Publications by authors named "C Hendrich"

Bacterial biofilm formation and attachment to hosts are mediated by carbohydrate-binding lectins, exopolysaccharides, and their interactions in the extracellular matrix (ECM). During tomato infection Ralstonia pseudosolanacearum (Rps) GMI1000 highly expresses three lectins: LecM, LecF, and LecX. The latter two are uncharacterized.

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Nucleosidic diarylethenes (DAEs) have evolved from an emerging class of photochromes into a well-established option for integrating photochromic functionalities into biological systems. However, a comprehensive understanding of how chemical structure influences their photochromic properties remains essential. While structural features, such as an inverse connection between the aryl residues and the ethene bridge, are well-documented for classical DAEs, their application to nucleosidic DAEs has been underexplored.

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Photochromism is a reversible phenomenon wherein a material undergoes a change in color upon exposure to light. In organic photochromes, this effect often results from light-induced isomerization reactions, leading to alterations in either the spatial orientation or electronic properties of the photochrome. The incorporation of photochromic moieties into biomolecules, such as proteins or nucleic acids, has become a prevalent approach to render these biomolecules responsive to light stimuli.

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causes bacterial wilt disease on diverse plant hosts. cells enter a host from soil or infested water through the roots, then multiply and spread in the water-transporting xylem vessels. Despite the low nutrient content of xylem sap, grows very well inside the host, using denitrification to respire in this hypoxic environment.

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Pathogenic variants in the Parkin-gene () are among the most common genetic causes of early onset Parkinson's disease (EOPD). Patients with EOPD can present with atypical clinical features and misdiagnosis is frequent. Here, we report a clinical phenotype with atypical signs and symptoms of a 35-year-old male patient with EOPD caused by a compound heterozygous -gene deletion of exons 2 and 4.

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