Bin Bai

Air Force Medical University

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Qingchuan Zhao

National Clinical Research Center for Digestive Diseases

Zhengyan Li

Shanghai University of Traditional Chinese Medicine

Shiqi Wang

First Affiliated Hospital of Henan University

Pengfei Yu

Xijing Hospital

Xiaonan Zhang

Bengbu Medical College

Yanjiao Zhao

Northeastern University

Bing Wang

Qingdao University

Tao Wang

Guizhou Provincial People's Hospital

Yang Yu

Second Affiliated Hospital of Harbin Medical University

Jiahui Zhao

China Guangzhou Analysis and Testing Center

Cooperative Institutions

John Wiley & Sons (United States)

John Wiley & Sons (United Kingdom)

Air Force Medical University

Interface (United Kingdom)

Xijing Hospital

University of East Asia

Zhejiang University

Chinese Academy of Sciences

National Clinical Research Center for Digestive Diseases

Sun Yat-sen University

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Emergency Transcatheter Arterial Embolization for Massive Hemoptysis Due to Pulmonary Tuberculosis and Tuberculosis Sequelae

Cell Biochemistry and Biophysics (2014)

Xu Wei Honghui Wang Bin Bai

Bronchial artery

Arterial Embolization

10.1007/s12013-014-0182-3

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Citations (7)

PTPN22 activates the PI3K pathway via 14‐3‐3τ in T cells

FEBS Journal (2023)

Bin Bai Tao Wang Xiaonan Zhang Xinlei Ba Na Zhang

The protein tyrosine phosphatase PTPN22 inhibits T cell activation by dephosphorylating some essential proteins in the T cell receptor-mediated signalling pathway, and its negative regulatory function protects organisms from autoimmune disease. 14-3-3τ is an adaptor protein that regulates target protein function through its intracellular localization. In the present study, we determined that PTPN22 binds to 14-3-3τ via the PTPN22-Ser640 phosphorylation side. PTPN22 binding to 14-3-3τ resulted in 14-3-3τ-Tyr179 dephosphorylation, and reduced the association between 14-3-3τ and Shc, which competitively increased 14-3-3ζ binding to Shc and activated phosphoinositide 3-kinase (PI3K) by bringing it to the membrane. In addition, PTPN22 decreased the tyrosine phosphorylation of p110 to activate PI3K. These two pathways cooperatively affect PI3K activity and the expression of PI3K downstream proteins, such as phosphorylated Akt, mammalian target of rapamycin and forkhead box O1, which inhibited the expression of some proinflammatory factors such as interleukin-1β, interleukin-2, interleukin-6, interferon-γ and tumour necrosis factor-α. Our research provides a preliminary theory for PTPN22 regulating T cell activation, development and immune response via the PI3K/Akt/mammalian target of rapamycin pathway and brings new information for clarifying the functions of PTPN22 in autoimmune diseases.

PTPN22

10.1111/febs.16878

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Citations (1)

Preventative effects of prostaglandin E1 in combination with iodized olive oil on liver fibrosis after transcatheter arterial chemoembolization in a rabbit model of CCl₄-induced liver fibrosis

Canadian Journal of Physiology and Pharmacology (2015)

Shu-Qiang Jin Haili Cao Kaibing Wang Ying Li Bin Bai

To explore the preventative effects of prostaglandin E1 (PGE1) on a rabbit model of CCl4-induced liver fibrosis after transcatheter arterial chemoembolization (TACE), we generated a rabbit model of CCl4-induced liver fibrosis by treatment with 40% CCl4 in iodized olive oil for 16 weeks. Body mass and serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total protein (TP), albumin (ALB), albumin:globulin ratio (A:G), total bilirubin (TBIL), and direct bilirubin (DBIL) were measured. After TACE, the levels of hyaluronic acid (HA), procollagen III (PC III), laminin (LN), and collagen IV (IV-C) were measured, and the severity of liver fibrosis as well as the morphology of liver tissues were determined. Body mass in the model group was significantly decreased from 10 to 16 weeks, and the serum levels of ALT, AST, TP, TBIL, and DBIL levels were significantly increased while the model was being generated; the levels of ALB and A:G were significantly decreased. After TACE, serum levels of HA, PC III, and LN in the group injected with 1.0 mL iodized olive oil (Group B) were higher than in the group that were injected with 1.0 mL iodized olive oil + 0.2 mL PGE1 (Group C), whereas the serum levels of IV-C were lower. The severity of liver fibrosis was ameliorated in Group C. The combination of PGE1 and iodized olive oil prevented the development of liver fibrosis following TACE.

