Anti-Actc1a polyclonal antibody (CABT-B369)

Rabbit Anti-Zebrafish Actc1a polyclonal antibody for IHC-P, WB, IHC-Wmt


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Application Notes
IHC-P: 1:100-1:1000
WB: 1:500-1:3000
IHC-Wmt: 1:100-1:500
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.


Alternative Names
cardiac muscle 1a; alpha cardiac actin; actin, alpha; cardiac muscle 1 like; actin, alpha, cardiac muscle like


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We offer labeled antibodies using our catalogue antibody products and a broad range of intensely fluorescent dyes and labels including HRP, biotin, ALP, Alexa Fluor® dyes, DyLight® Fluor dyes, R-phycoerythrin (R-PE), at scales from less than 100 μg up to 1 g of IgG antibody. Learn More

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Data on the role of cardiac alpha-actin (ACTC1) gene mutations on SRF-signaling


Authors: Rangrez, Ashraf Yusuf; Kilian, Lucia; Stiebeling, Katharina; Dittmann, Sven; Yadav, Pankaj; Schulze-Bahr, Eric; Frey, Norbert; Frank, Derk

We recently reported a novel, heterozygous, and non-synonymous ACTC1 mutation (p.Gly247Asp or G247D) in a large, multi-generational family, causing atrial-septal defect followed by late-onset dilated cardiomyopathy (DCM). We also found that the G247D ACTC1 mutation negatively regulated serum response (SRF)-signaling thereby contributing to the late-onset DCM observed in human patients carrying this mutation ("A cardiac aactin (ACTC1) p. Gly247Asp mutation inhibits SRF-signaling in vitro in neonatal rat cardiomyocytes" [1]). There are some ACTC1 mutations known to date, majority of which, though, have not been investigated for their functional consequence. We thus aimed at determining the functional impact of various ACTC1 gene mutations on SRF-signaling using SM22-response element driven firefly luciferase activity assays in C2C12 cells. (C) 2019 The Author(s). Published by Elsevier Inc.

Changing pattern of gene expression is associated with ventricular myocyte dysfunction and altered mechanisms of Ca2+ signalling in young type 2 Zucker diabetic fatty rat heart


Authors: Howarth, F. C.; Qureshi, M. A.; Hassan, Z.; Al Kury, L. T.; Isaev, D.; Parekh, K.; Yammahi, S. R. K. D.; Oz, M.; Adrian, T. E.; Adeghate, E.

The association between type 2 diabetes and obesity is very strong, and cardiovascular complications are the major cause of morbidity and mortality in diabetic patients. The aim of this study was to investigate early changes in the pattern of genes encoding cardiac muscle regulatory proteins and associated changes in ventricular myocyte contraction and Ca2+ transport in young (9- to 13-week-old) type 2 Zucker diabetic fatty (ZDF) rats. The amplitude of myocyte shortening was unaltered; however, time-to-peak shortening and time to half-relaxation of shortening were prolonged in ZDF myocytes (163 +/- 5 and 127 +/- 7 ms, respectively) compared with age-matched control rats (136 +/- 5 and 103 +/- 4 ms, respectively). The amplitude of the Ca2+ transient was unaltered; however, time-to-peak Ca2+ transient was prolonged in ZDF myocytes (66.9 +/- 2.6 ms) compared with control myocytes (57.6 +/- 2.3 ms). The L-type Ca2+ current was reduced, and inactivation was prolonged over a range of test potentials in ZDF myocytes. At 0 mV, the density of L-type Ca2+ current was 1.19 +/- 0.28 pA pF-1 in ZDF myocytes compared with 2.42 +/- 0.40 pA pF-1 in control myocytes. Sarcoplasmic reticulum Ca2+ content, release and uptake and myofilament sensitivity to Ca2+ were unaltered in ZDF myocytes compared with control myocytes. Expression of genes encoding various L-type Ca2+ channel proteins (Cacna1c, Cacna1g, Cacna1h and Cacna2d1) and cardiac muscle proteins (Myh7) were upregulated, and genes encoding intracellular Ca2+ transport regulatory proteins (Atp2a2 and Calm1) and some cardiac muscle proteins (Myh6, Myl2, Actc1, Tnni3, Tnn2, and Tnnc1) were downregulated in ZDF heart compared with control heart. A change in the expression of genes encoding myosin heavy chain and L-type Ca2+ channel proteins might partly underlie alterations in the time course of contraction and Ca2+ transients in ventricular myocytes from ZDF rats.

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