SCUBA

SLFN11 — Schlafen family member 11

SLFN11 belongs to a gene co-expression module in 1 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

SLFN11's module in each cell type

Cell typeModuleShares the module with
EndothelialVascular EC Identity
Endothelial cell development
AMOTL1, ARFGEF3, ATN1, CAMK1D, CASP10, CCNY, CFLAR, F11R +13 moreView in SCUBA

About the gene

SynonymsFLJ34922
Chromosome17: 35350305-35373701
Predicted locationIntracellular
Essential geneNo
Protein classPredicted intracellular proteins
Molecular functionDNA-binding, Endonuclease, Helicase, Hydrolase, Nuclease, RNA-binding, tRNA-binding
Biological processAntiviral defense, DNA damage, Immunity

Function

Inhibitor of DNA replication that promotes cell death in response to DNA damage. Acts as a guardian of the genome by killing cells with defective replication. Persistently blocks stressed replication forks by opening chromatin across replication initiation sites at stressed replication forks, possibly leading to unwind DNA ahead of the MCM helicase and block fork progression, ultimately leading to cell death. Upon DNA damage, inhibits translation of ATR or ATM based on distinct codon usage without disrupting early DNA damage response signaling. Antiviral restriction factor with manganese- dependent type II tRNA endoribonuclease. A single tRNA molecule is bound and cleaved by the SLFN11 dimer. Specifically abrogates the production of retroviruses such as human immunodeficiency virus 1 (HIV-1) by acting as a specific inhibitor of the synthesis of retroviruses encoded proteins in a codon-usage-dependent manner. Impairs the replication of human cytomegalovirus (HCMV) and some Flaviviruses. Exploits the unique viral codon bias towards A/T nucleotides. Also acts as an interferon (IFN)-induced antiviral protein which acts as an inhibitor of retrovirus protein synthesis.

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.