更新于：2024-11-01

TAGLN2

更新于：2024-11-01

基本信息

别名

Epididymis tissue protein Li 7e、HA1756、KIAA0120

+ [4]

简介-

关联

项与 TAGLN2 相关的药物

TSG1180

靶点

TAGLN2

作用机制

TAGLN2 激动剂

在研机构

上海中医药大学

原研机构

上海中医药大学

在研适应症

哮喘

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 TAGLN2 相关的临床结果

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100 项与 TAGLN2 相关的转化医学

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0 项与 TAGLN2 相关的专利（医药）

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214

项与 TAGLN2 相关的文献（医药）

2025-01-01·Journal of Affective Disorders

Identifying clinical and proteomic markers for early diagnosis and prognosis prediction of major psychiatric disorders

Article

作者: Kim, Minah ; Kim, Jayoun ; Park, Dong Yeon ; Rhee, Sang Jin ; Baik, Myungjae ; Jung, Hee Yeon ; Ha, Kyooseob ; Lee, Junhee ; Roh, Sungwon ; Lee, Hyunju ; Ahn, Yong Min ; Lee, Yunna ; Han, Dohyun ; Kim, Eun Young ; Lee, Tae Young ; Kim, Hyeyoon ; Kwon, Jun Soo ; Kim, Se Hyun

BACKGROUNDTo clarify if blood proteins can predict disease progression among individuals at clinical high-risk of severe mental illness (CHR-SMI), we developed a statistical model incorporating clinical and blood protein markers to distinguish the transition group (who developed severe mental illness) (CHR-SMI-T) and from non-transition group (CHR-SMI-NT) at baseline.METHODSNinety individuals (74 at CHR-SMI: 16 patients) were monitored for ≤4 years and were the focus of predictive models. Three predictive models (1 [100 clinical variables], 2 [158 peptides], and 3 [100 clinical variables +158 peptides]) were evaluated using area under the receiver operating characteristic (AUROC) values. Clinical and protein feature patterns were evaluated by linear mixed-effect analysis within the model at 12 and 24 months among patients who did (CHR-SMI-T) and did not transition (CHR-SMI-NT) and the entire group.RESULTEighteen CHR-SMI individuals with major psychiatric disorders (first episode psychosis: 2; bipolar II disorder: 13; major depressive disorder; 3) developed disorders over an average of 17.7 months. The combined model showed the highest discriminatory performance (AUROC = 0.73). Cytosolic malate dehydrogenase and transgelin-2 levels were lower in the CHR-SMI-T than the CHR-SMI-NT group. Complement component C9, inter-alpha-trypsin inhibitor heavy chain H4, von Willebrand factor, and C-reactive protein were lower in the patient than the CHR-SMI-NT group. These differences were non-significant after FDR adjustment.LIMITATIONSSmall sample, no control for medication use.CONCLUSIONThis exploratory study identified clinical and proteomic markers that might predict severe mental illness early onset, which could aid in early detection and intervention. Future studies with larger samples and controlled variables are needed to validate these findings.

2024-12-31·Experimental Lung Research

Exosomes derived from hypoxic alveolar epithelial cells promote the phenotypic transformation of pulmonary artery smooth muscle cells via the Rap1 pathway

Article

作者: Yang, Yongju ; Liu, Xingrui ; Zhou, Feifei ; Hu, Jian ; Gao, Yating ; Sun, Guifang ; Zhu, Caiyan ; Liu, Bin ; Feng, Yusen ; Zhao, Fangyun ; Liu, Fei ; Du, Zhiqin ; Jiang, Yue

Background: Hypoxic pulmonary hypertension (HPH) is one of the important pathophysiological changes in chronic pulmonary heart disease. Hypoxia promotes the phenotypic transformation of pulmonary artery smooth muscle cells (PASMCs). Extracellular exosomes regulate vascular smooth muscle cell (VSMC) phenotypic switch. Aim: Given the importance of exosomes and alveolar epithelial cells (AECs) in HPH, the present study aimed to address the issue of whether AEC-derived exosomes promote HPH by triggering PASMC phenotypic switch. Methods: Cell Counting Kit-8 (CCK-8), TRITC-phalloidin staining, and Western blotting were used to examine the effects of AEC-derived exosomes on cell proliferation, intracellular actin backbone distribution, and expression of phenotypic marker proteins in PASMCs. Transcriptomics sequencing was used to analyze differentially expressed genes (DEGs) between groups. Results: Hypoxia-induced exosomes (H-exos) could promote the proliferation of PASMCs, cause the reduction of cellular actin microfilaments, promote the expression of synthetic marker proteins (ELN and OPN), reduce the expression of contractile phenotypic marker proteins (SM22-α and α-SMA), and induce the phenotypic transformation of PASMCs. Transcriptomics sequencing analysis showed that the Rap1 signaling pathway was involved in the phenotypic transformation of PASMCs induced by H-exos. Conclusion: The present study identified that hypoxia-induced AEC-derived exosomes promote the phenotypic transformation of PASMCs and its mechanism is related to the Rap1 signaling pathway.

2024-10-01·Journal of Oral Pathology & Medicine

Metformin Radiosensitizing Effect on Hypoxic Oral Squamous Cell Carcinoma Cells by GAPDH and TAGLN2

Article

作者: Santiago, Luiza ; Santos, Sérgio Henrique Sousa ; de Souza, Marcela Gonçalves ; Santos, Eliane Macedo Sobrinho ; de Souza, Pericles Crisostomo ; Guimarães, Talita Antunes ; de Jesus, Sabrina Ferreira ; De‐Paula, Alfredo Maurício Batista ; D'Angelo, Marcos Flávio Silveira Vasconcelos ; Santos, Eloá Mangabeira ; Guimarães, André Luiz Sena ; Farias, Lucyana Conceição

ABSTRACTObjectiveTumor hypoxia is associated with a poorer prognosis in cancer patients and can diminish the efficacy of radiation therapy (RT). This study investigates the potential of metformin to enhance radiosensitivity in hypoxic cancer cells.MethodsPreliminary experiments were conducted to validate the impact of hypoxia on radiation response. Reactive oxygen species (ROS) levels, cell migration, and cell death were assessed in hypoxic, radiated cells treated with metformin. Proteomic and ontological analyses were employed to identify molecular targets associated with the radiosensitizing effect of metformin. Proteomic and ontological findings were validated through patient samples and in vitro studies.ResultsMetformin amplified cell death, induced DNA fragmentation, decreased cell migration, and elevated ROS levels in hypoxic, radiated cells. Proteomic analyses revealed that GAPDH and TAGLN2 were identified as pivotal targets linked to the radiosensitizing effect of metformin. Oral cancer patients exhibited elevated levels of TAGLN2 and reduced levels of GAPDH. Metformin downregulated TAGLN2 and upregulated GAPDH in hypoxic, radiated cells. Additionally, metformin reduced levels of mutated p53.ConclusionsThis study suggests that metformin can enhance radiosensitivity in hypoxic cells, operating through modulation of GAPDH and TAGLN2. Furthermore, metformin effectively reduces mutated p53 levels in radiated cells under hypoxic conditions.