Disease relevance of Azetidinecarboxylic acid

• Hyperthermia, the calcium ionophore A23187, and amino acid analogs (L-azetidine-2-carboxylic acid and L-canavanine) induced the formation of the major stress proteins, but failed to increase synthesis of p32 and p34 [1].
• An assessment of the importance of error-prone repair and point mutations to forward mutation to L-azetidine-2-carboxylic acid resistance in Escherichia coli [2].
• The toxicity of MPMS was much lower than that of the L-proline analogues L-azetidine-2-carboxylic acid and 3,4-dehydro-DL-proline [3].
• Effects of azetidine-2-carboxylic acid on treatments of hepatoma cells with single or fractionated X-ray irradiations and on thermal radiosensitization in normal and thermotolerant cells [4].
• Structural changes of hair after incorporation of the proline analogue L-azetidine-2-carboxylic acid. A model of hair disease by alteration of primary structure [5].

Psychiatry related information on Azetidinecarboxylic acid

• D-Proline, L-pyroglutamic acid, L-azetidine-2-carboxylic acid, DL-pipecolic acid, L-glutamic acid diethylester, L-isoleucine and L-norleucine neither depressed SD nor caused retrograde amnesia [6].

High impact information on Azetidinecarboxylic acid

• Furthermore, AZCA rapidly inhibits the synthesis of proline from glutamic acid in wild-type but not the resistant cell lines [7].
• We have isolated variants of Chinese hamster lung (CHL) fibroblasts with decreased sensitivity to the toxic proline analog, L-azetidine-2-carboxylic acid (AZCA) [7].
• Two AZCA-resistant cell lines overproduce and excrete more proline than wild-type cells [7].
• The drugs L-azetidine-2-carboxylic acid (LACA) and alpha, alpha'-dipyridyl, which interfere with collagen synthesis, prevent the formation of fibrils in cultured epithelial primordia and in cultures of whole thyroids [8].
• Substitution of the proline by 3,4-dehydroproline or l-azetidine-2-carboxylic acid, but not any other residue, led to a high rate of uncoupled 2-oxoglutarate decarboxylation with no hydroxylation [9].

Biological context of Azetidinecarboxylic acid

• Induction of ER stress by tunicamycin, dithiothreitol, or l-azetidine 2-carboxylic acid did not result in depletion of ER calcium, showing that such depletion was not necessary for up-regulation of SERCA2b expression or UPR activation in general [10].
• Control experiments with colchicine indicated that the delay in the rate of collagen secretion, which was observed in the presence of azetidine-2-carboxylic acid, did not in itself affect the degree of glycosylations of collagen [11].
• Methylation rates showed no increases following 12 hr incubations with the amino acid analogs L-azetidine-2-carboxylic acid or L-canavanine [12].
• Genomic Southern analysis and gene disruption showed that two copies of the novel gene with one amino acid change at position 85 required for L-azetidine-2-carboxylic acid resistance were present on chromosomes X and XIV of Sigma 1278b background strains [13].
• Deletion analysis indicated that one open reading frame encoding a predicted protein of 229 amino acids is indispensable for L-azetidine-2-carboxylic acid resistance [13].

Anatomical context of Azetidinecarboxylic acid

• Resistance to AZCA is a stable characteristic of these cell lines since it is maintained after 40 generations in nonselective medium [7].
• Incubation of reticulocytes with 1, 5, and 10 mM L-azetidine-2-carboxylic acid reduced L-[U-14-C]proline (0.10 mM) incorporation into hemoglobin by 25, 58, and 72%, respectively [14].
• The proline analogues cis-hydroxyproline and L-azetidine-2-carboxylic acid were shown to inhibit epithelial cell spreading and to suppress the collagen synthesis that occurs during serum-supported cell spreading [15].
• Both the mRNA levels and the secretion of osteonectin increased concurrently when Pam and HSC-1 cells cultured in low calcium medium were exposed to various stresses including heat shock and treatment with sodium arsenite or L-azetidine-2-carboxylic acid [16].
• Additional experiments indicated that azetidine-2-carboxylic acid did not increase the collagen glycosyltransferase activities in the tendon cells or the rate of glycosylation reactions when added directly to the enzyme incubation mixture [11].

