers and point out the direction for future in-depth research.

01 Jun 2025·Biomedicine & Pharmacotherapy

CNPY2 drives DSS-induced colitis via the macrophage-ROS axis

Article

Author: Li, Zihai ; Zhang, Wenqing ; Hong, Feng ; Meng, Lingbin ; Zhang, Xiaoli

Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the gastrointestinal tract, driven by genetic, environmental, and immune system factors. However, its exact mechanisms remain unclear. Here, we demonstrate that CNPY2 plays a critical role in colitis by modulating macrophage activity. Mice with whole-body Cnpy2 knockout (KO) exhibited significantly reduced dextran sodium sulfate (DSS)-induced colitis compared to wild-type controls. Cnpy2 KO mice showed less mucosal barrier disruption and fewer lamina propria macrophages (LPMφs) following DSS treatment. Proinflammatory cytokine production was also diminished in the colons of Cnpy2 KO mice. Furthermore, Cnpy2 KO macrophages generated markedly lower levels of reactive oxygen species (ROS), partly through CHOP regulation. Notably, treatment with the ROS scavenger N-acetyl-L-cysteine (NAC) completely abolished DSS-induced colitis in Cnpy2 KO mice. Thus, CNPY2 exacerbates DSS-induced colitis primarily through macrophage-specific effects, with ROS upregulation being central to its pathogenic role.

01 Apr 2025·Cancer Letters

A novel TLR4 accessory molecule drives hepatic oncogenesis through tumor-associated macrophages

Article

Author: Li, Zihai ; Ouyang, Yuli ; Allen, Carter A ; Meng, Lingbin ; Zhang, Xiaoli ; Chung, Dongjun ; Zhang, Wenqing ; Kim, Doyeon ; Hong, Feng

Tumor-associated macrophages (TAMs) play a crucial role in the tumor microenvironment, yet the roles and mechanisms of TAMs in inflammation-associated oncogenesis remain enigmatic. We report that protein canopy homolog 2 (CNPY2) functions as a novel TLR4 regulator, promoting cytokine production in macrophages. CNPY2 binds directly to TLR4. Cnpy2 deficiency reduces cell surface expression of TLR4, nuclear translocation of NFκB and cytokine production in macrophages. Macrophage-specific CNPY2 deficiency significantly decreases cytokine production in macrophages and reduces hepatocarcinogenesis in a diethylnitrosamine (DEN)-induced liver cancer model. RNA-sequencing analysis revealed Cnpy2 knockout decreased the mRNA level and cell surface expression of two VEGF receptors, Flt1 and Kdr, compared to those in WT counterparts, resulting in inhibition of macrophage tumor infiltration. Cnpy2 knockout inhibits NFκB2/p52-mediated transcription of Flt1 and Kdr in macrophages. These findings demonstrate that CNPY2 regulates macrophages in both inflammation and hepatocarcinogenesis and may serve as a therapeutic target for cancer.

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CNPY2

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