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Literature summary for 4.6.1.19 extracted from

  • Zhang, A.; Dong, B.; Doucet, A.J.; Moldovan, J.B.; Moran, J.V.; Silverman, R.H.
    RNase L restricts the mobility of engineered retrotransposons in cultured human cells (2014), Nucleic Acids Res., 42, 3803-3820.
    View publication on PubMedView publication on EuropePMC

Activating Compound

Activating Compound Comment Organism Structure
2',5'-Oligoadenylate
-
Homo sapiens

Cloned(Commentary)

Cloned (Comment) Organism
expression of FLAG-tagged wild-type, R667A mutant, and NDELTA385 deletion enzyme mutant in HeLa-M cells Homo sapiens

Protein Variants

Protein Variants Comment Organism
additional information deletion mutant NDELTA385 is a constitutively active form of RNase L Homo sapiens
R667A a catalytically inactive RNase L mutant Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
HeLa cell e.g. ATCC CCL-2 and S3, express normal enzyme level, while strain HeLa-M is defective in RNase L expression Homo sapiens
-

Synonyms

Synonyms Comment Organism
RNase L
-
Homo sapiens

General Information

General Information Comment Organism
malfunction siRNA-mediated depletion of endogenous enzyme in the human ovarian cancer cell line Hey1b increased the levels of LINE-1 retrotransposition by about 2fold. Recombinant expression of wild-type and a constitutively active deletion mutant enzyme form, but not a catalytically inactive enzyme mutant R667A, impair the mobility of engineered human LINE-1 and mouse intracisternal A-type particle retrotransposons in cultured human cells Homo sapiens
physiological function the enzyme might function as a suppressor of structurally distinct retrotransposons, endogenous RNase L restricts L1 retrotransposition, overview. Wild-type enzyme, but not enzyme mutant R667A, prevents formation of LINE-1 cytoplasmic foci Homo sapiens