antibody

MAb to Troponin I-Cardiac

MBS311155

1 mg

560 USD

monoclonal

mouse

nonconjugated

western blot, enzyme immunoassay

Antibody

MAb to Troponin I-Cardiac

[Troponin I-Cardiac (87-91 Region)]

[Monoclonal Antibody to Human Cardiac Troponin I (cTnI)]

[troponin I, cardiac muscle; Troponin I, cardiac muscle; troponin I, cardiac muscle; troponin I type 3 (cardiac); Cardiac troponin I]

[TNNI3; TNNI3; CMH7; RCM1; cTnI; CMD2A; TNNC1; CMD1FF; MGC116817; TNNC1]

TNNI3_HUMAN

Monoclonal

IgG1

Mouse

Reacts equally with free cardiac troponin I (cTnI) and cTnI forming complexes with other troponin components. Not affected by heparin, phosphorylation, oxidation and troponin complex formation. Recognizes an epitope located between amino acid residues 86 and 90 of cTnI. No cross-reactivity with skeletal muscle troponin I. Reactive with cTnI from human, bovine, porcine, goat, canine, rabbit and feline. Not reactive with cTnI from rat, mouse or fish.

>90% pure (SDS-PAGE). Protein A chromatography

Purified, Liquid

7.7mg/ml (Sigma protein assay kit)

Store at 2-8°C.

Suitable for use in ELISA (EIA), Immunoaffinity purification and Western Blot (WB).

Each laboratory should determine and optium working titer for use in its particular application. Other applications have not been tested but use in such assays should not necessarily be excluded . Recommended pairs for sandwich immunoassay:. Capture: MBS311155; Detection: MBS319676

Source: Ascites. Immunogen: Native troponin complex

Buffer: PBS, pH 7.4. Preservative: 0.1% Sodium azide. Important Note: Centrifuge before opening to ensure complete recovery of vial contents. Warnings: This product contains sodium azide, which has been classified as Xn (Harmful), in European Directive 67/548/EEC in the concentration range of 0.1-1.0 %. When disposing of this reagent through lead or copper plumbing, flush with copious volumes of water to prevent azide build-up in drains.

Monoclonal Antibodies to Cardiac Markers

MAb to Troponin I-Cardiac. Monoclonal Antibody to Human Cardiac Troponin 1 (cTnl). This one component water bases tetramethybenzidine (TMB) chromogenic substrate is ideal for color development of horseradish peroxide (HRP) based ELISA systems. It is identical to the TMB substrate supplied in our ELISA kits. For best results, add 100 ul to each well and shake at 300 rpm at room temperature for 2-15 mins Quench reaction with 50 ul of 1N (0.5M) H2SO4, mix gently, and read plate at 450 nm. Store at 4°C and bring to room temperature before use.

151101270

NP_000354.4

NM_000363.4

P19429

Cardiac Muscle Contraction Pathway (93344); Cardiac Muscle Contraction Pathway (93992); Dilated Cardiomyopathy Pathway (121494); Dilated Cardiomyopathy Pathway (121285); Hypertrophic Cardiomyopathy (HCM) Pathway (114229); Hypertrophic Cardiomyopathy (HCM) Pathway (106591); Muscle Contraction Pathway (106261); Striated Muscle Contraction Pathway (106262); Striated Muscle Contraction Pathway (198903)

Troponin I (TnI), along with troponin T (TnT) and troponin C (TnC), is one of 3 subunits that form the troponin complex of the thin filaments of striated muscle. TnI is the inhibitory subunit; blocking actin-myosin interactions and thereby mediating striated muscle relaxation. The TnI subfamily contains three genes: TnI-skeletal-fast-twitch, TnI-skeletal-slow-twitch, and TnI-cardiac. This gene encodes the TnI-cardiac protein and is exclusively expressed in cardiac muscle tissues. Mutations in this gene cause familial hypertrophic cardiomyopathy type 7 (CMH7) and familial restrictive cardiomyopathy (RCM). [provided by RefSeq]

Function: Troponin I is the inhibitory subunit of troponin, the thin filament regulatory complex which confers calcium-sensitivity to striated muscle actomyosin ATPase activity. Subunit structure: Binds to actin and tropomyosin. Interacts with TRIM63. Ref.7. Involvement in disease: Defects 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. Ref.10 Ref.11 Ref.13 Ref.15 Ref.17Defects 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. Ref.16Defects 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 similarities: Belongs to the troponin I family.

1 mg

560 USD