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anti-Human ACTC1 Anticorps:
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Goat Monoclonal ACTC1 Primary Antibody pour IHC (fro), ELISA - ABIN920523
Suurmeijer, Clément, Francesconi, Bocchi, Angelini, Van Veldhuisen, Spagnoli, Gabbiani, Orlandi: Alpha-actin isoform distribution in normal and failing human heart: a morphological, morphometric, and biochemical study. dans The Journal of pathology 2003
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Chicken Monoclonal ACTC1 Primary Antibody pour EIA, IHC (fro) - ABIN112213
Franke, Stehr, Stumpp, Kuhn, Heid, Rackwitz, Schnoelzer, Baumann, Holzhausen, Moll: Specific immunohistochemical detection of cardiac/fetal alpha-actin in human cardiomyocytes and regenerating skeletal muscle cells. dans Differentiation, research in biological diversity 1996
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Chicken Monoclonal ACTC1 Primary Antibody pour ELISA, IHC - ABIN224333
Itier, Ret, Viale, Sweet, Bangari, Caron, Le-Gall, Bénichou, Leonard, Deleuze, Orsini: Effective clearance of GL-3 in a human iPSC-derived cardiomyocyte model of Fabry disease. dans Journal of inherited metabolic disease 2014
Studies indicate that The change in F-actin or G-actin contents in a cell would translate to a number of biological endpoints such as change in cell shape, disrupted cell division, altered cell-cell adhesion, cell survival, and cell migration or motility.
Novel p.(Ala21Val) mutation of ACTC1 causes myofibrillar and intercalated disc alteration leading to familial hypertrophic cardiomyopathy and LV myocardial noncompaction with transmural crypts.
arrhythmogenesis was evident in all E99K-ACTC1 human induced pluripotent stem cell-derived cardiomyocytes.
ACTC1 is expressed in a large subset of gliomas, especially high-grade tumors. ACTC1-positive gliomas indicated poorer prognosis compared with ACTC1-negative gliomas.
These findings suggest that the familial ostium secundum atrial septal defect (ASDII)may be a result of an ACTC1 3'UTR gain-of-function mutation caused by the introduction of a new miR-139-5p target site. Our results provide the first evidence of a pathogenic mutation in the ACTC1 3'UTR that may be associated with familial isolated ASDII.
In conclusion, given that ACTC1 upregulation is associated with improved muscle function in certain myopathies, we hypothesize that upregulation of ACTC1 may represent a compensatory response to androgen deprivation therapy-induced muscle loss
highly penetrant, novel, heterozygous ACTC1I289T mutation is associated with a family with left ventricular noncompaction.
We reported a case of mirror-type dextrocardia who developed HCM in adulthood exhibiting multiple genetic mutation related to sarcomere proteins
A heterozygous missense mutation was found (c.251T>C, p.(Met84Thr)) in the ACTC1 gene
The first step of hypertrophic cardiomyopathy pathogenesis with E99K is increased calcium sensitivity and decreased calcium cooperativity, which result in larger tension during partial activation to cause a diastolic problem.
In this study, there was no association of the analyzed SNPs located in RASGRF1. GJD2, and ACTC1 with pathological myopia.
In adult Hypertrophic Cardiomyopathy patients, thin-filament gene ACTC1 mutations are associated with increased likelihood of advanced Left Ventricular dysfunction and heart failure compared with thick-filament disease.
Genetic variations at the ACTC1 gene may contribute to progression to chronic Chagas Cardiomyopathy
Change in the ability of cMyBP-C to bind cardiac actin modified filaments might contribute to the development of disease.
Our results provide further evidence supporting a causative role for ACTC1 mutations in ASD. Massively parallel sequencing of the exome allows for the detection of novel rare variants causing CHD without the limitations of a candidate gene approach.
The authors demonstrate that clathrin promotes clustering of the vaccinia virus actin tail nucleator A36 and host N-WASP, which activates actin nucleation through the Arp2/3 complex.
ACTC1 mutations Y166C and M305L are associated with hypertrophic cardiomyopathy
Data show that HMGN2 inhibited the attachment of bacteria, and then decreased bacteria-induced ERK1/2 activation and actin polymerization, which might contribute to bacterial internalization into T24 cells.
propose that the ACTC E99K mutation causes higher myofibrillar Ca(2+) sensitivity that is responsible for the sudden cardiac death, apical hypertrophy, and subsequent development of heart failure in humans and mice.
Reduced ACTC1 expression might play a role in the onset of congenital heart defects through induction of cardiomyocyte apoptosis.
Variations in ACTC1 is associated with refractive errors and myopia.
This study provides novel insights into the complex genetic regulation of Actc1 expression in early adult skeletal muscles.
Analogous to the findings in human skeletal muscle, Actc1 expression in mouse gastrocnemius muscle increased after testosterone deprivation in orchidectomized mice compared with sham controls
ACTC E361G mutation uncouples the relationship between Ca(2+) sensitivity and troponin I phosphorylation, predisposing the heart to dilated cardiomyopathy under conditions of chronic stress.
results demonstrate that in ACTC(Co)/KO myofibres, the presence of cardiac alpha-actin instead of skeletal muscle alpha-actin alters actin conformational changes upon activation; this later finely modulates the strain of individual actomyosin interactions and overall lowers myofibre force production
Data indicate that the tri-helix bundle is important to the regulatory role of cMyBP-C, likely through actin-binding interactions.
Other actin isoforms cannot compensate for the lack of cardiac alpha-actin, and this seems to induce apoptosis in defective cardiac myocytes, which are not able to cope with the increased workload in the perinatal phase.
These results demonstrate the importance of the Emb-MEF2D-histone transacetylase p300 complex in the transcriptional regulation of the cardiac actin gene and suggest a potential role in chromatin remodeling associated with muscle gene activation.
there is a cardiac-specific enhancer located within -2.354/-1.36 kbp of Actc1
Tm affects the conformation of actin so as to increase the area of hydrophobic interaction between actin and myosin molecules
Actins are highly conserved proteins that are involved in various types of cell motility. Polymerization of globular actin (G-actin) leads to a structural filament (F-actin) in the form of a two-stranded helix. Each actin can bind to four others. The protein encoded by this gene belongs to the actin family which is comprised of three main groups of actin isoforms, alpha, beta, and gamma. The alpha actins are found in muscle tissues and are a major constituent of the contractile apparatus. Defects in this gene have been associated with idiopathic dilated cardiomyopathy (IDC) and familial hypertrophic cardiomyopathy (FHC).
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, actin alpha cardiac 1
, actin, alpha, cardiac 1
, alpha-actin cardiac
, Actin alpha 1
, Alpha-cardiac actin
, actin, alpha, cardiac muscle 1
, actin, alpha cardiac muscle 1-like