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http://dx.doi.org/10.1038/s41594-024-01475-4 | DOI Listing |
Nat Struct Mol Biol
February 2025
Department of Reproductive Endocrinology, University Hospital Zurich, University of Zurich, Schlieren, Switzerland.
J Neurol Surg B Skull Base
August 2024
Department of Otolaryngology and Head and Neck Surgery, Thomas Jefferson University Hospitals, Philadelphia, Pennsylvania, United States.
Understanding the genetic basis for the molecular classification of sinonasal undifferentiated carcinoma (SNUC) based on SMARCB1 may improve our understating regarding the nature of the disease. The objective of the study was to compare the genetic profile of SMARCB1-retained (SR-SNUC) and SMARCB1-deficient SNUC (SD-SNUC). Formalin-fixed, paraffin-embedded tissue from treatment-naive patients with SNUC were selected.
View Article and Find Full Text PDFNat Cell Biol
September 2023
Key Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China.
Front Cell Neurosci
October 2021
State Key Laboratory of Bioelectronics, Jiangsu Province High-Tech Key Laboratory for Bio-Medical Research, School of Life Sciences and Technology, Southeast University, Nanjing, China.
The super elongation complex (SEC) has been reported to play a key role in the proliferation and differentiation of mouse embryonic stem cells. However, the expression pattern and function of the SEC in the inner ear has not been investigated. Here, we studied the inner ear expression pattern of three key SEC components, AFF1, AFF4, and ELL3, and found that these three proteins are all expressed in both cochlear hair cells (HCs)and supporting cells (SCs).
View Article and Find Full Text PDFStem Cell Rev Rep
December 2020
Department of Hematology, the First Affiliated Hospital of Xiamen University and Institute of Hematology, School of Medicine, Xiamen University, 55 Zhenhai Road, Xiamen, 361003, Fujian, China.
Both HOX gene expression and CTCF regulation have been well demonstrated to play a critical role in regulating maintenance of leukemic stem cells (LSCs) that are known to be resistant to BET inhibitor (BETi). To investigate the regulatory role of CTCF boundary in aberrant HOX gene expression and the therapeutic sensitivity of BETi in AML, we employed CRISPR-Cas9 genome editing technology to delete 47 base pairs of the CTCF binding motif which is located between HOXA7 and HOXA9 genes (CBS7/9) in different subtypes of AML with either MLL-rearrangement or NPM1 mutation. Our results revealed that HOXA9 is significantly downregulated in response to the CBS7/9 deletion.
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