AI Article Synopsis
- The 16-amino-acid fragment IG(46-61) from the B3 domain of protein G was studied using CD and NMR spectroscopy and differential scanning calorimetry to assess its structure and stability.
- The peptide maintains an organized three-dimensional structure resembling a beta-hairpin at various temperatures, stabilized by hydrophobic interactions among nonpolar side chains.
- The melting temperature of the peptide is approximately 320 K, indicating its potential as a folding initiation site for the B3 domain of the immunoglobulin binding protein G.
Article Abstract
The structure and stability of the 16-amino-acid-residue fragment [IG(46-61)] corresponding to the C-terminal beta-hairpin of the B3 domain of the immunoglobulin binding protein G from Streptococcus was investigated by means of CD and NMR spectroscopy and by differential scanning calorimetry. The CD and 2D NMR experiments were carried out (i) in water at different temperatures and (ii) at one temperature (305 K), with only CD, at different TFE concentrations. Our results show that the IG(46-61) peptide possesses organized three-dimensional structure at all investigated temperatures. The three-dimensional structure of the IG(46-61) peptide resembles the general shape of a beta-hairpin that is also observed for this peptide in the experimental structure of the B3 domain in the whole G protein; the structure is stabilized by hydrophobic interactions between nonpolar side chains. Our study shows that the melting temperature of the IG(46-61) peptide is about 320 K which supports the hypothesis that the investigated peptide can serve as a folding initiation site of the B3 domain of the immunoglobulin binding protein G.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2766666 | PMC |
| http://dx.doi.org/10.1002/bip.21080 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Antigen receptor ITAMs provide tonic signaling by acting as guanine nucleotide exchange factors to directly activate R-RAS2.
Sci Signal
January 2025
Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, 28049 Madrid, Spain.
The small GTPase R-RAS2 regulates homeostatic proliferation and survival of T and B lymphocytes and, when present in high amounts, drives the development of B cell chronic lymphocytic leukemia. In normal and leukemic lymphocytes, R-RAS2 constitutively binds to antigen receptors through their immunoreceptor tyrosine-based activation motifs (ITAMs) and promotes tonic activation of the phosphatidylinositol 3-kinase (PI3K) signaling pathway. Here, we examined the molecular mechanisms underlying this direct interaction and its consequences for R-RAS2 activity.
View Article and Find Full Text PDFEULAR recommendations for the treatment of systemic sclerosis: 2023 update.
Ann Rheum Dis
January 2025
Department of Rheumatology, Université Paris Cité UFR de Médecine, Paris, France.
Objectives: To update the 2017 European Alliance of Associations for Rheumatology (EULAR) recommendations for treatment of systemic sclerosis (SSc), incorporating new evidence and therapies.
Methods: An international task force was convened in line with EULAR standard operating procedures. A nominal group technique exercise was performed in two rounds to define questions underpinning a subsequent systematic literature review.
Rethinking Optimal Immunogens to Face SARS-CoV-2 Evolution Through Vaccination.
Influenza Other Respir Viruses
January 2025
Área de Investigación en Vacunas, Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunitat Valenciana, Valencia, Spain.
SARS-CoV-2, which originated in China in late 2019, quickly fueled the global COVID-19 pandemic, profoundly impacting health and the economy worldwide. A series of vaccines, mostly based on the full SARS-CoV-2 Spike protein, were rapidly developed, showing excellent humoral and cellular responses and high efficacy against both symptomatic infection and severe disease. However, viral evolution and the waning humoral neutralizing responses strongly challenged vaccine long term effectiveness, mainly against symptomatic infection, making necessary a strategy of repeated and updated booster shots.
View Article and Find Full Text PDFTIM-1 attenuates airway mucus hypersecretion and inflammation induced by cigarette smoke via the PI3K/Akt signaling pathway.
Pharmazie
December 2024
Department of Respiratory Medicine, Fourth Affiliated Hospital, Harbin Medical University Harbin, Heilongjiang, China.
Cigarette smoke extract (CSE)-induced airway mucus hypersecretion and inflammation are prominent features of chronic obstructive pulmonary disease (COPD). As a factor associated with inflammation regulation, T cell immunoglobulin and mucin domain-1 (TIM-1) is found to be involved in various inflammatory disorders such as asthma and COPD. In this study, the GEO database provides two human COPD gene expression datasets (GSE67472, n = 62) along with the relevant controls (n = 43) for differentially expressed gene (DEG) analyses.
View Article and Find Full Text PDFTargeted barcoding of variable antibody domains and individual transcriptomes of the human B-cell repertoire using Link-Seq.
PNAS Nexus
January 2025
Institute of Bioengineering, School of Engineering, École Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland.
Here, we present Link-Seq, a highly efficient droplet microfluidic method for combined sequencing of antibody-encoding genes and the transcriptome of individual B cells at large scale. The method is based on 3' barcoding of the transcriptome and subsequent single-molecule PCR in droplets, which freely shift the barcode along specific gene regions, such as the antibody heavy- and light-chain genes. Using the immune repertoire of COVID-19 patients and healthy donors as a model system, we obtain up to 91.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!