Jue Zhang

ORCID: 0000-0001-8331-2496
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About
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Research Areas
  • Ion Transport and Channel Regulation
  • Caveolin-1 and cellular processes
  • Pluripotent Stem Cells Research
  • Immune cells in cancer
  • Magnesium in Health and Disease
  • Peroxisome Proliferator-Activated Receptors
  • CRISPR and Genetic Engineering
  • Electrospun Nanofibers in Biomedical Applications
  • Cancer, Hypoxia, and Metabolism
  • Bone Metabolism and Diseases
  • Pancreatitis Pathology and Treatment
  • Mitochondrial Function and Pathology
  • ATP Synthase and ATPases Research
  • Cancer, Lipids, and Metabolism
  • Atherosclerosis and Cardiovascular Diseases
  • Bone health and osteoporosis research
  • Bone health and treatments
  • Renal and related cancers
  • Dyeing and Modifying Textile Fibers
  • Adipokines, Inflammation, and Metabolic Diseases
  • Phagocytosis and Immune Regulation
  • Fibroblast Growth Factor Research
  • Advanced Glycation End Products research
  • Ferroptosis and cancer prognosis
  • Cell Image Analysis Techniques

Versiti Blood Center of Wisconsin
2020-2025

Sichuan University
2025

West China Hospital of Sichuan University
2025

Guangzhou University of Chinese Medicine
2025

Foshan Hospital of TCM
2025

Peking University
2024

Center for Interdisciplinary Studies
2024

Morgridge Institute for Research
2013-2024

Medical College of Wisconsin
2024

Nanjing Medical University
2013-2022

Human pluripotent stem cells offer the best available model to study underlying cellular and molecular mechanisms of human embryonic lineage specification. However, it is not fully understood how individual exit state transition towards their respective progenitor states. Here, we analyze transcriptomes cell-derived lineage-specific progenitors by single-cell RNA-sequencing (scRNA-seq). We identify a definitive endoderm (DE) transcriptomic signature that leads us pinpoint critical time...

10.1186/s13059-016-1033-x article EN cc-by Genome biology 2016-08-17

Rationale: A hallmark of chronic inflammatory disorders is persistence proinflammatory macrophages in diseased tissues. In atherosclerosis, this associated with dyslipidemia and oxidative stress, but mechanisms linking these phenomena to macrophage activation remain incompletely understood. Objective: To investigate dyslipidemia, through modulation immunometabolism explore therapeutic potential targeting specific metabolic pathways. Methods Results: Using a combination biochemical,...

10.1161/circresaha.119.315833 article EN Circulation Research 2019-10-18

Helicobacter pylori (H. pylori) infection was identified as a substantial risk factor for gastric cancer development, but the eradication of H. did not necessarily lead to reduction in incidence cancer. Non-Helicobacter (non-H. bacteria stomach are involved transformation gastritis carcinoma. The aim this study characterize microbiome composition mucosa and its functions non-H. pylori-negative) patients with chronic atrophic (CAG) non-atrophic (CNAG). Fourteen CNAG samples twenty-three CAG...

10.1186/s12876-025-03900-4 article EN cc-by-nc-nd BMC Gastroenterology 2025-04-29

Fibroblast growth factor receptor 2 (Fgfr2) signaling is critical in maintaining ureteric branching architecture and mesenchymal stromal morphogenesis the kidney. substrate 2α (Frs2α) a major docking protein for Fgfr2 with downstream targets including Ets variant (Etv) 4 Etv5 other systems. Furthermore, global deletion of Frs2α causes early embryonic lethality. The purpose study was to determine role mediating epithelium. To that end, we generated mice conditional epithelium ( UB−/− ) point...

10.1152/ajprenal.00262.2009 article EN AJP Renal Physiology 2009-09-10

Contractile to synthetic phenotypic switching of smooth muscle cells (SMCs) contributes stenosis in vascular disease and transplants. To generate more contractile SMCs, we performed a high-throughput differentiation screen using MYH11-NLuc-tdTomato human embryonic stem cell reporter line. We identified RepSox as factor that promotes MYH11-positive by promoting NOTCH signaling. induces SMCs exhibit phenotype than generated PDGF-BB TGF-β1, two factors previously used for SMC but which also...

