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BHLHE40 Cooperates with GATA2/3 to Control Human Syncytiotrophoblast Lineage Differentiation.
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Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 201204, China.
Syncytiotrophoblasts (STBs) constitute one of the core components of the placenta, responsible for synthesizing pregnancy-sustaining hormones such as human chorionic gonadotropin (HCG). Deficient syncytialization of cytotrophoblasts affects the hormonal secretion and placental development, contributing to pregnancy-associated disorders, including spontaneous miscarriage. To date, the molecular mechanisms, particularly the role of transcription factors (TFs), in STB lineage specification remain incompletely understood.
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Department of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science, 6-3-1 Niijuku, Katsushika-ku, Tokyo, 125-8585, Japan.
Mucosal mast cells (MMCs) are distinguished from connective tissue mast cells (MCs) by the specific cell-surface expression of integrin CD103 (also known as integrin αE/β7; αE is encoded by Itgae) and mast cell protease 1 and 2 (Mcpt1 and Mcpt2, respectively). Although the expression of the Mcpt1 and Mcpt2 genes is cooperatively regulated by the transcription factor GATA-binding protein 2 (GATA2) and transforming growth factor beta (TGF-β) signaling in MMCs, the transcriptional mechanism of the cell-surface expression of CD103 remains unknown. We herein found that surface CD103 and Itgae mRNA levels were significantly increased by the knockdown (KD) of Gata2 in mouse bone marrow-derived MCs (BMMCs), which was accelerated by TGF-β stimulation.
View Article and Find Full Text PDFThe CBFA2T3::GLIS2 (CG) fusion protein causes aggressive pediatric acute megakaryoblastic leukemia (AMKL). Although dysregulated molecular pathways in AMKL have been identified, their role in early pre-leukemic transformation remains poorly understood. We developed a disease model utilizing genetically modified human induced pluripotent stem cells (hiPSC) physiologically and conditionally expressing CG.
View Article and Find Full Text PDFRevealing lactylation-mediated mechanisms and hub genes in heart failure pathogenesis.
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Department of Paediatrics, The Second Affiliated Hospital of Anhui Medical University, Hefei City, China.
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