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The protein encoded by TNNT2 is the tropomyosin-binding subunit of the troponin complex, which is located on the thin filament of striated muscles and regulates muscle contraction in response to alterations in intracellular calcium ion concentration. De plus, nous expédions Cardiac Troponin T2 Kits (69) et Cardiac Troponin T2 Protéines (35) et beaucoup plus de produits pour cette protéine.
Showing 10 out of 374 products:
Human Polyclonal Cardiac Troponin T2 Primary Antibody pour EIA, WB - ABIN951043
Millat, Chanavat, Créhalet, Rousson: Development of a high resolution melting method for the detection of genetic variations in hypertrophic cardiomyopathy. dans Clinica chimica acta; international journal of clinical chemistry 2010
Show all 3 references for ABIN951043
Cow (Bovine) Polyclonal Cardiac Troponin T2 Primary Antibody pour WB - ABIN2776953
Klaassen, Probst, Oechslin, Gerull, Krings, Schuler, Greutmann, Hürlimann, Yegitbasi, Pons, Gramlich, Drenckhahn, Heuser, Berger, Jenni, Thierfelder: Mutations in sarcomere protein genes in left ventricular noncompaction. dans Circulation 2008
Chicken Monoclonal Cardiac Troponin T2 Primary Antibody pour IF, IHC (p) - ABIN180606
Malouf, McMahon, Oakeley, Anderson: A cardiac troponin T epitope conserved across phyla. dans The Journal of biological chemistry 1992
Human Monoclonal Cardiac Troponin T2 Primary Antibody pour EIA, FACS - ABIN1105666
Hershberger, Pinto, Parks, Kushner, Li, Ludwigsen, Cowan, Morales, Parvatiyar, Potter: Clinical and functional characterization of TNNT2 mutations identified in patients with dilated cardiomyopathy. dans Circulation. Cardiovascular genetics 2009
Human Monoclonal Cardiac Troponin T2 Primary Antibody pour IA, WB - ABIN265695
Qiao, Tang, Munske, Dutta, Ivory, Dong: Enhanced fluorescence anisotropy assay for human cardiac troponin I and T detection. dans Journal of fluorescence 2011
Generated is a gene-targeted knock-in murine model of the autosomal dominant Arg141Trp (R141W) mutation in human Tnnt2. Tnnt2 R141W mutation causes a Ca2 (Montrer CA2 Anticorps)+ desensitization and mice adapt by increasing Ca2 (Montrer CA2 Anticorps)+-transient amplitudes, which impairs Ca2 (Montrer CA2 Anticorps)+ handling dynamics, metabolism and responses to beta-adrenergic activation.
A myosin activator improves actin assembly and sarcomere function of human-induced pluripotent stem cell-derived cardiomyocytes with a troponin T point mutation.
Our study supports that mutations in MYH7 (Montrer MYH7 Anticorps) and MYBPC3 (Montrer MYBPC3 Anticorps) should be the first focus of moleculargenetic analysis in HCM, and that mutations in TNNT2 have a low prevalence in Brazilian population. All mutations detected were missense mutations, whereas two mutations in MYH7 (Montrer MYH7 Anticorps) had not been described before.
Dyrk1A modulates SRp55-promoted cTnT exon 5 inclusion
Our results suggest that multiple enzymes are involved in cTnT degradation, and that thrombin (Montrer F2 Anticorps) plays an important role.
In patients with clinically stable angina pectoris, slightly elevated hs-cTnT levels may indicate the presence of complex coronary artery disease.
TNNT2 gene mutation is associated with Early-Onset Hypertrophic Cardiomyopathy.
The results showed that MYBPC3 25-bp deletion polymorphism was significantly associated with elevated risk of left ventricular dysfunction (LVD), while TTN 18 bp I/D, TNNT2 5 bp I/D and myospryn K2906N polymorphisms did not show any significant association with LVD.
A novel heterozygous mutation (MYH7 (Montrer MYH7 Anticorps), p.Asn885Thr), and a variant of uncertain significance (TNNT2, p.Arg296His) were identified in 2 patients with familial hypertrophic cardiomyopathy.
