Key features and details
- Rabbit polyclonal to cardiac Troponin I (phospho T143)
- Suitable for: WB
- Reacts with: Mouse, Rat, Human
- Isotype: IgG
Product nameAnti-cardiac Troponin I (phospho T143) antibody
See all Cardiac Troponin I primary antibodies
DescriptionRabbit polyclonal to cardiac Troponin I (phospho T143)
SpecificityDetects endogenous levels of cardiac Troponin I only when phosphorylated at threonine 142.
Tested applicationsSuitable for: WBmore details
Species reactivityReacts with: Mouse, Rat, Human
Synthetic phosphopeptide (Human) from around the phosphorylation site of threonine 142 (RPTPLR)
Storage instructionsShipped at 4°C. Store at -20°C. Stable for 12 months at -20°C.
Storage bufferpH: 7.40
Preservative: 0.02% Sodium azide
Constituents: PBS, 50% Glycerol, 0.87% Sodium chloride
Without Mg+2 and Ca+2
Concentration information loading...
PurityImmunogen affinity purified
Purification notesAffinity purified from rabbit antiserum by affinity chromatography using epitope specific phosphopeptide. The antibody against non phosphopeptide was removed by chromatography using non phosphopeptide corresponding to the phosphorylation site.
Our Abpromise guarantee covers the use of ab58546 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/500 - 1/1000. Detects a band of approximately 30 kDa (predicted molecular weight: 24 kDa).|
FunctionTroponin I is the inhibitory subunit of troponin, the thin filament regulatory complex which confers calcium-sensitivity to striated muscle actomyosin ATPase activity.
Involvement in diseaseDefects in TNNI3 are the cause of cardiomyopathy familial hypertrophic type 7 (CMH7) [MIM:613690]. Familial hypertrophic cardiomyopathy is a hereditary heart disorder characterized by ventricular hypertrophy, which is usually asymmetric and often involves the interventricular septum. The symptoms include dyspnea, syncope, collapse, palpitations, and chest pain. They can be readily provoked by exercise. The disorder has inter- and intrafamilial variability ranging from benign to malignant forms with high risk of cardiac failure and sudden cardiac death.
Defects in TNNI3 are the cause of cardiomyopathy familial restrictive type 1 (RCM1) [MIM:115210]. RCM1 is an heart muscle disorder characterized by impaired filling of the ventricles with reduced diastolic volume, in the presence of normal or near normal wall thickness and systolic function.
Defects in TNNI3 are the cause of cardiomyopathy dilated type 2A (CMD2A) [MIM:611880]. Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death.
Defects in TNNI3 are the cause of cardiomyopathy dilated type 1FF (CMD1FF) [MIM:613286]. Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death.
Sequence similaritiesBelongs to the troponin I family.
- Information by UniProt
- cardiac muscle antibody
- Cardiac troponin I antibody
- cardiomyopathy, dilated 2A (autosomal recessive) antibody
All lanes : Anti-cardiac Troponin I (phospho T143) antibody (ab58546) at 1/500 dilution
Lane 1 : Mouse heart extract without immunizing peptide
Lane 2 : Mouse heart extract with immunizing peptide
Predicted band size: 24 kDa
Observed band size: 30 kDa why is the actual band size different from the predicted?
ab58546 has been referenced in 5 publications.
- Parikh VN et al. Apelin and APJ orchestrate complex tissue-specific control of cardiomyocyte hypertrophy and contractility in the hypertrophy-heart failure transition. Am J Physiol Heart Circ Physiol 315:H348-H356 (2018). PubMed: 29775410
- Wu SC et al. Nuclear localization of a1A-adrenergic receptors is required for signaling in cardiac myocytes: an “inside-out” a1-AR signaling pathway. J Am Heart Assoc 3:e000145 (2014). PubMed: 24772522
- Wang H et al. TNNI3K is a novel mediator of myofilament function and phosphorylates cardiac troponin I. Braz J Med Biol Res 46:128-37 (2013). PubMed: 23369981
- Boontje NM et al. Enhanced myofilament responsiveness upon ß-adrenergic stimulation in post-infarct remodeled myocardium. J Mol Cell Cardiol 50:487-99 (2011). WB ; Pig . PubMed: 21156182
- Ladage D et al. Inhibition of PKCa/ß with ruboxistaurin antagonizes heart failure in pigs after myocardial infarction injury. Circ Res 109:1396-400 (2011). WB ; Pig . PubMed: 21998327