Rat Cardiac Troponin Ⅰ(cTn-Ⅰ) ELISA kit

Product Details

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Customer Reviews and Q&A

Target Background

Product Details

Target Name

Cardiac Troponin Ⅰ(cTn-Ⅰ)

Alternative Names

Tnni3 ELISA Kit; Ctni ELISA Kit; Tni ELISA Kit; Troponin I ELISA Kit; cardiac muscle ELISA Kit; Cardiac troponin I ELISA Kit

Abbreviation

cTn-I

Uniprot No.

P23693

Species

Rattus norvegicus (Rat)

Sample Types

serum, plasma, tissue homogenates

Detection Range

31.25pg/mL-2000pg/mL

Sensitivity

15.6pg/mL

Assay Time

1-5h

Sample Loading Volume

50-100ul

Detection Wavelength

450 nm

Research Area

Cardiovascular

Assay Principle

quantitative

Measurement

Sandwich

Precision

Linearity

To assess the linearity of the assay, samples were spiked with high concentrations of rat cTn-Ⅰ in various matrices and diluted with the Sample Diluent to produce samples with values within the dynamic range of the assay.

	Sample	Serum(n=4)
1:1	Average %	92
	Range %	85-98
1:2	Average %	89
	Range %	82-96
1:4	Average %	97
	Range %	92-103
1:8	Average %	106
	Range %	100-111

Recovery

Typical Data

These standard curves are provided for demonstration only. A standard curve should be generated for each set of samples assayed.


pg/ml	OD1	OD2	Average	Corrected
2000	2.793	2.634	2.713	2.575
1000	2.422	2.367	2.394	2.256
500	1.825	1.778	1.802	1.663
250	0.992	0.979	0.986	0.847
125	0.568	0.551	0.559	0.421
62.5	0.349	0.353	0.351	0.213
31.25	0.258	0.264	0.261	0.122
0	0.142	0.135	0.139

ELISA Data Analysis

ELISA Standard Curve & Curve Expert software

Troubleshooting
and FAQs

ELISA kit FAQs

Storage

Store at 2-8°C. Please refer to protocol.

Shelf Life

6 months

Lead Time

3-5 working days

Description

This ELISA kit provides quantitative measurement of cardiac troponin I (cTn-I) in rat serum, plasma, and tissue homogenates, supporting cardiovascular injury research. Because cTn-I is the gold-standard biomarker for myocardial damage yet circulates at extremely low concentrations in baseline and early injury states, this kit is engineered to resolve subtle changes in troponin release across both systemic and tissue-level compartments.

Detection Range: The 31.25–2000 pg/mL range spans from near-baseline circulating cTn-I levels in healthy rats through the elevated concentrations seen after ischemia-reperfusion or cardiotoxic drug exposure, minimizing the need for serial dilutions in most acute injury models.

Sensitivity: At 15.6 pg/mL, the kit detects the trace cTn-I elevations characteristic of early or subclinical myocardial insult, enabling researchers to capture the onset of cardiomyocyte membrane compromise before overt necrosis.

Sample Compatibility: Validation across serum, plasma, and tissue homogenates allows direct correlation between circulating cTn-I and residual cardiac tissue content within the same study, critical for distinguishing active leakage from cumulative myocardial depletion.

Assay Efficiency: The 1–5 hour protocol and 50–100 µL sample volume accommodate the limited blood volumes obtainable from serial rat sampling and high-throughput cardiotoxicity screening designs.

This kit is directly applicable to doxorubicin cardiotoxicity studies, myocardial ischemia-reperfusion models, and preclinical cardiac safety pharmacology assessments.

Target Background

Function
(From Uniprot)

Troponin I is the inhibitory subunit of troponin, the thin filament regulatory complex which confers calcium-sensitivity to striated muscle actomyosin ATPase activity.

