JPT2

Last update 08 May 2025

Basic Info

Synonyms

C16orf34, FLJ13092, Hematological and neurological expressed 1-like protein

+ [6]

Introduction

Nicotinic acid adenine dinucleotide phosphate (NAADP) binding protein required for NAADP-evoked intracellular calcium release (PubMed:33758061, PubMed:33758062). Confers NAADP-sensitivity to the two pore channels (TPCs) complex (PubMed:33758061). Enables NAADP to activate Ca(2+) release from the endoplasmic reticulum through ryanodine receptors (PubMed:33758062). (Microbial infection) Involved in the endolysosomal trafficking of human coronavirus SARS-CoV-2.

100 Clinical Results associated with JPT2

100 Translational Medicine associated with JPT2

0 Patents (Medical) associated with JPT2

Literatures (Medical) associated with JPT2

01 Jul 2025·Physiological Reviews

TPCs: FROM PLANT TO HUMAN

Review

Author: Grimm, Christian ; Klingl, Yvonne Eileen ; Jaślan, Dawid ; Petrauskas, Arnas

In 2005, the Arabidopsis thaliana two-pore channel TPC1 channel was identified as a vacuolar Ca2+-release channel. In 2009, three independent groups published studies on mammalian TPCs as nicotinic acid adenine dinucleotide phosphate (NAADP)-activated endolysosomal Ca2+ release channels, results that were eventually challenged by two other groups, claiming mammalian TPCs to be phosphatidylinositol-3,5-bisphosphate [PI(3,5)P2]-activated Na+ channels. By now this dispute seems to have been largely reconciled. Lipophilic small molecule agonists of TPC2, mimicking either the NAADP or the PI(3,5)P2 mode of channel activation, revealed, together with structural evidence, that TPC2 can change its selectivity for Ca2+ versus Na+ in a ligand-dependent fashion (N- vs. P-type activation). Furthermore, the NAADP-binding proteins Jupiter microtubule-associated homolog 2 protein (JPT2) and Lsm12 were discovered, corroborating the hypothesis that NAADP activation of TPCs only works in the presence of these auxiliary NAADP-binding proteins. Pathophysiologically, loss or gain of function of TPCs has effects on autophagy, exocytosis, endocytosis, and intracellular trafficking, e.g., LDL cholesterol trafficking leading to fatty liver disease or viral and bacterial toxin trafficking, corroborating the roles of TPCs in infectious diseases such as Ebola or COVID-19. Defects in the trafficking of epidermal growth factor receptor and β1-integrin suggested roles in cancer. In neurodegenerative lysosomal storage disease models, P-type activation of TPC2 was found to have beneficial effects on both in vitro and in vivo hallmarks of Niemann-Pick disease type C1, Batten disease, and mucolipidosis type IV. Here, we cover the latest on the structure, function, physiology, and pathophysiology of these channels with a focus initially on plants followed by mammalian TPCs, and we discuss their potential as drug targets, including currently available pharmacology.

01 Jun 2024·Journal of Pharmaceutical Analysis

Oxalate regulates crystal-cell adhesion and macrophage metabolism via JPT2/PI3K/AKT signaling to promote the progression of kidney stones

Article

Author: Xiong, Yunhe ; Ke, Hu ; Song, Qianlin ; Su, Xiaozhe ; He, Ziqi ; Chen, Xin ; Dong, Caitao ; Liao, Wenbiao ; Yang, Sixing ; Song, Chao ; Zhou, Jiawei

Oxalate is an organic dicarboxylic acid that is a common component of plant foods. The kidneys are essential organs for oxalate excretion, but excessive oxalates may induce kidney stones. Jupiter microtubule associated homolog 2 (JPT2) is a critical molecule in Ca²⁺ mobilization, and its intrinsic mechanism in oxalate exposure and kidney stones remains unclear. This study aimed to reveal the mechanism of JPT2 in oxalate exposure and kidney stones. Genetic approaches were used to control JPT2 expression in cells and mice, and the JPT2 mechanism of action was analyzed using transcriptomics and untargeted metabolomics. The results showed that oxalate exposure triggered the upregulation of JPT2, which is involved in nicotinic acid adenine dinucleotide phosphate (NAADP)-mediated Ca²⁺ mobilization. Transcriptomic analysis revealed that cell adhesion and macrophage inflammatory polarization were inhibited by JPT2 knockdown, and these were dominated by phosphatidylinositol 3-kinase (PI3K)/AKT signaling, respectively. Untargeted metabolomics indicated that JPT2 knockdown inhibited the production of succinic acid semialdehyde (SSA) in macrophages. Furthermore, JPT2 deficiency in mice inhibited kidney stones mineralization. In conclusion, this study demonstrates that oxalate exposure facilitates kidney stones by promoting crystal-cell adhesion, and modulating macrophage metabolism and inflammatory polarization via JPT2/PI3K/AKT signaling.

01 Apr 2024·Advanced Science

JPT2 Affects Trophoblast Functions and Macrophage Polarization and Metabolism, and Acts as a Potential Therapeutic Target for Recurrent Spontaneous Abortion

Article

Author: Cao, Ming Liang ; Ji, Rui ; Guo, Duan Ying ; Yang, Jing ; Chen, Xin ; Song, Qian Lin ; Wang, Jia Yu ; Zhang, Yan

AbstractRecurrent spontaneous abortion (RSA) is a pregnancy‐related condition with complex etiology. Trophoblast dysfunction and abnormal macrophage polarization and metabolism are associated with RSA; however, the underlying mechanisms remain unknown. Jupiter microtubule‐associated homolog 2 (JPT2) is essential for calcium mobilization; however, its role in RSA remains unclear. In this study, it is found that the expression levels of JPT2, a nicotinic acid adenine dinucleotide phosphate‐binding protein, are decreased in the villous tissues of patients with RSA and placental tissues of miscarried mice. Mechanistically, it is unexpectedly found that abnormal JPT2 expression regulates trophoblast function and thus involvement in RSA via c‐Jun N‐terminal kinase (JNK) signaling, but not via calcium mobilization. Specifically, on the one hand, JPT2 deficiency inhibits trophoblast adhesion, migration, and invasion by inhibiting the JNK/atypical chemokine receptor 3 axis. On the other hand, trophoblast JPT2 deficiency contributes to M1 macrophage polarization by promoting the accumulation of citrate and reactive oxygen species via inhibition of the JNK/interleukin‐6 axis. Self‐complementary adeno‐associated virus 9‐JPT2 treatment alleviates embryonic resorption in abortion‐prone mice. In summary, this study reveals that JPT2 mediates the remodeling of the immune microenvironment at the maternal–fetal interface, suggesting its potential as a therapeutic target for RSA.

Analysis

Perform a panoramic analysis of this field.

view full example data

Chat with Hiro

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis

JPT2

Basic Info

Related

Analysis