The TNI-3 antibody targets troponin I type 3 (TNNI3), a cardiac-specific protein critical for regulating muscle contraction. TNNI3 is a subunit of the troponin complex, which modulates calcium-sensitive interactions between actin and myosin in cardiac muscle. Mutations in the TNNI3 gene are linked to cardiomyopathies, including hypertrophic (CMH7) and restrictive (RCM1) forms . Antibodies against TNNI3 are essential tools for diagnostic assays, biomarker detection, and cardiovascular research.
TNNI3 phosphorylation at specific residues (e.g., Ser-23, Ser-24, Thr-31) modulates calcium sensitivity and contractility. For example:
Phosphorylation by PRKCA/PKCe at Ser-42/44 alters myocardium contractile dynamics .
STK4/MST1-mediated phosphorylation at Thr-31 affects binding to TNNC1 (troponin C) and TNNT2 (troponin T) .
Hypertrophic Cardiomyopathy (HCM): Over 20 TNNI3 mutations (e.g., R145W, K178E) disrupt troponin complex stability, leading to diastolic dysfunction .
Autoantibodies: Anti-cTnI antibodies occur in ~10% of post-MI patients and 20% with chronic cardiomyopathy, potentially interfering with diagnostic assays .
In C. elegans, the TNI-3 isoform (distinct from human TNNI3) regulates myoepithelial sheath contraction during ovulation. A rabbit polyclonal antibody against Ascaris TNI cross-reacts with C. elegans TNI-3, revealing compensatory upregulation of TNI-1 in unc-27-null mutants .
HyTest’s monoclonal antibodies target distinct linear epitopes along cTnI (Figure 1 ):
Critical Regions: Residues 84–96 (MF4), 110–130 (C5), and 160–180 (Y501) are commonly targeted for high-affinity binding .
| Residue | PTM Type | Enzyme | Functional Impact |
|---|---|---|---|
| Ser-23 | Phosphorylation | PRKD1, PRKACA | Reduces calcium sensitivity |
| Thr-31 | Phosphorylation | STK4 | Alters TNNC1 binding |
| Lys-40 | Methylation | N/A | Regulatory function |