Disease relevance of arabinose

• Expression of the L-arabinose BAD operon in Escherichia coli is regulated by AraC protein which acts both positively in the presence of arabinose to induce transcription and negatively in the absence of arabinose to repress transcription [1].
• Of a total of 16 arabinose-dependent TnAraOut mutants characterized in Vibrio cholerae, four were found to carry insertions upstream of known essential genes (gyrB, proRS, ileRS, and aspRS) whereas the other strains carried insertions upstream of known and hypothetical genes not previously shown to encode essential gene products [2].
• At the protein level the rns gene product is homologous to AraC, a positive regulator of the arabinose operon of enteric bacteria, and to RhaR and RhaS, which regulate the rhamnose operon of E. coli [3].
• Acute hypertension, occlusion of the superior venae cavae, and hyperosmolar arabinose produced leaky sites primarily in venules [4].
• A family of monoglycosyl polyprenylphosphates was isolated from Mycobacterium smegmatis, containing arabinose, ribose, and mannose [5].

High impact information on arabinose

• The others (maltose-binding protein, arabinose-binding protein, omp A protein, lam B protein and alkaline phosphatase) showed both modes of processing, although the amount of cotranslational processing varied considerably among the individual proteins of this class [6].
• A specific increase in S7 synthesis caused by stimulation in transcription originating from the arabinose promoter decreased the synthetic rate for EF-G but had no effect on S12 or EF-Tu synthesis [7].
• EMB inhibits the polymerization of cell wall arabinan, and results in the accumulation of the lipid carrier decaprenol phosphoarabinose, which suggests that the drug interferes with the transfer of arabinose to the cell wall acceptor [8].
• Here we address this issue directly by construction of a strain in which ffh expression is arabinose-dependent [9].
• The addition of arabinose, which induces the operon, breaks the loop, and shifts the interactions from the distal araO2 site to the previously unoccupied half of the araI site [1].

Chemical compound and disease context of arabinose

• Arabinose-binding protein, maltose-binding protein, and lambda receptor are synthesized in vitro on membrane-bound polysomes from Escherichia coli [10].
• In addition, by developing an in vitro assay using recombinant Escherichia coli expressing Mt-aftA and use of cell wall galactan as an acceptor, we demonstrated the transfer of arabinose from beta-D-arabinofuranosyl-1-monophosphoryldecaprenol to galactan, and unlike the Mt-Emb proteins, Mt-AftA was not inhibited by ethambutol [11].
• The tertiary structure has been compared to that of the Escherichia coli arabinose binding protein (Gilliland, G.L., and Quiocho, F. A. (1981) J. Mol. Biol. 146, 341-362), a periplasmic receptor which is involved in transport, but not in chemotaxis [12].
• The XylS protein exhibits homology with the AraC protein of Escherichia coli, a protein that stimulates transcription from ara promoters when it is activated by arabinose or benzoate [13].
• Xylose, arabinose, and rhamnose fermentation by Bacteroides ruminicola [14].

Biological context of arabinose

• The differing abilities of ribose, 2'-deoxyribose, and arabinose nucleotides to base-pair within an RNA.RNA duplex and to contribute a nucleophilic 2'-OH group were exploited to analyze the paired/unpaired disposition of the branch site nucleotide [15].
• The dimeric AraC protein of Escherichia coli binds specifically to DNA sequences upstream of promoters whose transcription is regulated by arabinose [16].
• Gene expression from plasmids containing the araBAD promoter can be regulated by the concentration of arabinose in the growth medium [17].
• One provides a dimerization capability and binds the ligand arabinose, and the other provides a site-specific DNA-binding capability and activates transcription [18].
• First, dimethyl sulfate methylation protection measurements on normally growing cells show that the AraC regulatory protein occupies the araI site in the presence and absence of the inducer arabinose [19].

Anatomical context of arabinose

• The blood-brain barrier of rats was opened reversibly by infusing a hyperosmotic solution of arabinose into the external carotid artery [20].
• Right brain regions of anesthetized rats were loaded with [3,5,7-3H]methotrexate ([3H]MTX) or with [14C]sucrose by infusing the tracers into the right carotid artery, after the blood-brain barrier had been opened by right carotid infusion of a hypertonic arabinose solution [21].
• When monolayers of the endothelial cells were exposed briefly to a calcium-free solution or treated with 1.6 M arabinose, distinctive morphological changes occurred in the intercellular contacts [22].
• Incubation of microsomes with UDP-[(14)C]-beta-L-arabinopyranose resulted in incorporation of radioactivity into two different products, although most of the radioactivity was present in xylose (Xyl), indicating a high degree of UDP-arabinose (Ara) epimerization [23].
• RESULTS: Cell walls were found to be rich in NSPs, particularly arabinose-rich polysaccharides, with a high concentration of phenolic compounds detected in the seed coat cell wall [24].

Associations of arabinose with other chemical compounds

• Art v 1, the major allergen of mugwort (Artemisia vulgaris) pollen contains galactose and arabinose [25].
• The absolute configuration of the arabinose was determined after reduction and acylation with a pure enantiomer of Mosher's acid chloride [26].
• Whereas the fermentation of glucose can be carried out efficiently, the bioconversion of the pentose fraction (xylose and arabinose, the main pentose sugars obtained on hydrolysis of hemicellulose), presents a challenge [27].
• High-level expression of MGS severely compromised growth on xylose, arabinose and glycerol [28].
• Although P0 rat neurons are strictly postmitotic, topoisomerase II inhibitors teniposide and mitoxantrone induced them to die by apoptosis in the presence of NGF with the same apparent time-course as arabinose treatment or NGF withdrawal [29].

Gene context of arabinose

• Excision events that produce an in-frame fusion of lacZ to araB result in a cell (here designated Ara-Lac+) that can grow on lactose if arabinose is present as an inducer [30].
• The cloning, DNA sequence, and overexpression of the gene araE coding for arabinose-proton symport in Escherichia coli K12 [31].
• In this study, we examined whether overexpression of TLR2 or TLR4 would affect the ability of cells to become tolerant to LPS or the mycobacterial components, arabinose-capped lipoarabinomannan (LAM) and soluble tuberculosis factor (STF) [32].
• However, when expression of the cloned misL gene was driven by the Escherichia coli arabinose promoter, MisL could be detected in the S [33].
• Mutant RNase P RNA alleles (rnpBC292 and rnpBC293) caused severe growth defects in the E. coli rnpB mutant strain DW2 and abolished growth in the newly constructed mutant strain BW, in which chromosomal rnpB expression strictly depended on the presence of arabinose [34].

Analytical, diagnostic and therapeutic context of arabinose

• Sequence analysis of regions flanking the transposon insertion revealed the presence of an arabinose assimilation operon consisting of nine genes [35].
• Northern-blot analysis showed that abf51A was efficiently transcribed, whereas no transcript derived from abf62A was detected in the presence of arabinose-containing polysaccharides [36].
• In the study presented here, we use analytical ultracentrifugation to determine the oligomeric state of the AraC dimerization domain in the presence and absence of arabinose [37].
• The data also support the view that hypophysectomy renders adipocytes more susceptible than normal to the cell isolation procedure which maximally accelerates glucose utilization and inward transport of arabinose in these cells [38].
• Western blot (immunoblot) analyses of sigmaS produced from natural or arabinose-regulated promoters revealed that acid shock and MviA posttranscriptionally regulate sigmaS levels [39].

References