Troponin I-Cardiac (65-74 Region), free cTnI, Monoclonal Antibody

Monoclonal Antibody to Troponin I-Cardiac (a.a. 65-74)

For Research Use Only. Not for use in diagnostic procedures.

Chromosome: 19; NC_000019.9 (55663135..55669100, complement). Location: 19q13.4

Monoclonal

IgG1

B158M

Host: Mouse. Hybridization of Sp2/0 myeloma cells with spleen cells from Balb/c mice.
Source: Ascites

Troponin I-Cardiac (65-74 Region), free cTnI
Reacts with free cardiac troponin I (cTnI). Does not react with cTnI forming complexes with other troponin components. Not affected by phosphorylation. Recognizes an epitope between amino acid residues 65 an

Protein A chromatography

Purified, Liquid

Store at 2 to 8 degree C.

Manufactured in an ISO 13485:2003 and EN ISO 13485:2012 Certified Laboratory.

Small volumes of anti-TNNI3 antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Monoclonal Antibodies to Cardiac Markers

EIA/ELISA, Western Blot, Immunohistochemistry, Immunoprecipitation

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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.

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