Go Annotations as Summary Text (Tabular View) (GO Graph)

GO curators for mouse genes have assigned the following annotations to the gene product of Tnni3. (This text reflects annotations as of Wednesday, January 23, 2013.) MGI curation of this mouse gene is considered complete, including annotations derived from the biomedical literature as of March 12, 2007. If you know of any additional information regarding this mouse gene please let us know. Please supply mouse gene symbol and a PubMed ID.

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Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] 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, Jul 2008]

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Summary text based on GO annotations supported by experimental evidence in mouse

• Researchers have inferred from direct assay, that the gene product of Tnni3
  • participates in the following biological processes:
    • cellular calcium ion homeostasis ^[4]
    • heart development ^[1]
    • regulation of muscle contraction ^[3]
    • striated muscle contraction ^{[4, 6]}
    • vasculogenesis ^[1]
  • is located in the following cellular components:
    • sarcomere ^[2]
• Researchers have inferred, based on phenotypic analysis of mouse mutants, that the gene product of Tnni3
  • participates in the following biological processes:
    • cellular calcium ion homeostasis ^[5]
    • regulation of systemic arterial blood pressure by ischemic conditions ^[5]

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Summary text based on GO annotations supported by experimental evidence in other organisms

• From comparative sequence analysis (see table for details), MGI curators have determined that the gene product of Tnni3:
  • participates in the following biological processes:
    • cardiac muscle contraction
    • heart contraction
    • negative regulation of ATPase activity
    • regulation of smooth muscle contraction
    • ventricular cardiac muscle tissue morphogenesis
  • performs the following molecular functions:
    • actin binding
    • calcium channel inhibitor activity
    • calcium-dependent protein binding
    • protein domain specific binding
    • protein kinase binding
    • troponin C binding
    • troponin T binding
  • is located in the following cellular components:
    • contractile fiber
    • cytoplasm
    • sarcomere
    • troponin complex

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References

1. Barbato JC et al. (2005) Proteolytic N-terminal truncation of cardiac troponin I enhances ventricular diastolic function. J Biol Chem, 280:6602-9. (PubMed:15611140)
2. Bennett PM et al. (2006) The transitional junction: a new functional subcellular domain at the intercalated disc. Mol Biol Cell, 17:2091-100. (PubMed:16481394)
3. Burkart EM et al. (2003) Phosphorylation or glutamic acid substitution at protein kinase C sites on cardiac troponin I differentially depress myofilament tension and shortening velocity. J Biol Chem, 278:11265-72. (PubMed:12551921)
4. Kogler H et al. (2001) Maintained contractile reserve in a transgenic mouse model of myocardial stunning. Am J Physiol Heart Circ Physiol, 280:H2623-30. (PubMed:11356618)
5. MacGowan GA et al. (2001) Ischemic dysfunction in transgenic mice expressing troponin I lacking protein kinase C phosphorylation sites. Am J Physiol Heart Circ Physiol, 280:H835-43. (PubMed:11158984)
6. Murphy AM et al. (2000) Transgenic mouse model of stunned myocardium. Science, 287:488-91. (PubMed:10642551)

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Gene Ontology Evidence Code Abbreviations:

EXP Inferred from experiment

IC Inferred by curator

IDA Inferred from direct assay

IEA Inferred from electronic annotation

IGI Inferred from genetic interaction

IMP Inferred from mutant phenotype

IPI Inferred from physical interaction

ISS Inferred from sequence or structural similarity

ISO Inferred from sequence orthology

ISA Inferred from sequence alignment

ISM Inferred from sequence model

NAS Non-traceable author statement

ND No biological data available

RCA Reviewed computational analysis

TAS Traceable author statement

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