更新于：2024-11-01

PTPRD

更新于：2024-11-01

基本信息

别名

HPTP、protein tyrosine phosphatase receptor type D、Protein-tyrosine phosphatase delta

+ [4]

简介

Can bidirectionally induce pre- and post-synaptic differentiation of neurons by mediating interaction with IL1RAP and IL1RAPL1 trans-synaptically. Involved in pre-synaptic differentiation through interaction with SLITRK2.

关联

靶点

PTPRD

作用机制

PTPRD抑制剂

在研机构

Cold Spring Harbor Laboratory, Inc.

原研机构

Cold Spring Harbor Laboratory, Inc.

在研适应症

乳腺癌

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

NHB-1109

靶点

PTPRD

作用机制

PTPRD抑制剂

在研机构

The University of New Mexico [+1]

原研机构

University of Maryland School of Medicine

在研适应症

未指明的药物依赖

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 PTPRD 相关的临床结果

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100 项与 PTPRD 相关的转化医学

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0 项与 PTPRD 相关的专利（医药）

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441

项与 PTPRD 相关的文献（医药）

2024-10-18·Nanomaterials (Basel, Switzerland)

Exploring the Potential of Bimetallic PtPd/C Cathode Catalysts to Enhance the Performance of PEM Fuel Cells.

Article

作者: Guterman, Vladimir ; Menshikov, Vladislav ; Alekseenko, Anastasia ; Novomlinskaya, Irina ; Paperzh, Kirill ; Belenov, Sergey ; Pankov, Ilya ; Moguchikh, Elizaveta

Bimetallic platinum-containing catalysts are deemed promising for electrolyzers and proton-exchange membrane fuel cells (PEMFCs). A significant number of laboratory studies and commercial offers are related to PtNi/C and PtCo/C electrocatalysts. The behavior of PtPd/C catalysts has been studied much less, although palladium itself is the metal closest to platinum in its properties. Using a series of characterization methods, this paper presents a comparative study of structural characteristics of the commercial PtPd/C catalysts containing 38% wt. of precious metals and the well-known HiSpec4000 Pt/C catalyst. The electrochemical behavior of the catalysts was studied both in a three-electrode electrochemical cell and in the membrane electrode assemblies (MEAs) of hydrogen-air PEMFCs. Both PtPd/C samples demonstrated higher values of the electrochemically active surface area, as well as greater specific and mass activity in the oxygen reduction reaction in comparison with conventional Pt/C, while not being inferior to the latter in durability. The MEA based on the best of the PtPd/C catalysts also exhibited higher performance in single tests and long-term durability testing. The results of this study conducted indicate the prospects of using bimetallic PtPd/C materials for cathode catalysts in PEMFCs.

2024-09-06·Journal of Proteome Research

Proteomics and Metabolic Characteristics of Boar Seminal Plasma Extracellular Vesicles Reveal Biomarker Candidates Related to Sperm Motility

Article

作者: Ding, Ning ; Zhang, Yu ; Jiang, Li ; Liu, Jianfeng ; Cao, Jinkang ; Zhang, Chun ; Zhang, Jing

Although seminal plasma extracellular vesicles (SPEVs) play important roles in sperm function, little is known about their metabolite compositions and roles in sperm motility. Here, we performed metabolomics and proteomics analysis of boar SPEVs with high or low sperm motility to investigate specific biomarkers affecting sperm motility. In total, 140 proteins and 32 metabolites were obtained through differentially expressed analysis and weighted gene coexpression network analysis (WGCNA). Seven differentially expressed proteins (DEPs) (ADIRF, EPS8L1, PRCP, CD81, PTPRD, CSK, LOC100736569) and six differentially expressed metabolites (DEMs) (adenosine, beclomethasone, 1,2-benzenedicarboxylic acid, urea, 1-methyl-l-histidine, and palmitic acid) were also identified in WGCNA significant modules. Joint pathway analysis revealed that three DEPs (GART, ADCY7, and NTPCR) and two DEMs (urea and adenosine) were involved in purine metabolism. Our results suggested that there was significant correlation between proteins and metabolites, such as IL4I1 and urea (r = 0.86). Furthermore, we detected the expression level of GART, ADCY7, and CDC42 in sperm of two groups, which further verified the experimental results. This study revealed that several proteins and metabolites in SPEVs play important roles in sperm motility. Our results offered new insights into the complex mechanism of sperm motility and identified potential biomarkers for male reproductive diseases.

