SCUBA

SMARCA5 — SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 5

SMARCA5 belongs to a gene co-expression module in 6 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.

SMARCA5's module in each cell type

Cell typeModuleShares the module with
CD4⁺ T cellsChromatin Regulation
DNA/chromatin regulation
ADI1, ASXL2, BTG3, CASP8, CHD3, CTSS, CWF19L2, DENND2D +17 moreView in SCUBA
EndothelialInflammatory Kinase Signaling
Inflammation
ANKRD28, CBL, CDC123, CNN2, DGKH, EOGT, FADS3, FYN +7 moreView in SCUBA
Gamma-delta T cellsHippo Pathway Signaling
TCR Signaling
ADAR, ARL8B, BAZ2A, CASC3, CCDC85C, CCNK, CDC73, CDK12 +24 more
Innate lymphoid cellsRNA Chromatin Regulation
RNA processing & translation
BTBD7, CCDC59, CWC25, DDX3Y, DNTTIP2, HNRNPU, KRR1, MRFAP1 +5 moreView in SCUBA
MacrophagesmRNA Splicing Processing
Housekeeping
AP3D1, BAZ1B, CCDC47, CHTOP, CTCF, EIF1AX, EIF3A, HDLBP +29 moreView in SCUBA
Mucosal-associated invariant T cellmRNA Processing Translation
RNA processing & translation
ACTN4, CDC42SE1, CSDE1, DDX5, EIF4G1, GDI1, HNRNPU, MSN +7 more

About the gene

SynonymshISWI, hSNF2H, ISWI
Chromosome4: 143513702-143557486
Predicted locationIntracellular
Essential geneYes
Protein classEssential proteins, Predicted intracellular proteins, Transcription factors
Molecular functionChromatin regulator, Hydrolase
Biological processHost-virus interaction

Function

ATPase that possesses intrinsic ATP-dependent nucleosome- remodeling activity. Catalytic subunit of ISWI chromatin-remodeling complexes, which form ordered nucleosome arrays on chromatin and facilitate access to DNA during DNA- templated processes such as DNA replication, transcription, and repair; this may require intact histone H4 tails. Within the ISWI chromatin-remodeling complexes, slides edge- and center-positioned histone octamers away from their original location on the DNA template. Catalytic activity and histone octamer sliding propensity is regulated and determined by components of the ISWI chromatin-remodeling complexes. The BAZ1A/ACF1-, BAZ1B/WSTF-, BAZ2A/TIP5- and BAZ2B- containing ISWI chromatin-remodeling complexes regulate the spacing of nucleosomes along the chromatin and have the ability to slide mononucleosomes to the center of a DNA template in an ATP-dependent manner. The CECR2- and RSF1-containing ISWI chromatin-remodeling complexes do not have the ability to slide mononucleosomes to the center of a DNA template. Binds to core histones together with RSF1, and is required for the assembly of regular nucleosome arrays by the RSF-5 ISWI chromatin-remodeling complex. Involved in DNA replication and together with BAZ1A/ACF1 is required for replication of pericentric heterochromatin in S-phase. Probably plays a role in repression of RNA polymerase I dependent transcription of the rDNA locus, through the recruitment of the SIN3/HDAC1 corepressor complex to the rDNA promoter (By similarity). Essential component of the WICH-5 ISWI chromatin- remodeling complex (also called the WICH complex), a chromatin- remodeling complex that mobilizes nucleosomes and reconfigures irregular chromatin to a regular nucleosomal array structure. The WICH-5 ISWI chromatin- remodeling complex regulates the transcription of various genes, has a role in RNA polymerase I transcription (By similarity). Within the B- WICH complex has a role in RNA polymerase III transcription. Mediates the histone H2AX phosphorylation at 'Tyr- 142', and is involved in the maintenance of chromatin structures during DNA replication processes (By similarity). Essential component of NoRC- 5 ISWI chromatin-remodeling complex, a complex that mediates silencing of a fraction of rDNA by recruiting histone-modifying enzymes and DNA methyltransferases, leading to heterochromatin formation and transcriptional silencing (By similarity).

Human Protein Atlas · Open Targets · UniProt

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