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Literature summary for 3.6.4.13 extracted from

  • Hug, N.; Caceres, J.F.
    The RNA helicase DHX34 activates NMD by promoting a transition from the surveillance to the decay-inducing complex (2014), Cell Rep., 8, 1845-1856.
    View publication on PubMedView publication on EuropePMC

Cloned(Commentary)

Cloned (Comment) Organism
recombinant expression of FLAG-tagged DHX34 in HEK-293T cells, co-expression with recombinant UPF1 protein, DHX34 and UPF1 interact directly, but weak interaction with UPF2 and UPF3b Homo sapiens

Protein Variants

Protein Variants Comment Organism
D279A site-directed mutagenesis, the mutation affects ATP hydrolysis Homo sapiens
K191S site-directed mutagenesis, the mutation affects ATP binding Homo sapiens

Metals/Ions

Metals/Ions Comment Organism Structure
Mg2+ required Homo sapiens

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
ATP + H2O Homo sapiens
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ADP + phosphate
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?

Organism

Organism UniProt Comment Textmining
Homo sapiens Q14147
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-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
ATP + H2O
-
Homo sapiens ADP + phosphate
-
?
additional information RNA-dependent interactions of DHX34 with UPF3b and the EJC component, MLN51, no interaction with PABP1, with the eukaryotic release factor eRF3, or with the NMD core factor UPF2. Interactions of DHX34 with RNA degradation factors such as the exonuclease XRN1, the exosome component DIS3, and the decapping enzyme DCP1, all of them independently of the presence of RNA. DHX34 interacts with UPF1 directly and preferentially associates with SURF complexes, and promoties UPF1 phosphorylation Homo sapiens ?
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?

Synonyms

Synonyms Comment Organism
DEAH box protein 34
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Homo sapiens
DHX34
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Homo sapiens
RNA helicase DHX34
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Homo sapiens

General Information

General Information Comment Organism
evolution enzyme DHX34 belongs to the DExH/D box family of proteins Homo sapiens
malfunction a reduction in the phosphorylation of endogenous UPF1 protein is observed upon DHX34 depletion. The levels of UPF1 phosphorylation are rescued upon the expression of an shRNA-resistant wild-type DHX34 construct, but not by the ATPase-deficient DHX34 mutants (K191S or D279A), which affect ATP binding or ATP hydrolysis, respectively. Overexpression of DHX34 affects the recruitment of SMG9, a subunit of the SMG1c complex, as well as the DHX34-dependent recruitment of UPF2 and eIF4A3 Homo sapiens
metabolism RNA helicase DHX34 activates nonsense-mediated decay (NMD), a surveillance mechanism that degrades aberrant mRNAs. A complex comprising SMG1, UPF1, and the translation termination factors eRF1 and eRF3 (SURF) is assembled in the vicinity of a premature termination codon. Subsequently, an interaction with UPF2, UPF3b, and the exon junction complex induces the formation of the decay-inducing complex (DECID) and triggers NMD. The central NMD factor is the ATP-dependent RNA helicase UPF1 Homo sapiens
physiological function RNA helicase DHX34 use ATP hydrolysis to promote directly or indirectly RNA-RNA unwinding, RNA-protein dissociation, and protein-protein interactions. It activates nonsense-mediated mRNA decay, a surveillance pathway that eliminates mRNAs that contain premature termination codons preventing the synthesis of truncated proteins mechanism, overview. Enzyme DHX34 promotes UPF1 phosphorylation. Role for helicase DHX34 in the active remodeling of the SURF complex promoting its transition to the DECID complex, overview. DHX34-dependent recruitment of UPF2 and eIF4A3 to UPF1 complexes. DHX34 supports the transition from SURF to DECID resulting in UPF1 phosphorylation and release of the eRFs from the PTC resulting in targeting of the faulty mRNA for degradation Homo sapiens