Review Article

Ankrd2 in Mechanotransduction and Oxidative Stress Response in Skeletal Muscle: New Cues for the Pathogenesis of Muscular Laminopathies

Table 1

Overview of the main structural and functional features of Ankrd2 (extensively reported in [122]).

FeatureRef.

Structural domains
Ankyrin repeats[123]
Coiled coil
Protein destabilization motif (PEST)
Nuclear localization signal (NLS)
Posttranslational modifications
Phosphorylation by Akt2 kinase[15]
Proteolytic cleavage by μ-calpain[9]
Expression profile
[4, 19, 123, 124]
Type I (slow) skeletal muscle fibers[8, 123]
Localized in nuclei of myoblasts and cytoplasm of myotubes[123]
Migrate from myofibrils to nucleus after muscle injury[10]
Proposed functions
Stress response in muscle (stretch, denervation, eccentric contractions, fatiguing jumping and other types of exercise, and injury)[8, 10, 16, 46, 47, 49, 50, 55]
Muscle adaptation[7, 10, 16, 20, 46, 47, 49, 50, 125, 126]
Transcriptional regulation[1, 10]
Communication between the sarcoplasm and the nucleus[1]
Myogenesis and myogenic differentiation[11, 13, 14]
Inflammatory response[12]
Interacting proteins
Titin[7]
Telethonin[1]
ZASP[30]
Calpain 3[9]
Akt2[15]
A-type lamins (lamin A, prelamin A, and lamin C)[98]
Proteins with PDZ and SH3 domains, including ZO-1 and β1-syntrophin[20]
Transcription factors, including YB1, p53, PML, PAX6, NFIL3, and MECP2[20]
Pathways affected by Ankrd2 silencing in human myoblasts
Intercellular communication[20]
 Cytokine-cytokine receptor interaction
 Focal adhesion
 Tight junction
 Gap junction
 Regulation of actin cytoskeleton
Signaling involved in intracellular communication
 Calcium
 Insulin
 MAPK
 p53
 TGF-β
 Wnt