Table 1.

Physiological and abnormal alternative splice forms of cardiac TnT.

Splice forms	Physiological and pathophysiological significance
Exon 4 splice-out	This exon encodes 4–5 amino acids and its alternative splicing results in relatively small change of N-terminal charge of cardiac TnT. Alternative splicing is normally found in rabbit, rat, mouse, and bovine hearts (Biesiadecki and Jin, 2002) and is increased in human heart failure (Anderson et al., 1991, 1995), human familial hypertrophic cardiomyopathy (Thierfelder et al., 1994), and the heart of diabetic rats (Akella et al., 1995).
Exon 5 splice-in	This exon encodes 9–10 mainly acidic amino acids. It is normally included in embryonic avian and mammalian cardiac TnT (Jin et al., 1992) and abnormally expressed in adult canine hearts of dilated cardiomyopathy (Biesiadecki et al., 2002). Its inclusion equips myofibrils with a higher tolerance to acidosis and higher Ca2+ sensitivity.
Exon 6 splice-out	This exon encodes 25 amino acids and its alternative splicing corresponds to a rather large structural change, abnormally occurring in adult Guinea pig hearts (Biesiadecki et al., 2002) with unknown functional effects.
Exon7 splice-out	This exon encodes 12 amino acids and is abnormally excluded in adult canine hearts with dilated cardiomyopathy, causing impairing systolic function (Biesiadecki et al., 2002).
Exon 8 splice-out	This exon encodes 12 amino acids equivalent to mammalian exon 7. Its abnormal exclusion in adult turkey hearts with dilated cardiomyopathy alters molecular conformation and binding affinity of cardiac TnT for cardiac TnI and tropomyosin (Biesiadecki and Jin, 2002).
Exon 13 splice-in/out	This exon encodes 2–3 amino acids. Its alternative splicing is independent of development and the functional significance is unknown (Jin et al., 1992).