Correction for 'Multivalent presentation of carbohydrates by 314-helical peptide templates: synthesis, conformational analysis using CD spectroscopy and saccharide recognition' by Nitin J. Pawar et al., Org. Biomol. Chem., 2015, 13, 11278-11285.
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Nesfatin-1 as a crucial mediator of glucose homeostasis in the reptile, Hemidactylus flaviviridis.
Sci Rep
December 2024
University of Jammu, Jammu and Kashmir, 180006, India.
Nesfatin-1 is a crucial regulator of energy homeostasis in mammals and fishes, however, its metabolic role remains completely unexplored in amphibians, reptiles, and birds. Therefore, present study elucidates role of nesfatin-1 in glucose homeostasis in wall lizard wherein fasting stimulated hepatic nucb2/nesfatin-1, glycogen phosphorylase (glyp), phosphoenolpyruvate carboxykinase (pepck), and fructose 1,6-bisphosphatase (fbp), while feeding upregulated pancreatic nucb2/nesfatin-1 and insulin, suggesting towards tissue-specific dual role of nesfatin-1 in glucoregulation. The glycogenolytic/gluconeogenic role of nesfatin-1 was further confirmed by an increase in media glucose levels along with heightened hepatic pepck and fbp expression and concomitant decline in liver glycogen content in nesfatin-1-treated liver of wall lizard.
View Article and Find Full Text PDFThe Cryo-EM structure of human CD163 bound to haptoglobin-hemoglobin reveals molecular mechanisms of hemoglobin scavenging.
Nat Commun
December 2024
Department of Biomedicine, Aarhus University, 8000, Aarhus C, Denmark.
CD163, a macrophage-specific receptor, plays a critical role in scavenging hemoglobin released during hemolysis, protecting against oxidative effects of heme iron. In the bloodstream, hemoglobin is bound by haptoglobin, leading to its immediate endocytosis by CD163. While haptoglobin's structure and function are well understood, CD163's structure and its interaction with the haptoglobin-hemoglobin complex have remained elusive.
View Article and Find Full Text PDFTowards designing improved cancer immunotherapy targets with a peptide-MHC-I presentation model, HLApollo.
Nat Commun
December 2024
Oncology Bioinformatics, Genentech, South San Francisco, CA, USA.
Based on the success of cancer immunotherapy, personalized cancer vaccines have emerged as a leading oncology treatment. Antigen presentation on MHC class I (MHC-I) is crucial for the adaptive immune response to cancer cells, necessitating highly predictive computational methods to model this phenomenon. Here, we introduce HLApollo, a transformer-based model for peptide-MHC-I (pMHC-I) presentation prediction, leveraging the language of peptides, MHC, and source proteins.
View Article and Find Full Text PDFPlasma Exchange and N-Acetylcysteine Therapy in a Case of Congenital Thrombotic Thrombocytopenic Purpura Presenting With Acute Renal Failure.
J Pediatr Hematol Oncol
January 2025
Departments of Pediatric Hematology.
Congenital thrombotic thrombocytopenic purpura (cTTP), which is associated with mutations in the gene for a disintegrin and metalloproteinase with a thrombospondin type 1 motif member 13 (ADAMTS13), is a chronic and lifelong disease. The clinical course is variable. Regularly using ADAMTS13-containing products such as fresh frozen plasma (FFP) for long-term prophylaxis is the most important treatment to prevent thrombotic microangiopathy (TMA) episodes.
View Article and Find Full Text PDFLike Father, Like Daughter: A Family With a Constitutional Thrombocytopenia Variant Due to a Novel Heterozygous Missense Mutation in GP1BA.
J Pediatr Hematol Oncol
January 2025
Department of Pediatrics, The University of North Carolina at Chapel Hill, Chapel Hill, NC.
Constitutional platelet disorders have become better understood since Bernard and Soulier first described a case in 1948. Their diagnosis can also be challenging due to overlap in clinical presentation and lab findings with platelet type von Willebrand. Bernard-Soulier syndrome is a disorder caused by GPIb receptor mutations that decrease its affinity for von Willebrand factor resulting in reduced platelet function and macrothrombocytopenia.
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