Disease relevance of Srl

• Drastic reduction of sarcalumenin in Dp427 (dystrophin of 427 kDa)-deficient fibres indicates that abnormal calcium handling plays a key role in muscular dystrophy [1].
• The control of virulence determinant expression in Staphylococcus aureus is a complex process involving global regulatory loci such as sar and agr [2].

High impact information on Srl

• sar: a genetic mouse model for human sarcosinemia generated by ethylnitrosourea mutagenesis [3].
• SAR-deficient skeletal muscle carrying irregular SR ultrastructures retained normal force generation but showed slow relaxation phases after contractions [4].
• The results obtained demonstrate that SAR plays important roles in improving the Ca2+ handling functions of the SR in striated muscle [4].
• Impaired Ca2+ store functions in skeletal and cardiac muscle cells from sarcalumenin-deficient mice [4].
• Cardiac myocytes from SAR-deficient mice showed slow contraction and relaxation accompanied by impaired Ca2+ transients, and the mutant mice exhibited a number of impairments in cardiac performance as determined in electrocardiography, ventricular catheterization, and echocardiography [4].

Biological context of Srl

• Our data suggest that systemic ablation of sarcalumenin caused enhanced resistance to muscle fatigue by compensatory changes in Ca2+ regulatory proteins that effect SOCE [5].
• Northern analysis of sar mutant clones containing these mutations carried on a shuttle plasmid revealed that all three sar-related transcripts are present [2].

Anatomical context of Srl

• Sarcalumenin (SAR), specifically expressed in striated muscle cells, is a Ca2+-binding protein localized in the sarcoplasmic reticulum (SR) of the intracellular Ca2+ store [4].

Associations of Srl with chemical compounds

• In the present study, we show that a key luminal Ca2+-binding protein SAR (sarcalumenin) is affected in mdx skeletal-muscle fibres [1].
• A new series of 12 dermorphin tetrapeptides, W-Tyr-D-MetO-Phe-Xaa-Y (W = H, H2NC = (NH); Xaa = Gly, Sar, D-Ala; Y = OH, OCH3, NH2) were prepared by traditional methods in solution and tested for opioid activity [6].
• In the present study, two analogues containing N-Me-Gly (Sarcosine, Sar) were synthesized to further investigate the structural-activity relationships of orphanin FQ/nociceptin (OFQ/NC, NC) [7].
• To examine pharmacological properties of D-Arg2-dermorphin tetrapeptides, six tetrapeptide analogs based on the following formulas, H-Tyr-D-Arg-Phe-Gly-OX (X = H, ethyl, n-propyl), H-Tyr-D-Arg-Phe-Sar-OX (Sar = sarcosine; X = H, methyl, ethyl), were prepared [8].
• The rank order of scratching duration was Phy > Sar-SP > SP [9].

Other interactions of Srl

• This included the main terminal cisternae constituent, calsequestrin, and the previously implicated Ca(2+)-shuttle element, sarcalumenin [10].

Analytical, diagnostic and therapeutic context of Srl

• Using anti-SarA monoclonal antibodies with defined epitopes in a competitive ELISA to determine the SarA protein level, we found that the introduction of a stop codon in ORF3 on a shuttle plasmid carrying the intact sar locus in a sar mutant led to a significant decrease in SarA protein level compared with the non-mutated control [2].
• A group of three male beagle dogs were treated with Sar CNU 10 mg/kg given both by i.v. infusion and orally in a crossover design [11].

References