ArticleBiochemical and biophysical research communications2025
Unraveling the mechanism of RNA duplex unwinding by DEAD-box helicase DDX3X: Insights into Cooperativity and roles of protomers.
Article in Biochemical and biophysical research communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- DEAD-box helicase intrinsically disordered domains and structural dynamics of HIV-1 RNA are required to reveal DDX3X catalytic efficiency.Nucleic acids research · 2025Article
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3 authors.
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Abstract
DDX3X, a human DEAD-box helicase involved in ATP-dependent unwinding of short RNA duplexes, plays a pivotal role in RNA metabolism, cancer progression, and HIV-1 infection. It is composed of an N-terminal region (N: residues 1-131), a helicase core containing two RecA-like domains (D1D2: residues 132-607), and a C-terminal tail (C: residues 608-662). Previous research has shown that D1D2 forms a pre-unwound complex with dsRNA, exhibiting two-molecule cooperativity for both RNA-unwinding and ATPase activities. However, the cooperative mechanism by which the full-length DDX3X (N-D1D2-C) unwinds RNA remains to be fully understood. Knowing that the C-terminal tail is crucial for oligomerization, we have created an N-truncated form of DDX3X (D1D2-C: residues 132-662) for further investigation. Our findings indicate that D1D2-C oligomerizes in the presence of RNA substrate, exhibits three-molecule cooperativity for RNA-unwinding activity, and displays two-molecule cooperativity for ATPase activity. Furthermore, D1 residue E186 and C-terminal tail are essential for the oligomerization of D1D2-C, enabling two types of subunit interface to form, one between two D1 domains (C-D2D1:D1D2-C) and the other between two C-terminal tails (D1D2-C:C-D2D1). These results offer new insights into the molecular mechanism of cooperative RNA unwinding by DDX3X.
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