The smallest and enzymatically active molecule, TetApuQ818, was localized within the C-terminal Q818 amino acid residue after serial C-terminal truncation analysis of the recombinant amylopullulanase molecule (TetApuM955) from Thermoanaerobacter pseudoethanolicus. Kinetic analyses indicated that the overall catalytic efficiency, k (cat)/K (m), of TetApuQ818 was 8-32% decreased for the pullulan and the soluble starch substrate, respectively. Changes to the substrate affinity, K (m), and the turnover rate, k (cat), were decreased significantly in both enzymatic activities of TetApuQ818. TetApuQ818 exhibited less thermostability than TetApuM955 when the temperature was raised above 85°C, but it had similar substrate-binding ability and hydrolysis products toward various substrates as TetApuM955 did. Both enzymes showed similar spectroscopies of fluorescence and circular dichroism, suggesting the active folding conformation was maintained after this C-terminal Q818 deletion. This study suggested that the binding ability of insoluble starch by TetApuM955 did not rely on the putative C-terminal carbohydrate binding module family 20 (CBM20) and two FnIII regions of TetApu, though the integrity of the AamyC module of TetApuQ818 was required for the enzyme activity.
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http://dx.doi.org/10.1007/s00792-012-0438-z | DOI Listing |
Mol Cell Biol
December 2024
Department of Biology, University of Iowa, Iowa City, Iowa, USA.
Med15 is a general transcriptional regulator and tail module subunit within the RNA Pol II mediator complex. The Med15 protein has a well-structured N-terminal KIX domain, three activator binding domains (ABDs) and several naturally variable polyglutamine (poly-Q) tracts (Q1, Q2, Q3) embedded in an intrinsically disordered central region, and a C-terminal mediator association domain (MAD). We investigated how the presence of ABDs and changes in length and composition of poly-Q tracts influences Med15 activity using phenotypic, gene expression, transcription factor interaction and phase separation assays of truncation, deletion, and synthetic alleles.
View Article and Find Full Text PDFbioRxiv
December 2024
Department of Molecular Biology, University of California, San Diego, La Jolla, CA.
APOBEC3B (A3B) is implicated in DNA mutations that facilitate tumor evolution. Although structures of its individual N- and C-terminal domains (NTD and CTD) have been resolved through X-ray crystallography, the full-length A3B (fl-A3B) structure remains elusive, limiting understanding of its dynamics and mechanisms. In particular, the APOBEC3B C-terminal domain (A3Bctd) active site is frequently closed in models and structures.
View Article and Find Full Text PDFProtein Sci
January 2025
Department of Chemistry and Biochemistry, The Ohio State University, Columbus, Ohio, USA.
After overexpression in a suitable host, recombinant protein purification often relies on affinity (e.g., poly-histidine) and solubility-enhancing (e.
View Article and Find Full Text PDFObjective: This study aimed to identify the binding sites for plasminogen (Pg) and its kringle-containing fragments within the αC-region of fibrin(ogen). This investigation is crucial while the conversion of fibrinogen into fibrin induces conformational changes that expose binding sites for Pg and tissue-type Pg activator (tPA), facilitating effective zymogen activation on the fibrin surface.
Methods: Two C-terminal fragments of the Aα chain ‒ 45 kDa (225Val-610Val) and 40 kDa (225Val-580Lys), were obtained through plasmin hydrolysis of human fibrinogen and subsequently characterized using MALDI TOF mass spectrometry.
FASEB J
December 2024
Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Peritoneum is the second most common site of metastasis in patients with pancreatic ductal adenocarcinoma (PDAC). Peritoneal colonization is impaired in PDAC cells with knockout (KO) of the cancer surface antigen mesothelin (MSLN) or by introducing Y318A mutation in MSLN to prevent binding to mucin-16 (MUC-16). MSLN has a membrane-bound form but is also shed to release soluble MSLN (sMSLN).
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