Gene References into Functions

Pim-1 is a novel kinase that phosphorylates cTnI primarily at Ser23/24 and Ser150 in cardiomyocytes, which in turn may modulate myofilament function under a variety of physiological and pathophysiological conditions. PMID: 29544221
Cardiac troponin I mutation P83S present in hypertrophic cardiomyopathy changes the contractile myofibril properties and modulation by PKA-mediated phosphorylation. PMID: 27150586
Troponin I interaction with calcium and Troponin C in cardiac muscle PMID: 28864299
Compared to cTnI(WT), both truncations displayed greater Ca(2+)-sensitivity and faster cross-bridge attachment rates at both SLs. Furthermore, cTnI(1-167) slowed MgADP release rate and enhanced cross-bridge binding. Our findings imply that cTnI-MD truncations affect the blocked-to closed-state transition(s) and destabilize the closed-state position of tropomyosin. PMID: 28958680
PKC phosphorylates cardiac troponin I (cTnI) S23/24, S43/45 and T144 to fine tune myocyte function. PMID: 28587770
These findings demonstrate that S-nitrosylation and S-glutathionylation exert opposing effects on Ca(2+) sensitivity in mammalian FT muscle fibers, mediated by competitive actions on Cys134 of TnIf. PMID: 27974300
the interaction between cTnC and cTnI in skinned papillary muscle strips is dependent on sarcomere length PMID: 26944554
cTnIS43/45N is a functionally conservative substitution, and may be appropriate for use as a phospho-null in rodent models designed for studies on PKC modulation of cardiac performance PMID: 26869200
This study suggests that cTnI point of care tests can accurately determine heat stroke (HS) severity and could serve as simple, portable, cost-effective HS field tests. PMID: 26290107
The present study utilizes viral gene transfer of cTnI with phosphomimetic S43D and/or S45D substitutions to evaluate their individual and combined influences on function in intact adult cardiac myocytes. PMID: 25481661
Results suggest that weakened troponin C interaction with cTnI, via PKA phosphorylation of cTnI, may slow thin filament activation and result in increased myofilament relaxation kinetics PMID: 25185555
The findings elucidate the pathogenesis of MI, and the gradual increase in serum adropin could be a novel diagnostic marker and serve as an alternative to troponin-I measurement for diagnosing MI. PMID: 24932661
molecular determinants of cardiac myocyte performance as conferred by isoform-specific TnI residues PMID: 24853739
Arsenic induced ventricular hypertrophy occurs via MEF2A/CAMKK2/CALM3/TNNI3 signaling. PMID: 25089838
Data indicate that the serum TnI level was significantly greater in the acute coronary syndrome (ACS) group compared to the control group. PMID: 23904327
A cutoff value of 4.8ng/mL for cTnI could be used as early as 8h after MI to accurately identify infarct in this model, whereas echocardiographic images taken 48h after MI predicted the infarcted area 14days after MI. PMID: 23764111
Mutation in the C helix of cTnC can reduce Ca2+ binding affinity and cTnC-cTnI interaction. PMID: 23454346
Hypertrophic cardiomyopathy related mutations R146G/Q and R163W impact interactions between cTnI and cardiac troponin C or actin. PMID: 23246786
Aan increase in calpain activity may enhance cTnI degradation in the myocardium of tail-suspended rats. PMID: 20945043
Normal developing myocardium and skeletal muscle transiently share both sk-fMHC and cTn-I proteins. PMID: 22808244
the functional impact of cardiac troponin I (cTnI) phosphorylation by protein kinase A PMID: 22684024
cTnC, cTnI, cTnT and cTm are not only present in myofilaments of ventricular cardiomyocytes in culture but are also within their nuclei; significantly, these four proteins appear between days 3 and 5 in both myofilaments and nuclei PMID: 22364878
differential histidine ionization may be necessary for cTnI A164H to act as a molecular sensor capable of modulating sarcomere performance in response to changes in the cytosolic milieu PMID: 22500757
Structural dynamics of C-domain of cardiac troponin I protein in reconstituted thin filament. PMID: 22207765
PKC phosphorylation of cTnI may be maladaptive and potentially associated with cardiac dysfunction PMID: 22052912
Cardiac function and phosphorylation of PLB and cTnI were compared in pacing, isoproterenol treatment, and combined pacing and isoproterenol treatment in isolated working heart. PMID: 21876643
Ulinastatin may protect myocardium from the damage resulted from sepsis in a rat model, probably by lowering expressions of cTnI, TNF-alpha and ET-1. PMID: 20594472
Data show that dual expression of two CM mutants, tropomyosin mutant A63V and cardiac troponin mutant R146G, were shown to additively slow myocyte relaxation beyond either mutant studied in isolation. PMID: 20161772
Time-dependent cTnI breakdown occurs during global ischemia independent of reperfusion. cTnI breakdown during ischemia is further increased in presence of antioxidants. ROS generated during ischemia may play cTnI protective role. PMID: 15142843
cardiac Troponin I Thr144 plays an important role in the acute acceleration of relaxation, whereas Ser23/Ser24 contributes to relaxation during more prolonged activation of protein kinase C by endothelin PMID: 16236710
GATA elements control repression of cTNI promoter activity in skeletal muscle cells. PMID: 17875210
Overexpression of heat shock protein 27 protects against ischaemia/reperfusion-induced cardiac dysfunction via stabilization of troponin I and T. PMID: 18397962
cTnI-R145G expression influences the response to adrenergic stimulation dependent on the receptor subtype PMID: 18548271
Metabolic inhibition of cardiomyocytes induces a parallel release of intact cTnI and its degradation products, starting only after onset of irreversible cardiomyocyte damage. PMID: 18721805
the nNOS-PMCA4b complex regulates contractility via cAMP and phosphorylation of both PLB and cTnI. PMID: 19278978

Hide All

Protein Families

Troponin I family

Database Links

KEGG: rno:29248

STRING: 10116.ENSRNOP00000024640

UniGene: Rn.64141

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Code	CSB-E08594r-IS
Size	96T,5×96T,10×96T
Price	Request a Quote
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Intra-assay Precision (Precision within an assay): CV%<8%

Three samples of known concentration were tested twenty times on one plate to assess.

Inter-assay Precision (Precision between assays): CV%<10%

Three samples of known concentration were tested in twenty assays to assess.