Target intelligence / Profile preview

Ankyrin repeat domain-containing protein 23 (ANKRD23)

Target
ANKRD23
Molecular classification
Other (Ankyrin repeat domain-containing protein, muscle ankyrin repeat protein family (MARP))
01

Overview

Ankyrin repeat domain-containing protein 23 (ANKRD23), also called diabetes-related ankyrin repeat protein (DARP) or muscle ankyrin repeat protein 3 (MARP3), is a member of the muscle ankyrin repeat protein family. It contains four tandem ankyrin-like repeats and localizes primarily to the nucleus where it acts as a transcriptional regulator. ANKRD23 is strongly expressed in striated muscle and is upregulated during conditions of metabolic stress, such as in insulin-resistant and diabetic models. Functionally, it regulates muscle metabolism by modulating AMP-activated protein kinase (AMPK) activity and influences both fatty acid and glucose metabolism. It also acts as a negative regulator of myoblast differentiation, impacting muscle growth. In addition to its nuclear regulatory activities, ANKRD23 may contribute to mechanotransduction signaling in muscle tissue and could serve as a biomarker for muscular diseases. There is no evidence that ANKRD23 is currently a direct pharmaceutical target, but it plays important roles in muscle physiology and metabolic regulation[1][2][3][5].

Other names
Diabetes-related ankyrin repeat proteinDARPMuscle ankyrin repeat protein 3MARP3FLJ32449
02

Biological functions

Transcription regulation (transcriptional regulator in the nucleus)Glucose homeostasis and energy metabolismMechanosensation in muscle (possible involvement in muscle stretch-signaling)Negative regulation of myoblast differentiation
03

Disease associations

Diabetes/metabolic syndrome (regulation of glucose uptake, upregulated in insulin resistance)Muscular disease (implicated in muscular dystrophy and cardiac/skeletal muscle pathophysiology)Cancer (expression associated with specific cancer subtypes, e.g., glioblastoma)
04

Biomarkers

Muscle disease (MARPs are used as biomarkers in cardiac and skeletal myopathies due to their deregulation in these diseases)

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