SCUBA

TWIST1 — Twist family bHLH transcription factor 1

TWIST1 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.

TWIST1's module in each cell type

Cell typeModuleShares the module with
CD4⁺ T cellsCD200 immunoregulation
Immune regulation
B3GNT2, CAV1, CD200, CD79A, CH25H, CHGB, DUOX1, ELF2 +23 moreView in SCUBA
FibroblastsActivated Myofibroblast State
Wound healing
BGN, BMP1, CPXM1, CTHRC1, EGFL6, FAP, KIAA0930, MASP1 +7 moreView in SCUBA

About the gene

SynonymsACS3, bHLHa38, BPES2, BPES3, CRS, CRS1, H-twist, SCS, TWIST
Chromosome7: 19020991-19117636
Predicted locationIntracellular
Essential geneNo
Protein classCancer-related genes, Disease related genes, Human disease related genes, Predicted intracellular proteins, Transcription factors
Molecular functionActivator, Developmental protein, DNA-binding, Repressor
Biological processBiological rhythms, Differentiation, Myogenesis, Transcription, Transcription regulation

Function

Acts as a transcriptional regulator. Inhibits myogenesis by sequestrating E proteins, inhibiting trans-activation by MEF2, and inhibiting DNA-binding by MYOD1 through physical interaction. This interaction probably involves the basic domains of both proteins. Also represses expression of pro-inflammatory cytokines such as TNFA and IL1B. Regulates cranial suture patterning and fusion. Activates transcription as a heterodimer with E proteins. Regulates gene expression differentially, depending on dimer composition. Homodimers induce expression of FGFR2 and POSTN while heterodimers repress FGFR2 and POSTN expression and induce THBS1 expression. Heterodimerization is also required for osteoblast differentiation. Represses the activity of the circadian transcriptional activator: NPAS2-BMAL1 heterodimer (By similarity).

Human Protein Atlas · Open Targets · UniProt

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