2024-09-01·Nature Neuroscience

Cerebellar Purkinje neurons enhance thirst via asprosin–PTPRD signaling

Article

Independent of its appetite- and body weight-modulating effects, the hormone asprosin activates its receptor PTPRD at cerebellar Purkinje neurons to enhance thirst and maintain fluid homeostasis.Surprisingly, this has no effect whatsoever on Purkinje neuron-mediated motor coordination and learning.

项与 PTPRD 相关的新闻（医药）

2023-12-22

·生物谷

JITC：在人类致死性癌症中识别出免疫检查点抑制剂的新型生物标志物

来自中国科学院上海营养与健康研究所等机构的科学家们通过研究在人类癌症中识别出了一种新型的免疫检查点抑制剂（ICIs）生物标志物。癌症免疫疗法能诱导持久性的肿瘤消退，但大多数患者并没有反应，SETD2的突变往往与免疫检查点抑制剂（ICIs）免疫疗法的疗效有关，SETD2失活的功能重要性以及如何调节免疫疗法的反应，至今研究人员并不清楚。近日，一篇发表在国际杂志Journal for ImmunoTherapy of Cancer上题为“Tumor cell-intrinsic SETD2 inactivation sensitizes cancer cells to immune checkpoint blockade through the NR2F1-STAT1 pathway”的研究报告中，来自中国科学院上海营养与健康研究所等机构的科学家们通过研究在人类癌症中识别出了一种新型的免疫检查点抑制剂（ICIs）生物标志物。 ICIs主要包括针对诸如程序性细胞死亡蛋白-1（PD-1）、程序性细胞死亡配体1（PD-L1）和细胞毒性T淋巴细胞相关抗原4（CTLA-4）等蛋白的抗体，ICIs免疫疗法在治疗很多致死性癌症上带来了革命性的变革，然而，仅有大约20%的患者能因这种疗法而获益，因此识别出哪些患者能因ICIs的治疗而获益就显得尤为重要了。 SETD2是唯一已知的组蛋白甲基转移酶，其主要负责组蛋白H3在酪氨酸36位点（H3K36me3）的三重甲基化作用，其通过H3K36me3在基因调节方面扮演着关键作用；SETD2的基因突变大约在5%的人类癌症中存在，而且其会促进多种人类癌症中肿瘤的进展和转移，比如透明细胞肾细胞癌、胰腺癌、结直肠癌、前列腺癌和乳腺癌等，然而，目前研究人员还没有开发出能靶向作用SETD2缺失的肿瘤及表现出治疗潜力的小分子或特殊抗体。在人类致死性癌症中识别出免疫检查点抑制剂的新型生物标志物。图片来源：Journal for ImmunoTherapy of Cancer (2023). DOI:10.1136/jitc-2023-007678 为了揭示SETD2基因和癌症免疫疗法之间的关联，研究人员分析了利用ICIs治疗的1662名患者，随后在这些患者的预后和组学数据集中识别出了与对免疫疗法产生积极反应相关的127个基因，除了已经建立的ICIs生物标志物（比如TP53, PAK7, TET1, PTPRD/PTPRT和STK1）外，SETD2是排名前三的基因，携带SETD2失活突变的患者往往能对免疫治疗表现出更有利的反应。功能实验结果表明，携带Setd2失活的小鼠同源性肿瘤对于ICIs也较为敏感，通过进行大量和单细胞RNA测序，研究人员进一步揭示了SETD2的失活或能重编程肿瘤内的免疫细胞并促使肿瘤微环境发炎。从机制上来讲，利用ATAC测序、CHIP测序和RNA测序的综合多组学分析结果表明，SETD2的失活能通过损伤H3K36me3的堆积和染色质可及性来降低NR2F1的转录，这反过来就会激活STAT1信号通路，从而增强趋化因子和PD-L1的表达，并改善抗原的呈递。综上，本文研究为深入理解SETD2失活调控的生物学特性提供了新的见解，并揭示了一种新型生物标志物，从而有望帮助识别出能因ICI治疗获益的癌症患者，尤其是胰腺癌、黑色素瘤和肾脏癌症等患者。（生物谷Bioon.com）原始出处： Xufen Zheng,Yuxiang Luo,Yangjie Xiong, et al. Tumor cell-intrinsic SETD2 inactivation sensitizes cancer cells to immune checkpoint blockade through the NR2F1-STAT1 pathway, Journal for ImmunoTherapy of Cancer (2023). DOI:10.1136/jitc-2023-007678