Discordant elevation of cTnT in the presence of normal CK plasma levels on admission is associated with increased mortality in STEMI patients undergoing primary PCI (Montrer SERPINA5 Anticorps).
We show that the phosphorylation of cTnI and alphaTm vary in the different chambers of the heart, whereas the phosphorylation of MLC2 and cTnT does not.
Significant changes in thin filament Ca2 (Montrer CA2 Anticorps)+-sensitivity, structure and kinetics are brought about through PKC (Montrer PKC Anticorps) phosphorylation of cardiac troponin T.
The mu-calpain-mediated proteolytic modification of TnT by removing the NH2-terminal variable region of TnT may act as an acute mechanism to adjust muscle contractility under stress conditions.
Substituting smooth muscle caldesmon for skeletal muscle troponin produces a similar decrease and re-increase in fluorescence, but the apparent rate constant for the increase is >10 times that observed with troponin.
In ischemic myocardium, the expression of cTnT showed prominent focal or flaky depletion in myocardial cytoplasm with no expression detected in interstitium.
TnTA30V mutation attenuated Ca(2 (Montrer CA2 Anticorps)+)-activated maximal tension and length-mediated cross-bridge recruitment against alpha-myosin (Montrer MYH6 Anticorps) heavy chain but augmented these parameters against beta-myosin heavy chain (Montrer MYH7 Anticorps), suggesting divergent contractile phenotypes.
The shift from cTnT exon 5 inclusion to exclusion during development was delayed in the heart of Ts65Dn mice due to Dyrk1A (Montrer DYRK1A Anticorps) overexpression.
for hypertrophic cardiomyopathy (HCM)-causing mutations in TnT (Montrer TNNI1 Anticorps), Ca(2 (Montrer CA2 Anticorps)+)-sensitisation together with uncoupling in vitro is the usual response and both factors may contribute to the HCM phenotype
cardiomyopathy mutation (R97L) in mouse cardiac troponin T has an effect on the muscle length-mediated recruitment of crossbridges and is modified divergently by alpha- and beta-myosin heavy chain (Montrer MYH7 Anticorps)
Data indicate that high-sensitivity troponin T (hs-TnT) levels are influenced by myocardial dysfunction/heart failure (HF) in acute exacerbation of chronic obstructive lung disease (AECOPD), but provide independent prognostic information.
cTnT elevation emerged as a strong, independent predictor of 30-day mortality and remained a modest, but significant, predictor throughout 2 years post transcatheter aortic valve implantation.
MBPC and troponin-I phosphorylation modulate myofilament length-dependent activation
Data indicate that the troponin T Tnnt2(MerCreMer/+) mouse model also provides a useful tool to trace myocardial lineage during development.
TnT (Montrer TNNI1 Anticorps) mutation F72L leads to contractile changes that are linked to dilated cardiomyopathy in the presence of MYH6 (Montrer MYH6 Anticorps) and hypertrophic cardiomyopathy in the presence of MYH7 (Montrer MYH7 Anticorps).
TNT increases slightly during low flux-hemodialysis. High-flux hemodialysis eliminates the biomarker and can mask increases caused by cardiac disease.
Data showed that CXCR4a was significantly more highly expressed in tnnt2 knocked down mutant at 48 and 60 hpf than controls.
We show that the zebrafish silent heart (sih) mutation affects the gene tnnt2.
Tnnt1 (Montrer TNNI1 Anticorps), Tnnt2, and Tnnt3b were conserved in the central tropomyosin (Montrer TPM2 Anticorps)- and C-terminal troponin I-binding domains but the N-terminal hypervariable regions were highly extended and rich in glutamic acid in polypeptides of Tnnt1 (Montrer TNNI1 Anticorps) and Tnnt2, but not Tnnt3b.
The protein encoded by this gene is the tropomyosin-binding subunit of the troponin complex, which is located on the thin filament of striated muscles and regulates muscle contraction in response to alterations in intracellular calcium ion concentration. Mutations in this gene have been associated with familial hypertrophic cardiomyopathy as well as with dilated cardiomyopathy. Transcripts for this gene undergo alternative splicing that results in many tissue-specific isoforms, however, the full-length nature of some of these variants has not yet been determined.
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