SCUBA

RASSF1 — Ras association domain family member 1

RASSF1 belongs to a gene co-expression module in 3 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.

RASSF1's module in each cell type

Cell typeModuleShares the module with
CD4⁺ T cellsCytotoxic Effector CD4
Cytotoxicity
ADAM8, ADRB2, CCL5, CHD9, DPP4, HIC1, HOPX, IFIT2 +13 moreView in SCUBA
Gamma-delta T cellsLymphocyte Homeostatic Regulation
Housekeeping
BSG, CTDSP1, FBXW5, HMGN4, IGSF8, IKBKG, LRP10, MFNG +8 more
Mucosal-associated invariant T cellTCR Signaling Identity
TCR Signaling
ACAP1, CASP4, CD3G, CENPT, CFAP97, DPP7, FBXW5, IL27RA +10 more

About the gene

Synonyms123F2, NORE2A, RDA32, REH3P21
Chromosome3: 50329782-50340980
Predicted locationIntracellular
Essential geneNo
Protein classHuman disease related genes, Predicted intracellular proteins, RAS pathway related proteins
Biological processCell cycle

Function

Potential tumor suppressor. Required for death receptor- dependent apoptosis. Mediates activation of STK3/MST2 and STK4/MST1 during Fas-induced apoptosis by preventing their dephosphorylation. When associated with MOAP1, promotes BAX conformational change and translocation to mitochondrial membranes in response to TNF and TNFSF10 stimulation. Isoform A interacts with CDC20, an activator of the anaphase-promoting complex, APC, resulting in the inhibition of APC activity and mitotic progression. Inhibits proliferation by negatively regulating cell cycle progression at the level of G1/S-phase transition by regulating accumulation of cyclin D1 protein. Isoform C has been shown not to perform these roles, no function has been identified for this isoform. Isoform A disrupts interactions among MDM2, DAXX and USP7, thus contributing to the efficient activation of TP53 by promoting MDM2 self-ubiquitination in cell-cycle checkpoint control in response to DNA damage.

Human Protein Atlas · Open Targets · UniProt

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