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Review
. 2010 May 18;121(19):2137-45.
doi: 10.1161/CIRCULATIONAHA.109.860171.

Cardiac titin: a multifunctional giant

Martin M LeWinter  1 , Henk Granzier
Affiliations
Review

Cardiac titin: a multifunctional giant

Martin M LeWinter et al. Circulation. .
No abstract available

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Figures

Figure 1
Figure 1
Schematic of titin in sarcomere.
Figure 2
Figure 2
Titin-based passive stiffness tuning-mechanisms. Differential splicing gives rise to isoforms of varying stiffness. During postnatal development (Devel) passive stiffness increases due to switching of fetal cardiac titin (FCT) to adult N2B and N2BA isoforms; hypothyroidism (HT) and dilated cardiomyopathy (DCM) alter splicing in the opposite direction. PKA and PKG phosphorylation reduce and PKC phosphorylation increases passive stiffness.
Figure 3
Figure 3
Proteins that bind to titin.
Figure 4
Figure 4
Schematic of N2B-based signalosome. Adaptor molecules belonging to the FHL family bind to N2B element and sequester kinases of the MAPK signaling pathway. Bottom: increased N2B strain (PEVK KO) results in additional signalosomes, shifting the balance towards hypertrophy; absence of the N2B element (N2B KO) results in hypertrophy.
See this image and copyright information in PMC

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References

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