SCUBA

ASF1A — Anti-silencing function 1A histone chaperone

ASF1A belongs to a gene co-expression module in 2 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.

ASF1A's module in each cell type

Cell typeModuleShares the module with
Gamma-delta T cellsDNA Damage Repair
DNA/chromatin regulation
ANKRD10, DDX18, DNAJC17, ENPP5, KLRC4, KLRD1, NARS1, NDUFV3 +15 more
Mucosal-associated invariant T cellMAIT Effector Maturation
T cell maturation
BET1, CRYZ, DAXX, ECI2, EOMES, FNTA, IRF3, LBH +10 more

About the gene

SynonymsCIA, DKFZP547E2110
Chromosome6: 118894152-118909171
Predicted locationIntracellular
Essential geneNo
Protein classPredicted intracellular proteins
Molecular functionChaperone, Chromatin regulator
Biological processDNA damage, Transcription, Transcription regulation

Function

Histone chaperone that facilitates histone deposition and histone exchange and removal during nucleosome assembly and disassembly. Cooperates with chromatin assembly factor 1 (CAF-1) to promote replication-dependent chromatin assembly and with HIRA to promote replication-independent chromatin assembly. Promotes homologous recombination-mediated repair of double-strand breaks (DSBs) at stalled or collapsed replication forks: acts by mediating histone replacement at DSBs, leading to recruitment of the MMS22L-TONSL complex and subsequent loading of RAD51. Also involved in the nuclear import of the histone H3-H4 dimer together with importin-4 (IPO4): specifically recognizes and binds newly synthesized histones with the monomethylation of H3 'Lys-9' and acetylation at 'Lys-14' (H3K9me1K14ac) marks, and diacetylation at 'Lys-5' and 'Lys-12' of H4 (H4K5K12ac) marks in the cytosol. Required for the formation of senescence-associated heterochromatin foci (SAHF) and efficient senescence-associated cell cycle exit.

Human Protein Atlas · Open Targets · UniProt

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