Xu Chen

ORCID: 0000-0002-3777-0514
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Ubiquitin and proteasome pathways
  • Mitochondrial Function and Pathology
  • Genetics and Neurodevelopmental Disorders
  • Macrophage Migration Inhibitory Factor
  • 14-3-3 protein interactions
  • Histone Deacetylase Inhibitors Research
  • Retinoids in leukemia and cellular processes
  • Cancer-related Molecular Pathways
  • Peptidase Inhibition and Analysis
  • Neuroscience and Neuropharmacology Research
  • Hippo pathway signaling and YAP/TAZ
  • Protein Tyrosine Phosphatases
  • RNA modifications and cancer
  • Ion channel regulation and function
  • Viral-associated cancers and disorders
  • Neurogenetic and Muscular Disorders Research
  • Muscle Physiology and Disorders
  • Phagocytosis and Immune Regulation
  • GDF15 and Related Biomarkers
  • TGF-β signaling in diseases
  • Acute Myeloid Leukemia Research
  • Cancer-related gene regulation
  • Cellular Mechanics and Interactions
  • Pneumocystis jirovecii pneumonia detection and treatment
  • Microtubule and mitosis dynamics

Shaanxi Normal University
2017-2024

Macau University of Science and Technology
2024

Sun Yat-sen Memorial Hospital
2023

Sun Yat-sen University
2023

University of California, San Francisco
2020

University of Baltimore
2011

Johns Hopkins University
2011

Abstract Background Metastatic prostate cancer (mPCa) has a poor prognosis with limited treatment options. The high mobility of tumor cells is the key driving characteristic metastasis. However, mechanism complex and far from clarified in PCa. Therefore, it essential to explore metastasis discover an intrinsic biomarker for mPCa. Methods Transcriptome sequencing data clinicopathologic features PCa multifarious public databases were used identify novel metastatic genes tissue cohort...

10.1186/s12967-023-04146-y article EN cc-by Journal of Translational Medicine 2023-05-05

Therapeutic approaches for acute myeloid leukaemia (AML) and myelodysplastic syndromes (MDS) differ due to distinct diagnostic criteria treatment strengths. However, reliable biomarkers differentiate AML from MDS are needed. This study investigated transfer RNA (tRNA) modifications, particularly hydroxy-wybutosine (OHyW), in the transition AML. We found a significant decrease OHyW its biosynthetic enzyme leucine carboxyl methyltransferase 2 (LCMT2, alias symbol is TYW4) levels compared MDS....

10.1111/bjh.19873 article EN British Journal of Haematology 2024-11-10

Leukemia is a malignant disease of hematopoietic tissue characterized by the differentiation arrest and proliferation immature precursor cells in bone marrow. ERG (ETS-related gene) an important member E26 transformation-specific (ETS) transcription factor family that plays crucial role physiological pathological processes. However, its modification leukemia remains underexplored. In present study, we stably knocked down or overexpressed observed significantly promotes inhibits AML (acute...

10.3389/fmolb.2021.652284 article EN cc-by Frontiers in Molecular Biosciences 2021-03-26

Endothelial-mesenchymal transition (EndoMT) is a complex biological process in which endothelial cells are transformed into mesenchymal cells, and dysregulated EndoMT causes variety of pathological processes. Transforming growth factor beta (TGF-β) signaling effectively induces the Smad2 critical protein TGF-β pathway. However, whether small ubiquitin-like modifier modification (SUMOylation) involved remains unclear. Here, we show that predominantly modified by SUMO1 at two major SUMOylation...

10.1016/j.jbc.2023.105244 article EN cc-by Journal of Biological Chemistry 2023-09-09

Sentrin/small ubiquitin-like modifier (SUMO)-specific protease 2 (SENP2)-deficient mice develop spontaneous seizures in early life because of a marked reduction M currents, which regulate neuronal membrane excitability. We have previously shown that hyper-SUMOylation the Kv7.2 and Kv7.3 channels is critically involved regulation currents conducted by these potassium voltage-gated channels. Here, we show proteins reduced binding to lipid secondary messenger PIP2. CaM1 has been be tethered Kv7...

10.1016/j.jbc.2021.101183 article EN cc-by-nc-nd Journal of Biological Chemistry 2021-09-10

Abstract Breast carcinoma exhibits the highest incidence among various cancers and is foremost cause of mortality in women. Increasing evidence shows that SUMOylation proteins plays a critical role progression breast cancer; however, SENP2 its molecular mechanism cancer remain underexplored. Here, we discerned promoted tumorigenesis both vitro vivo. Furthermore, identified ERK2 was SUMOylated played by deconjugating cancer. ubiquitin-proteasomal degradation, thus inhibiting...

10.1007/s00018-024-05505-8 article EN cc-by Cellular and Molecular Life Sciences 2024-11-23

Abstract Ovarian serous carcinoma (OSC) represents one of the most aggressive neoplastic diseases because cases present at an advanced stage when therapy is usually ineffective. We have previously reported that Notch3 gene amplification and overexpression occurs frequently in OSC. Activation signaling essential for survival OSC cells with overexpression, especially presence chemotherapeutic agents. pathway activation has been known to transcriptionally regulate array genes, including those...

10.1158/1538-7445.am2011-1987 article EN Cancer Research 2011-04-01

目的探讨微RNA-218(miRNA-218)对后纵韧带骨化症(OPLL)患者原代后纵韧带细胞骨化的影响及其作用机制。 方法原代培养5例OPLL患者及5例非OPLL者的韧带细胞,比较2组细胞miRNA-218的表达差异。利用agomir过表达或antagomir抑制OPLL患者韧带细胞中miRNA-218的表达水平后进行成骨诱导,通过检测茜素红染色水平、碱性磷酸酶活性及成骨相关基因的表达验证miRNA-218对韧带细胞骨化的作用。采用Target scan预测miRNA-218的靶基因,并采用双荧光素酶报告基因实验验证miRNA-218的靶向作用。 结果OPLL患者韧带细胞miRNA-218的表达水平低于非OPLL者,差异有统计学意义(P 结论miRNA-218能明显抑制原代后纵韧带细胞的骨化反应,其作用机制与抑制RUNX2和COL1A1基因表达相关。

10.3969/j.issn.1672-2957.2019.04.008 article KO 2019-08-28

Abstract Uveal Melanoma (UM) is a highly lethal cancer with 50% of patients developing metastatic disease, primarily the liver, currently no effective treatment options. UM driven by mutations constitutively activating Gαq pathway, about 90% affecting heterotrimeric G-protein alpha subunits GNAQ or GNA11 and less commonly (<10%) CYSLTR2 (a GNAQ/11 coupled receptor) PLCB4 direct effector Gαq). Directly targeting therefore could be therapeutic relevance for majority UMs. Here we found...

10.1158/1538-7445.am2020-1812 article EN Cancer Research 2020-08-15
Coming Soon ...