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BolA family member 2 (BOLA2) is a cytosolic protein that plays a central role in the regulation of cellular iron homeostasis by facilitating the assembly and transfer of iron–sulfur (Fe–S) clusters in partnership with monothiol glutaredoxins, especially GLRX3[1][2][3][5]. Human-specific duplications of BOLA2 have increased its dosage, which not only impacts the processing of Fe–S proteins but is also implicated in susceptibility to genetic rearrangements linked to developmental and hematological disorders, such as anemia and altered cranial size[1]. BOLA2 forms heterodimeric [2Fe–2S] complexes important for metabolic and redox processes and is highly integrated with cellular pathways like mTOR and PI3K-AKT signaling in cancer biology[1][3]. Dysregulation and overexpression of BOLA2 are associated with several malignancies and altered iron metabolism, positioning it as a suggested—but not yet validated—therapeutic target in oncology[1][3][5]. There are currently no drugs directly targeting BOLA2, and its major functions relate to core aspects of cell growth, iron handling, and stress responses[1][2][3][5].
Not applicable; no drugs targeting this molecule are currently described[1][2][3][5].
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