CD39L3

Last update 08 May 2025

Basic Info

Synonyms

CD39 antigen-like 3, CD39L3, Ecto-apyrase 3

+ [8]

Introduction

Has a threefold preference for the hydrolysis of ATP over ADP.

100 Clinical Results associated with CD39L3

100 Translational Medicine associated with CD39L3

0 Patents (Medical) associated with CD39L3

137

Literatures (Medical) associated with CD39L3

01 Apr 2025·Reproductive Sciences

Expression and Hormonal Regulation of Entpd3 at Various Estrous Cycle Stages in the Mouse Uterus

Article

Author: Li, Rong ; Zhou, Ping ; Mo, Dan ; Yang, Yihua ; Liu, Yusong ; Lin, Mingmei ; Hu, Kai-Lun ; Zeng, Zhonghong

Ectonucleoside triphosphate diphosphohydrolase 3 (ENTPD3), a plasma membrane-bound metabolic enzyme, converts extracellular nucleotides into nucleosides. ENTPD3 is involved in various pathophysiological processes, including cellular adhesion, metabolism, activation, and migration. However, its specific function in the uterus remains unclear. This study aimed to investigate the expression pattern and localization of Entpd3 in the mouse uterus throughout the estrous cycle using immunohistochemistry (IHC), quantitative real-time PCR, and western blot analysis. The effect of sex steroid hormones on Entpd3 expression was also examined in ovariectomized (OVX) mice treated with 17β-estradiol (E2)/progesterone (P4) and estrogen receptor antagonist (Fulvestrant)/progesterone receptor antagonist (Mifepristone). Results demonstrated that elevated levels of Entpd3 mRNA and protein were noted during estrus and metestrus, with a decline in diestrus and proestrus. IHC revealed abundant ENTPD3 in the cytoplasm of glandular and luminal epithelial cells during estrus and metestrus. Additionally, treatment with E2 or P4 in OVX mice downregulated the expression of Entpd3 in the mouse uterus, which was rescued by Fulvestrant or Mifepristone. This study demonstrated that the expression of Entpd3 in the mouse uterus varied dynamically throughout the estrous cycle and was steroid-dependent, suggesting a potential role for Entpd3 in female mice's reproductive function.

01 Dec 2024·Journal of Biochemical and Molecular Toxicology

Extracellular Vesicles Derived Ectonucleoside Triphosphate Diphosphohydrolase 3 Alleviates Mitochondrial Dysfunction of Osteoarthritis Chondrocytes via Ectonucleotide Pyrophosphatase/Phosphodiesterase 1‐Induced Suppression of the AKT/Notch2 Pathway

Article

Author: Tang, Xin ; Hao, Ye ; He, Jingsheng

ABSTRACTOsteoarthritis (OA) is the most common joint disease that usually starts from joint cartilage injury. Notch2, a versatile signaling in human development and diseases, was recently uncovered to be an important regulator in chondrocyte damage. However, in OA chondrocytes, how Notch2 activation is dysregulated is largely unknown. Here, integrated bioinformatic analysis was performed on GEO datasets (GSE199193 and GSE224255) to search potential extracellular vesicles (EVs) derived regulators of Notch2 in OA chondrocytes. Ectonucleoside triphosphate diphosphohydrolase 3 (Entpd3), a most differentially expressed gene both in LPS‐induced macrophage EV and Notch2 mutant chondrocytes, was screened as the candidate regulator of Notch2 in OA chondrocytes. Gain‐of‐function experiments in cultured human chondrocytes revealed that recombinant Entpd3 protein and macrophage EV both had a protective effect on LPS‐induced inflammation, oxidative stress, apoptosis, and collagen loss in chondrocytes. In terms of mechanism, Entpd3 directly interacted with ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1) and suppressed AKT/Notch2‐mediated mitochondrial dysfunction. Finally, we verified that either macrophage EV administration or Entpd3 overexpression was able to alleviate osteoarthritis in mice in vivo. In conclusion, Entpd3 is identified as a new regulator in OA, which alleviates mitochondrial dysfunction induced chondrocyte damage via ENPP1‐induced suppression of the AKT/Notch2 pathway.

21 Oct 2024·ACS Applied Bio Materials

Peptide-Coated Polycaprolactone-Benzalkonium Chloride Nanocapsules for Targeted Drug Delivery to the Pancreatic β-Cell

Article

Author: Collins, Jillian ; Farnsworth, Nikki L. ; Shilleh, Ali ; Holcomb, Keifer ; Broichhagen, Johannes ; Fremin, Ashton ; Russ, Holger A. ; Barra, Jessie M. ; Hodson, David J. ; Hays, Julianna K. ; Kratz, Austin ; Ocampo, Andres ; Sela, Amit ; Akolade, Jubril

Targeting current therapies to treat or prevent the loss of pancreatic islet β-cells in Type 1 Diabetes (T1D) may provide improved efficacy and reduce off-target effects. Current efforts to target the β-cell are limited by a lack of β-cell-specific targets and the inability to test multiple targeting moieties with the same delivery vehicle. Here, we fabricate a tailorable polycaprolactone nanocapsule (NC) in which multiple different targeting peptides can be interchangeably attached for β-cell-specific delivery. Incorporation of a cationic surfactant in the NC shell allows for the attachment of Exendin-4 and an antibody for ectonucleoside triphosphate diphosphohydrolase 3 (ENTPD3) for β-cell-specific targeting. The average NC size ranges from 250 to 300 nm with a polydispersity index under 0.2. The NCs are nontoxic, stable in media culture, and can be lyophilized and reconstituted. NCs coated with a targeting peptide were taken up by human cadaveric islet β-cells and human stem cell-derived β-like cells (sBC) in vitro with a high level of specificity. Furthermore, NCs successfully delivered both hydrophobic and hydrophilic cargo to human β-cells. Additionally, Exendin-4-coated NCs were stable and targeted the mouse pancreatic islet β-cell in vivo. Overall, our tailorable NCs have the potential to improve cell-targeted drug delivery and can be utilized as a screening platform to test the efficacy of cell-targeting peptides.

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CD39L3

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