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Permanent defects in renal medullary structure and function after reversal of urinary obstruction.
JCI Insight
January 2025
Division of Nephrology, Department of Medicine, Vanderbildt University Medical Center, Nashville, United States of America.
Urinary obstruction causes injury to the renal medulla, impairing the ability to concentrate urine, and increasing the risk of progressive kidney disease. However, the regenerative capacity of the renal medulla after reversal of obstruction is poorly understood. To investigate this, we developed a mouse model of reversible urinary obstruction.
View Article and Find Full Text PDFANKRD11 binding to cohesin suggests a connection between KBG syndrome and Cornelia de Lange syndrome.
Proc Natl Acad Sci U S A
January 2025
Shenzhen Key Laboratory of Biomolecular Assembling and Regulation, Department of Neuroscience, School of Life Sciences, Southern University of Science and Technology, Shenzhen 518055, China.
Ankyrin Repeat Domain-containing Protein 11 () is a causative gene for KBG syndrome, a significant risk factor for Cornelia de Lange syndrome (CdLS), and a highly confident autism spectrum disorder gene. Mutations of lead to developmental abnormalities in multiple organs/tissues including the brain, craniofacial and skeletal bones, and tooth structures with unknown mechanism(s). Here, we find that ANKRD11, via a short peptide fragment in its N-terminal region, binds to the cohesin complex with a high affinity, implicating why mutation can cause CdLS.
View Article and Find Full Text PDFThe LIM-domain-only protein LMO2 and its binding partner LDB1 are differentially required for class switch recombination.
Proc Natl Acad Sci U S A
January 2025
Department of Immunology and Microbiology, Key Laboratory of Tropical Disease Control of Ministry of Education, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong 510000, China.
The LIM-domain-only protein LMO2 interacts with LDB1 in context-dependent multiprotein complexes and plays key roles in erythropoiesis and T cell leukemogenesis, but whether they have any roles in B cells is unclear. Through a CRISPR/Cas9-based loss-of-function screening, we identified LMO2 and LDB1 as factors for class switch recombination (CSR) in murine B cells. LMO2 contributes to CSR at least in part by promoting end joining of DNA double-strand breaks (DSBs) and inhibiting end resection.
View Article and Find Full Text PDFComplement C3 of tumor-derived extracellular vesicles promotes metastasis of RCC via recruitment of immunosuppressive myeloid cells.
Proc Natl Acad Sci U S A
January 2025
Zhongda Hospital, School of Life Sciences and Technology, Advanced Institute for Life and Health, Southeast University, Nanjing 210096, China.
Heterogeneous roles of complement C3 have been implicated in tumor metastasis and are highly context dependent. However, the underlying mechanisms linking C3 to tumor metastasis remain elusive in renal cell carcinoma (RCC). Here, we demonstrate that C3 of RCC cell-derived extracellular vesicles (EVs) contributes to metastasis via polarizing tumor-associated macrophages (TAMs) into the immunosuppressive phenotype and recruiting polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs).
View Article and Find Full Text PDFSUMOylation of TRIM28 is positively modulated by the BTB/POZ domain of Kaiso.
Mol Biol Rep
January 2025
Federal Research Centre «Fundamentals of Biotechnology», Russian Academy of Sciences, Moscow, Russia, 119071.
Background: TRIM28 plays a crucial role in maintaining genomic stability and establishing imprinting, facilitated by the diversity of KRAB zinc finger proteins. The SUMOylation of TRIM28 is essential for its function and is enhanced in the presence of the KRAB domain. Previously, we demonstrated that Kaiso, another factor capable of interacting with TRIM28, can promote its SUMOylation.
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