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更新于：2025-05-07

PLD2

更新于：2025-05-07

基本信息

别名

Choline phosphatase 2、hPLD2、Phosphatidylcholine-hydrolyzing phospholipase D2

+ [4]

简介

Function as phospholipase selective for phosphatidylcholine (PubMed:9582313). May have a role in signal-induced cytoskeletal regulation and/or endocytosis (By similarity).

关联

项与 PLD2 相关的药物

ML299

靶点

PLD1 x PLD2

作用机制

PLD1 inhibitors [+1]

在研机构-

原研机构

Vanderbilt University Medical Center

在研适应症-

非在研适应症

胶质母细胞瘤

最高研发阶段无进展

首次获批国家/地区-

首次获批日期1800-01-20

ML298

靶点

PLD2

作用机制

PLD2 inhibitors

在研机构-

原研机构

Vanderbilt University Medical Center

在研适应症-

非在研适应症

胶质母细胞瘤

最高研发阶段无进展

首次获批国家/地区-

首次获批日期1800-01-20

ML395

靶点

PLD2

作用机制

PLD2 inhibitors

在研机构-

原研机构

Vanderbilt University Medical Center

在研适应症-

非在研适应症

流感病毒感染

最高研发阶段无进展

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 PLD2 相关的临床结果

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100 项与 PLD2 相关的转化医学

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0 项与 PLD2 相关的专利（医药）

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653

项与 PLD2 相关的文献（医药）

2025-04-03·Immunological Investigations

Differential Control of T-Cell Subsets by Recombinant Human PLD2 in a Mouse Model of Allergic Asthma

Article

作者: Zhu, Ling ; Yu, Xiu-Ming ; Lin, Jun-Jin ; Chen, Yi-Zhong ; Yu, Chuan-Xing ; Wang, Hui-Li

BACKGROUNDPhospholipase D2 (PLD2) enzymes are expressed on the cytoplasmic membrane of bacteria, fungi, plants, and animals. Recently, extensive research has linked PLD2 to the chronic inflammatory activity of cells. Allergic asthma is a chronic airway inflammation disease. In this context, a recombinant human phospholipase D2 (rhPLD2) was designed and modified from the wild-type PLD2 to study its effects in an ovalbumin (OVA) induced murine model of asthma.METHODSHematoxylin and eosin staining was used for lung histopathology. Cytokine concentrations in bronchoalveolar lavage fluid (BALF) were measured using ELISA kits. The ratio of T-bet and GATA-3 expression level in spleen and lymph nodes following rhPLD2 administration was assessed through RT-PCR. Phenotyping analysis of Treg cells from peripheral blood was performed by flow cytometry.RESULTSIt indicated that OVA-induced mice exhibited elevated pulmonary eosinophilia and allergic inflammation in the airways, along with increased expression of IFN-γ, IL-4 in the lung BALF. Administration of rhPLD2 alleviated lung inflammation and significantly reduce the number of eosinophils in peripheral blood and BALF. RhPLD2 also reversed the IFN-γ/IL-4 ratio at the molecular level in BALF and the T-bet/GATA-3 ratio in lymphocytes of the lung, spleen, lymph nodes at the genetic level. Furthermore, FACS analysis demonstrated that rhPLD2 increased the frequency of both IL-10⁺Treg cells and CD25⁺ Treg cells.CONCLUSIONFrom a therapeutic perspective, rhPLD2 alleviates allergic airway inflammation by balancing Th1/Th2 homeostasis and increasing Treg cells. It has been shown to function in immunoregulatory activities in OVA-induced asthma mice.

2025-04-01·The Journal of Nutritional Biochemistry

β-Hydroxy-β-methylbutyrate (HMB) increases muscle mass and diminishes weight gain in high-fat-fed mice

Article

作者: Froy, Oren ; Chapnik, Nava ; Cohen-Or, Meytal

β-Hydroxy-β-methylbutyrate (HMB) is a catabolite of leucine, which promotes muscle growth. However, little is known about the effect of HMB on body composition in the context of a high-fat diet. Our aim was to study the circadian metabolic effect of HMB on body weight. C57BL male mice were fed ad libitum chow diet (C), chow diet supplemented with 500mg Ca-HMB per 1 kg body weight (C+HMB), a high-fat diet (HFD) or HFD supplemented with 500mg Ca-HMB per 1 kg body weight (HFD+HMB) for 7 weeks. HMB led to reduced fat weight (30%, p<0.05) and body weight (7%, p<0.05) and increased muscle weight (17%, p<0.05) in the HFD+HMB group. HMB increased glucose oxidation (27%, p<0.0001) and reduced fatty acid oxidation (30%, p<0.0001) in the C group, but increased fatty acid oxidation in the HFD+HMB group (10%, p<0.05). At the molecular level, HMB did not affect metabolic proteins in the liver, but lowered NF-κB levels in adipose tissue (24%, p<0.05). In the muscle, HMB showed no activation of AKT and mTOR, but did show activation of P70S6K (67%, p<0.01) and S6 (42%, p<0.01). The activation of the P70S6K and S6 was independent of AKT and mTOR and was accompanied by increased activation of phospholipase D2 (PLD) (35%, p<0.0001). In addition, HMB led to altered circadian rhythms. In conclusion, mice fed a HFD supplemented with HMB have increased muscle weight and reduced fat mass and body weight presumably due to increased locomotor activity. HMB induces myogenesis by activating P70S6K and S6 via PLD2.

2025-02-01·Cancer Science

Phospholipase D2 downregulates interleukin‐1β secretion from tumor‐associated macrophages to suppress bladder cancer progression

Article

作者: Shiga, Masanobu ; Mathis, Bryan J. ; Sano, Keisuke ; Nagumo, Yoshiyuki ; Nitta, Satoshi ; Suzuki, Shuhei ; Negoro, Hiromitsu ; Tanuma, Kozaburo ; Hamada, Kazuki ; Nishiyama, Hiroyuki ; Funakoshi, Yuji ; Isoda, Bunpei ; Sakka, Shotaro ; Kandori, Shuya

AbstractThe tumor microenvironment (TME) modulates therapeutic response and prognosis in patients with bladder cancer (BC). The roles of two phospholipase D (PLD) isoforms, PLD1 and PLD2 (hydrolysis of phosphatidylcholine to phosphatidic acid), in cancer cells have been well‐studied in numerous cancer types, but their roles in the TME remain unclear. We used a mouse BC Pld2‐KO carcinogenesis model and global transcriptomic analysis to reveal that PLD2 was significantly involved in BC progression through immunosuppressive pathways in the TME. We therefore focused on PLD2 and tumor‐associated macrophages (TAMs), which were increased in Pld2‐KO mice and further associated with poor prognoses in BC patients. In vitro, we found that Pld2‐KO mouse TAMs had significantly enhanced proliferation, correlating closely with increased interleukin‐1β (IL‐1β) production. These results indicate that PLD2 suppresses BC progression by regulation of IL‐1β secretion from TAMs in the TME, suggesting that PLD2 could serve as a potential therapeutic target for modifying the TME in BC.

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