| Name | muscles |
|---|---|
| Synonyms | COX 7a M; COX VIIa M; COX7A; COX7A1; COX7A1 protein; COX7AH; COX7AM; Cytochrome c oxidase subunit 7a H… |
| Name | streptomycin |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 17005404 | Whitehead NP, Streamer M, Lusambili LI, Sachs F, Allen DG: Streptomycin reduces stretch-induced membrane permeability in muscles from mdx mice. Neuromuscul Disord. 2006 Dec;16(12):845-54. Epub 2006 Sep 26. |
164(2,2,2,4) | Details |
| 15948207 | Willems ME, Stauber WT: Streptomycin and EDTA decrease the number of desmin-negative fibers following stretch injury. Muscle Nerve. 2005 Sep;32(3):310-5. In both streptomycin-and EDTA-treated rats, the percent of injured (i.e., desmin-negative) myofibers in TA was reduced compared to untreated, injured muscles (S, 0.35 +/- 0.08%; EDTA, 0.64 +/- 0.19%; C, 1.81 +/- 0.43%). |
83(1,1,1,3) | Details |
| 18367238 | Ward ML, Williams IA, Chu Y, Cooper PJ, Ju YK, Allen DG: Stretch-activated channels in the heart: contributions to length-dependence and to cardiomyopathy. Prog Biophys Mol Biol. 2008 Jun-Jul;97(2-3):232-49. Epub 2008 Feb 13. Streptomycin also decreased the increase in Ca2+ transient amplitude 60s after the stretch from 43.5+/-12.7% to 5.7+/-3.5% (P <0.05, n=4), and reduced the stretch-dependent increase in intracellular Ca2+ in quiescent muscles when stretched. |
81(1,1,1,1) | Details |
| 15298539 | Allen DG: Skeletal muscle function: role of ionic changes in fatigue, damage and disease. Clin Exp Pharmacol Physiol. 2004 Aug;31(8):485-93. Recently, we demonstrated that the elevation of Na+ occurs through a stretch-activated channel that can be blocked by either gadolinium or streptomycin. Repeated activity of skeletal muscle causes a variety of changes in its properties: muscles become weaker with intense use (fatigue), may feel sore and weak after repeated contractions involving stretch and can degenerate in some disease conditions. |
6(0,0,0,6) | Details |
| 19127190 | Butterfield TA, Best TM: Stretch-activated ion channel blockade attenuates adaptations to eccentric exercise. Med Sci Sports Exerc. 2009 Feb;41(2):351-6. Specifically, we investigated if daily injections of streptomycin (a known SAC blocker) would abrogate the muscle's adaptive resistance to the damaging effects of eccentric exercise over a 4-wk period. RESULTS: Although blocking the SAC function completely eliminated the expected adaptive response in biomechanical parameters during the exercise regimen, there remained evidence of an acquired RBE, albeit with an attenuated response when compared with the muscles with intact SAC function. |
2(0,0,0,2) | Details |
| 17910510 | Larsson K, Almgren A, Undeland I: Hemoglobin-mediated lipid oxidation and compositional characteristics of washed fish mince model systems made from cod (Gadus morhua), herring (Clupea harengus), and salmon (Salmo salar) muscle. J Agric Food Chem. 2007 Oct 31;55(22):9027-35. Epub 2007 Oct 2. The aim of this study was to systematically investigate whether washed mince model systems useful in Hb-mediated oxidation studies could be prepared also from herring (Clupea harengus) and salmon (Salmo salar) light muscles. A 20 microM portion of Hb and 200 ppm streptomycin was then added, followed by adjustment of pH and moisture to 6.3 and 86%, respectively. |
2(0,0,0,2) | Details |
| 15298550 | Yeung EW, Allen DG: Stretch-activated channels in stretch-induced muscle damage: role in muscular dystrophy. Clin Exp Pharmacol Physiol. 2004 Aug;31(8):551-6. This muscle damage is caused, in part, by ionic entry through stretch-activated channels and blocking these channels with Gd3+ or streptomycin reduces the force deficit associated with damage. 2. Dystrophin-deficient muscles are more susceptible to stretch-induced muscle injury and the recovery from injury can be incomplete. |
2(0,0,0,2) | Details |
| 15105296 | von Lewinski D, Stumme B, Fialka F, Luers C, Pieske B: Functional relevance of the stretch-dependent slow force response in failing human myocardium. Circ Res. 2004 May 28;94(10):1392-8. Epub 2004 Apr 22. Muscles were stretched from 88% of optimal length to 98% of optimal length. The resulting immediate and delayed (ie, slow force response [SFR]) increases in twitch force were assessed without and after blockade of the sarcoplasmic reticulum (SR; cyclopiazonic acid and ryanodine), stretch-activated ion channels (SACs; gadolinium, streptomycin), L-type Ca2+-channels angiotensin II type-1 (AT1) receptors (candesartan), endothelin (ET) receptors (PD145065 or BQ123), Na+/H+ exchange (NHE1; HOE642), or reverse-mode Na+/Ca+ exchange (NCX; KB-R7493). |
1(0,0,0,1) | Details |
| 15312831 | Nicolosi AC, Kwok CS, Bosnjak ZJ: Antagonists of stretch-activated ion channels restore contractile function in hamster dilated cardiomyopathy. J Heart Lung Transplant. 2004 Aug;23(8):1003-7. METHODS: Left ventricular papillary muscles from Syrian hamsters with a genetic DCM (n = 26), and from non-myopathic controls (n = 26), were superfused and stimulated to contract. Gadolinium (10 micromol/liter) and streptomycin (40 micromol/liter) were used separately to antagonize SACs. |
1(0,0,0,1) | Details |
| 16179399 | Spangenburg EE, McBride TA: Inhibition of stretch-activated channels during eccentric muscle contraction attenuates p70S6K activation. J Appl Physiol. 2006 Jan;100(1):129-35. Epub 2005 Sep 22. The TA muscles performed four sets of six repetitions of EC. In vivo blockade of SAC was performed by a continuous oral treatment with streptomycin in the drinking water (4 g/l) or by intravenous infusion of 80 micromol/kg gadolinium (Gd3+). |
1(0,0,0,1) | Details |
| 15235080 | Calaghan S, White E: Activation of Na+-H+ exchange and stretch-activated channels underlies the slow inotropic response to stretch in myocytes and muscle from the rat heart. J Physiol. 2004 Aug 15;559(Pt 1):205-14. Epub 2004 Jul 2. Papillary muscles were stretched from 88 to 98% of the length at which maximum tension is generated (L (max)). We saw a significant reduction (P < 0.05) in the slow force response in the presence of the SAC blocker streptomycin in both muscle (80 microm) and myocytes (40 microm). |
1(0,0,0,1) | Details |
| 18199588 | Sonobe T, Inagaki T, Poole DC, Kano Y: Intracellular accumulation following eccentric contractions in rat skeletal muscle in vivo: role of stretch-activated channels. Am J Physiol Regul Integr Comp Physiol. 2008 Apr;294(4):R1329-37. Epub 2008 Jan 16. The following hypotheses were tested. 1) For 90 min at rest, an in vivo vs. in vitro preparation would better maintain initial [Ca2+] i. 2) Compared with ISO, ECC contractions (50 contractions, 10 sets, 5-min interval) would lead to a greater increase of [Ca2+] i. 3) Elevated [Ca2+] i during ECC would be reduced or prevented by the stretch-activated ion channel blockers streptomycin and gadolinium (Gd3+). |
0(0,0,0,0) | Details |