Growth arrest-specific protein 2 (GAS2)

Growth arrest-specific protein 2 (GAS2) is a multifunctional, cytoskeleton-associated protein originally identified as being upregulated in cells during growth arrest[1][2][5]. The protein contains an N-terminal calponin homology (CH) domain that binds actin filaments and a C-terminal GAS2-related (GAR) domain that binds microtubules, enabling it to cross-link actin and microtubules and regulate cytoskeletal dynamics[2][3][4]. GAS2 functions as a caspase-3 substrate, plays a role in controlling cell shape changes during apoptosis, and modulates susceptibility to p53-dependent apoptosis partly by inhibiting calpain activity[1]. It participates in processes such as cell cycle progression, cellular homeostasis, and death, and its family members are considered miniversions of spectraplakins (a class of cytoskeletal cross-linkers)[2][5]. GAS2 has been implicated in cancer due to its role in apoptosis and cytoskeletal reorganization, but it is not recognized as a classical therapeutic target such as a receptor, enzyme, or transporter[1][2][5]. There are currently no known drugs acting directly on GAS2, nor is it established as a clinical biomarker or associated with specific therapeutic safety concerns.

Other names

Growth arrest-specific 2GAS-2DFNB125growth arrest-specific protein 2