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Probing the properties of PTEN specific botulinum toxin type E mutants.
J Neural Transm (Vienna)
January 2025
Institut für Zellbiochemie, OE 4310, Medizinische Hochschule Hannover, 30623, Hannover, Germany.
Botulinum neurotoxins (BoNT) are established biopharmaceuticals for neuromuscular and secretory conditions based on their ability to block neurotransmitter release from neurons by proteolyzing specific soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins. Recently, a mutant catalytic domain of serotype E (LC/E) exhibiting 16 mutations was reported to cleave the phosphatase and tensin homolog (PTEN). This molecule represents an attractive new target in neurons as several reports support PTEN knockdown as a strategy to stimulate axonal regeneration after injury.
View Article and Find Full Text PDFSanjad-Sakati Syndrome in a 35-day-old Iraqi Infant: A Case Report.
Oman Med J
January 2024
Department of Pediatrics, Fallujah Teaching Hospital for Women and Children, Fallujah, Iraq.
Sanjad-Sakati syndrome is a rare autosomal recessive genetic disorder that presents solely in Arabian people. Our case was reported from the Fallujah Teaching Hospital for Women and Children in Fallujah, Iraq. This syndrome is associated with hypoparathyroidism, growth retardation, atypical facial appearance, and a variable degree of mental retardation.
View Article and Find Full Text PDFPeptide Binding to HLA-E Molecules in Humans, Nonhuman Primates, and Mice Reveals Unique Binding Peptides but Remarkably Conserved Anchor Residues.
J Immunol
November 2020
Department of Infectious Diseases, Leiden University Medical Center, 2333 ZA Leiden, the Netherlands; and.
Ag presentation via the nonclassical MHC class Ib molecule HLA-E, with nearly complete identity between the two alleles expressed in humans, HLA-E*01:01 and HLA-E*01:03, can lead to the activation of unconventional T cells in humans. Despite this virtual genetic monomorphism, differences in peptide repertoires binding to the two allelic variants have been reported. To further dissect and compare peptide binding to HLA-E*01:01 and HLA-E*01:03, we used an UV-mediated peptide exchange binding assay and an HPLC-based competition binding assay.
View Article and Find Full Text PDFAfrican individuals harbor molecular RH variants, which permit alloantibody formation to high-prevalence Rh antigens after transfusions. Genotyping identifies such RH variants, which are often missed by serologic blood group typing. Comprehensive molecular blood group analysis using 3 genotyping platforms, nucleotide sequencing, and serologic evaluation was performed on a 7-year-old African male with sickle cell disease who developed an "e-like" antibody shortly after initiating monthly red blood cell (RBC) transfusions for silent stroke.
View Article and Find Full Text PDFA novel RHCE*ce 48C, 733G allele with Nucleotide 941C in Exon 7 encodes an altered red blood cell e antigen.
Transfusion
January 2011
Laboratory of Immunochemistry, New York Blood Center, New York, New York 10065, USA.
Background: Several RHCE*ce alleles have in common a 733C>G (Leu245Val) change. Some encode an altered expression of e on red blood cells (RBCs) and individuals with such RBCs can make e-like alloantibodies. The identification of an apparent anti-hr(B) in the serum of an E-e+ African American patient prompted us to analyze her DNA, which revealed a novel RHCE*ce allele.
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