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http://dx.doi.org/10.1016/0162-3109(96)00129-4 | DOI Listing |
Sci Adv
November 2024
Department of Biochemistry and Cellular and Molecular Biology, The University of Tennessee, Knoxville, TN, USA.
Optimal gene transcription is achieved through precise interactions between transcription factors and their DNA binding sites. We provide evidence that conserved distally located 5'-flanking sequences interact directly with the intrinsically disordered amino-terminal region of the thyroid receptor-α (TRα) to control transcriptional activity. Simulated modeling and dynamics with multiple ChIP-seq-derived sequences consistently reveal specific lysine/arginine-DNA minor groove interactions.
View Article and Find Full Text PDFInt J Mol Sci
November 2024
Sagol Department of Neurobiology, Faculty of Natural Sciences, University of Haifa, Haifa 3103301, Israel.
N-methyl-D-aspartate receptors (NMDARs) are critical components of the mammalian central nervous system, involved in synaptic transmission, plasticity, and neurodevelopment. This review focuses on the structural and functional characteristics of NMDARs, with a particular emphasis on the GRIN2 subunits (GluN2A-D). The diversity of GRIN2 subunits, driven by alternative splicing and genetic variants, significantly impacts receptor function, synaptic localization, and disease manifestation.
View Article and Find Full Text PDFReplicative helicases are assembled on chromosomes by helicase loaders before initiation of DNA replication. Here, we investigate mechanisms used by the bacterial DnaB replicative helicase and the DciA helicase loader. In the present structure of the DnaB-ssDNA•ATPγS complex, the amino-terminal (NTD) tier, previously found as an open spiral in a GDP•AlF4 complex, was observed to adopt a closed planar arrangement.
View Article and Find Full Text PDFSci Adv
November 2024
Cancer Program, Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800, Australia.
Tuberous sclerosis complex (TSC) is targeted to the lysosomal membrane, where it hydrolyzes RAS homolog-mTORC1 binding (RHEB) from its GTP-bound to GDP-bound state, inhibiting mechanistic target of rapamycin complex 1 (mTORC1). Loss-of-function mutations in TSC cause TSC disease, marked by excessive tumor growth. Here, we overcome a high degree of continuous conformational heterogeneity to determine the 2.
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