Associations of Azetidinecarboxylic acid with other chemical compounds

• When an analog of proline, L-azetidine-2-carboxylic acid (LACA), was added at a concentration of 80 microgram/ml with insulin, cortisol, and prolactin at the beginning of culture, collagen production in cultured tissue was inhibited by 75% during a 3-day incubation period [17].
• Inhibition of procollagen triple-helix formation by the addition of cis-hydroxyproline or azetidine-2-carboxylic acid increased the synthesis of 3-hydroxy[14C]proline 1.7-1.8-fold in pulse-chase experiments with freshly isolated chick-embryo tendon cells [18].
• Analogues of [Sar1]angiotensin II, Sarilesin (type I antagonist), and Sarmesin (type II antagonist) with L-azetidine-2-carboxylic acid (Aze) and L-pipecolic acid (Pip) at position 7 have been prepared by the solid-phase method, purified by reverse-phase HPLC, and bioassayed in the rat uterus [19].
• Inhibitors of collagen synthesis were used (cis-hydroxy proline and L-azetidine-2-carboxylic acid) in addition to a proteoglycan inhibitor (p-nitrophenyl-xylopyranoside) and a secretion inhibitor (monensin) [20].
• While substitution of the proline by proline homologs (L-pipecolic acid or L-azetidine-2-carboxylic acid) increased the K(m) value 2- to 4-fold at utmost, substitution by N-methylamino acids (sarcosine, L-N-methylalanine, L-N-methylvaline, or L-N-methylleucine) increased the K(m) value 7- to 40-fold for cdc2 kinase [21].

Gene context of Azetidinecarboxylic acid

• Rac1N17 also inhibited HSF activation by l-azetidine-2-carboxylic acid, a proline analog, and heavy metals (CdCl)), suggesting that Rac1 may be linked to HSF activation by denaturation of polypeptides in response to various proteotoxic stresses [22].
• The present study shows that accumulation of aberrant proteins, caused by the proteasome inhibitor MG132 or the incorporation of the amino acid analogue AZC (L-azetidine-2-carboxylic acid), increased both clusterin protein and mRNA levels in the human glial cell line U-251 MG [23].
• In cells experiencing the metabolic stress due to azetidine-2-carboxylic acid, BSDL was additionally associated with a protein of 46 kDa [24].
• Incubation of K562 at either 42 degrees C or with the amino acid analogue L-azetidine-2-carboxylic acid induced synthesis of hsp70, but not of hsc70 [25].
• The wild-type strain is sensitive to two toxic proline analogs (azetidine-2-carboxylic acid and 3,4-dehydroproline) also transported by the putP permease [26].

Analytical, diagnostic and therapeutic context of Azetidinecarboxylic acid

• The effect of a proline analog, L-azetidine-2-carboxylic acid (LACA), on protein matrix secretion by odontoblasts and ameloblasts was compared by light and electron microscopic radioautography after injection of 3H-glycine in young mice [27].
• A single 75 kDa band was detected by Western blot of cytoplasmic proteins which was not greatly altered after thermal stress or treatment with L-azetidine-2-carboxylic acid or nonactin [28].
• Three sets of proteins with molecular weights of 70, 84, and 110 kilodaltons were elevated simultaneously from constitutive levels after treatment with azetidine-2-carboxylic acid (AzC), an amino acid analogue of proline [29].
• After the freezing procedure, the rats were divided into 3 groups: nothing addition was done to the control group, while the other 2 groups received daily intraperitoneal administration of antifibrotic substances (colchicine or L-azetidine-2-carboxylic acid (AZC)) for 6 weeks [30].

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