The structure, phylogeny and in vivo function of the base pair formed between nucleotides 32 and 38 of the tRNA anticodon loop are reviewed. The A32-U38 pair, which is highly conserved in tRNA2(Ala) and sometimes observed in tRNA2(Pro), was recently found to decrease the affinity of tRNAs to the ribosomal A site relative to other 32-38 combinations. This suggests that the role of 32-38 pair is to tune the tRNA affinity in the A site to a uniform value. New experiments presented here show that the U32C mutation in tRNA1(Gly) increases its affinity to the cognate codon and to codons with third position mismatches in the A site. This suggests that one reason for uniform tRNA binding to evolve was to avoid incorrect codon recognition.
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http://dx.doi.org/10.1016/j.biochi.2006.06.005 | DOI Listing |
J Clin Endocrinol Metab
January 2025
Metabolic Diseases Branch, Bldg. 10/Rm 8C-101, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892.
Establishing genotype-phenotype correlations in disorders of hereditary endocrine neoplasia is important for clinical screening, genetic counseling, prognostication, surveillance, and surgical strategy, and may also provide clues about disease pathogenesis. Important genotype-phenotype correlations are recognized, for example, in pheochromocytoma/paraganglioma and multiple endocrine neoplasia type 2A. The presence of such correlations has been less clear in other familial endocrine disorders associated with primary hyperparathyroidism including multiple endocrine neoplasia type 1 (MEN1), and the hyperparathyroidism-jaw tumor syndrome (HPT-JT).
View Article and Find Full Text PDFUnlabelled: The T cell receptor (TCR) repertoire of intestinal CD4+ T cells is enriched for specificity towards microbiome-encoded epitopes shared among many microbiome members, providing broad microbial reactivity from a limited pool of cells. These cells actively coordinate mutualistic host-microbiome interactions, yet many epitopes are shared between gut symbionts and closely related pathobionts and pathogens. Given the disparate impacts of these agents on host health, intestinal CD4+ T cells must maintain strain-level discriminatory power to ensure protective immunity while preventing inappropriate responses against symbionts.
View Article and Find Full Text PDFMol Cell
January 2025
Department of Biochemistry, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA. Electronic address:
While most of the regulation of translation initiation occurs in the cytosol predominantly through phosphorylation, Ly et al. have discovered the first instance of regulation via protein concentration due to disruption of the nuclear membrane at mitosis. Only eIF1 appears to be involved in this regulation, and its release at mitosis enhances translational accuracy of start codon recognition.
View Article and Find Full Text PDFGenes Genet Syst
December 2024
Laboratory of Chromosome Function and Regulation, Graduate School of Engineering, Kochi University of Technology.
Strict control of the expression levels of heterologously introduced protein-coding genes is important for the functional analysis of the protein of interest and its effective use in new situations. For this purpose, various promoters with different expression strengths, codon optimization, and expression stimulation by low molecular weight compounds are commonly used. However, methods to control protein expression levels by combining regulation of translation efficiency have not been studied in detail.
View Article and Find Full Text PDFJ Hum Genet
December 2024
Department of Neurology, Qilu Hospital of Shandong University (Qingdao), Qingdao, Shandong, China.
Congenital disorder of glycosylation type Iy (CDG-Iy) is an X-linked monogenic inherited disease caused by variants in the SSR4 gene. To date, a total of 11 variants have been identified in 14 CDG-Iy patients. Our study identified a novel canonical splicing variant, c.
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