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TRIM71 NHL Domain is a critical driver of various cellular process and is dysregulated in several medical conditions like non-small cell lung cancer, hepatocellular carcinoma and congenital hydrocephalus. However, its pathways and binding with CDKN1A has not been well studied. To investigate its interaction with CDKN1A, we expressed TRIM71 NHL domain in SF9 (Spodoptera frugiperda) insect cells using the pFastBacTM HT B plasmid, was purified by size exclusion chromatography and its crystal structure was determined successfully (PDB ID: 9JUR). Fluorescence polarization (Kd = 0.42 ± 0.04 μM) and EMSA confirmed strong and specific binding to CDKN1A mRNA, indicating its role in repressing CDKN1A expression to promote cancer cell proliferation. To further delve into its therapeutic implication, we screened a library of 2517 phytochemicals from 48 medicinal plants to identify potential natural inhibitors of the TRIM71 NHL domain. Epigallocatechin Gallate and Cyanidin 3-O-galactoside demonstrated binding affinities of -9.1 kcal/mol and -9.0 kcal/mol, respectively, while SPR confirmed their affinities with Kd values of 3.2 μM and 17.3 μM, accordingly. Molecular dynamics simulations confirmed protein-ligand complexes stability. In summary, human TRIM71 NHL domain crystal structure provides a foundation for understanding its structural features while exploring two potential inhibitors for therapeutic applications.
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http://dx.doi.org/10.1016/j.ijbiomac.2025.142764 | DOI Listing |
Int J Biol Macromol
May 2025
Center for Advanced Interdisciplinary Science and Biomedicine of IHM, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230027, China; Ministry of Education Key Laboratory for Membraneless Organelles and Cellular Dynamics, Division of Life Sciences and Medi
TRIM71 NHL Domain is a critical driver of various cellular process and is dysregulated in several medical conditions like non-small cell lung cancer, hepatocellular carcinoma and congenital hydrocephalus. However, its pathways and binding with CDKN1A has not been well studied. To investigate its interaction with CDKN1A, we expressed TRIM71 NHL domain in SF9 (Spodoptera frugiperda) insect cells using the pFastBacTM HT B plasmid, was purified by size exclusion chromatography and its crystal structure was determined successfully (PDB ID: 9JUR).
View Article and Find Full Text PDFLife Sci Alliance
April 2025
Molecular Immunology and Cell Biology, Life & Medical Sciences Institute (LIMES), University of Bonn, Bonn, Germany
The transition of an embryo from gastrulation to organogenesis requires precisely coordinated changes in gene expression, but the underlying mechanisms remain unclear. The RNA-binding protein Trim71 is essential for development and serves as a potent regulator of post-transcriptional gene expression. Here, we show that global deficiency of induces severe defects in mesoderm-derived cells at the onset of organogenesis.
View Article and Find Full Text PDFBrain
December 2024
Department of Neurosurgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
Congenital hydrocephalus, characterized by cerebral ventriculomegaly, is one of the most common reasons for paediatric brain surgery. Recent studies have implicated lin-41 (lineage variant 41)/TRIM71 (tripartite motif 71) as a candidate congenital hydrocephalus risk gene; however, TRIM71 variants have not been systematically examined in a large patient cohort or conclusively linked with an OMIM syndrome. Through cross-sectional analysis of the largest assembled cohort of patients with cerebral ventriculomegaly, including neurosurgically-treated congenital hydrocephalus (totalling 2697 parent-proband trios and 8091 total exomes), we identified 13 protein-altering de novo variants (DNVs) in TRIM71 in unrelated children exhibiting variable ventriculomegaly, congenital hydrocephalus, developmental delay, dysmorphic features and other structural brain defects, including corpus callosum dysgenesis and white matter hypoplasia.
View Article and Find Full Text PDFSci Bull (Beijing)
January 2024
State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy, Nankai University, Tianjin 300353, China. Electronic address:
Autophagy
May 2024
Institute of Molecular Virology, Ulm University Medical Center, Ulm, Baden-Wuerttemberg, Germany.
Macroautophagy/autophagy is a tightly regulated cellular process integral to homeostasis and innate immunity. As such, dysregulation of autophagy is associated with cancer, neurodegenerative disorders, and infectious diseases. While numerous factors that promote autophagy have been characterized, the key mechanisms that prevent excessive autophagy are less well understood.
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