10.1016/j.stemcr.2019.04.013 article EN cc-by-nc-nd Stem Cell Reports 2019-05-09

Objective: Metastasis and therapeutic resistance are the major determinants of lung cancer progression high mortality. Epithelial-mesenchymal transition (EMT) plays a key role in metastasis resistance. Highly expressed glucose-regulated protein 78 (GRP78) is poor prognostic factor possibly correlated with EMT. This study aims to examine whether up-regulation GRP78 involved EMT adenocarcinoma explore underlying downstream molecular pathways. Study Design: was assessed by analysis cell...

10.3389/fonc.2019.00137 article EN cc-by Frontiers in Oncology 2019-03-12

Of the four Na-K-ATPase α-isoforms, ubiquitous α1 possesses both ion transport and Src-dependent signaling functions. Mechanistically, we have identified two putative pairs of domain interactions between Src that are critical for function. Our subsequent report α2 lacks these Src-binding sites fails to carry on further supported our proposed model direct interaction but fell short providing evidence a causative role. This hypothesis was specifically tested here by introducing key residues...

10.1152/ajpcell.00124.2017 article EN AJP Cell Physiology 2017-12-06

Hypoimmune gene edited human pluripotent stem cells (hPSCs) are a promising platform for developing reparative cellular therapies that evade immune rejection. Existing first-generation hypoimmune strategies have used CRISPR/Cas9 editing to modulate genes associated with adaptive (e.g., T cell) responses, but largely not addressed the innate monocytes, neutrophils) mediate inflammation and rejection processes occurring early after graft transplantation. We identified adhesion molecule ICAM-1...

10.1101/2024.06.07.597791 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-06-09

Recent studies have highlighted a critical role for CD40 in the pathogenesis of renal injury and fibrosis. However, little is currently understood about regulation this setting.We use novel Na/K-ATPase cell lines inhibitors order to demonstrate regulatory function with regards expression function. We utilize 5/6 partial nephrectomy as well direct infusion ligand mechanism exists vivo.We that knockdown α1 isoform causes reduction while rescue but not α2 restores epithelial cells. Second,...

10.1093/ndt/gfx334 article EN Nephrology Dialysis Transplantation 2017-11-17

We have reported that the reduction in plasma membrane cholesterol could decrease cellular Na/K-ATPase α1-expression through a Src-dependent pathway. However, it is unclear whether regulate other α-isoforms and molecular mechanisms of this regulation are not fully understood. Here we used cells expressing different α isoforms found by U18666A decreased expression α1-isoform but α2- or α3-isoform. Imaging analyses showed redistribution α1 α3 α2. Moreover, led to late endosomes/lysosomes,...

10.1152/ajpcell.00083.2020 article EN AJP Cell Physiology 2020-09-30

Several signaling events have been recognized as essential for regulating cell lineage specification and organogenesis in animals. We find that the gain of an amino-terminal caveolin binding motif (CBM) α subunit Na/K-adenosine triphosphatase (ATPase) (NKA) is required early stages both mice Caenorhabditis elegans. The evolutionary CBM occurred at same time acquisition sites Na+/K+. Loss this does not affect or initiation organogenesis, but arrests further organ development. Mechanistically,...

10.1126/sciadv.aaw5851 article EN cc-by-nc Science Advances 2020-05-27

A Na/K-ATPase α1 caveolin-binding motif regulates adipogenesis. Mutation of this binding in the mouse leads to reduced fat with increased extracellular matrix production and inflammation. RNA-seq analysis pharmacological interventions human iPSC-derived adipocytes revealed that TGF-β signal, rather than Na/K-ATPase-mediated ion transport, is a key mediator NKA regulation

10.1152/ajpcell.00168.2024 article EN AJP Cell Physiology 2024-05-06

In the present study, we investigated whether high dietary Ca and exogenous parathyroid hormone 1–34 fragments (PTH 1–34) have synergistic effects on bone formation in adult mice, explored related mechanisms. Adult male mice were fed a normal diet, high-Ca PTH-treated or diet combined with subcutaneously injected PTH (80 μg/kg per d) for 4 weeks. Bone mineral density, trabecular volume, osteoblast number, alkaline phosphatase (ALP)- type I collagen-positive areas, expression levels of...

10.1017/s0007114514004309 article EN cc-by British Journal Of Nutrition 2015-03-06
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