Hepatic fibrosis

10.1139/cjpp-2014-0561

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Citations (7)

Expression of iron-regulators in the bone tissue of rats with and without iron overload

BioMetals (2018)

Yanqin Li Bin Bai Yaohui Zhang

Osteocyte

DMT1

Bone remodeling

Transferrin receptor

Ferroportin

10.1007/s10534-018-0133-3

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Citations (17)

Surgical and long-term oncologic outcomes of laparoscopic and open gastrectomy for serosa-positive (pT4a) gastric cancer: A propensity score-matched analysis

Surgical Oncology (2019)

Zhengyan Li Yezhou Liu Yiming Hao Bin Bai Deliang Yu

Surgical oncology

10.1016/j.suronc.2019.01.003

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Citations (22)

Divalent Metal Transporter 1 Expression and Regulation in Human Placenta

Biological Trace Element Research (2011)

Yanqin Li Bin Bai Xiaoxiao Cao Yaohui Zhang Hong Yan

DMT1

Syncytiotrophoblasts

10.1007/s12011-011-9214-7

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Citations (23)

PTPN18 Serves as a Potential Oncogene for Glioblastoma by Enhancing Immune Suppression

Oxidative Medicine and Cellular Longevity (2023)

Tao Wang Yang Yu Xinlei Ba Xiaonan Zhang Na Zhang

Glioblastoma is characterized as one of the deadliest cancers in humans. The survival time is not improved by standard treatment. Although immunotherapy has revolutionized cancer treatment, the current therapy targets for glioblastoma patients are not satisfied. We systematically analyzed the expression patterns, predictive values, and immunological characteristics of PTPN18 in glioblastoma. The independent datasets and functional experiments were employed to validate our findings. Our data showed that PTPN18 is potentially cancerogenic in glioblastoma with advanced grades and poor prognosis. High expression of PTPN18 correlated with CD8+ T cell exhaustion and immune suppression in glioblastoma. In addition, PTPN18 facilitates glioblastoma progression by accelerating glioma cell prefiltration, colony formation, and tumor growth in mice. PTPN18 also promotes cell cycle progression and inhibits apoptosis. Our results illustrate the characterization of PTPN18 in glioblastoma and highlight the potential value as an immunotherapeutic target for glioblastoma treatment.

Tumor progression

10.1155/2023/2994316

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Citations (1)

PTPN22 and the pathogenesis of ulcerative colitis: Insights into T cell differentiation and the JAK/STAT signaling pathway

Cellular Signalling (2024)

Yang Yu Xinlei Ba Tong Li Wenying Xu Jiahui Zhao

PTPN22

Pathogenesis

10.1016/j.cellsig.2024.111551

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Citations (0)

Enhanced Recovery After Surgery Programs for Laparoscopic Abdominal Surgery: A Systematic Review and Meta‐analysis

World Journal of Surgery (2018)

Zhengyan Li Qingchuan Zhao Bin Bai Gang Ji Yezhou Liu

Cardiothoracic surgery

Vascular surgery

10.1007/s00268-018-4656-0

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Citations (27)

Proteomic Profiling of Gastric Signet Ring Cell Carcinoma Tissues Reveals Characteristic Changes of the Complement Cascade Pathway

Molecular & Cellular Proteomics (2021)

Fan Yang Bin Bai Yuting Liang Yan Ren Yanxia Liu

Signet ring cell carcinoma (SRCC) is a histological subtype of gastric cancer with distinct features in multiple aspects compared with adenocarcinomas (ACs). The lack of a systematic molecular overview of this disease has led to slow progress in its clinical practice. In the present proteomics study, gastric tissues were collected from tumors and adjacent tissues, including 14 SRCCs and 34 ACs, and laser capture microdissection (LCM) was employed to eradicate the cellular heterogeneity of the tissues. The proteomes of tissues were profiled by data-independent acquisition (DIA) mass spectrometry (MS). Based on the over 6000 proteins quantified, univariate analysis and pathway enrichment revealed that some proteins and pathways demonstrated differences between SRCC and ACs. Importantly, the upregulation of a majority of complement-related proteins was notable for SRCC but not for ACs. A hypothesis, based on the proteomics evidence, was proposed that the complement cascade was evoked in the SRCC microenvironment upon infiltration, and the SRCC cells survived the complement cytotoxicity by secreting endogenous negative regulators. Moreover, an attempt was made to establish appropriate cell models for gastric SRCC through proteomic comparison of the 15 gastric cell lines and gastric tumors. The predictions of a supervised classifier suggested that none of these gastric cell lines qualified to mimic SRCC. This study discovered that the complement cascade is activated at a higher level in gastric SRCC than in ACs.

Laser capture microdissection

Proteome

10.1016/j.mcpro.2021.100068

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Citations (12)