Aliases for RASSF1 Gene
External Ids for RASSF1 Gene
Previous GeneCards Identifiers for RASSF1 Gene
This gene encodes a protein similar to the RAS effector proteins. Loss or altered expression of this gene has been associated with the pathogenesis of a variety of cancers, which suggests the tumor suppressor function of this gene. The inactivation of this gene was found to be correlated with the hypermethylation of its CpG-island promoter region. The encoded protein was found to interact with DNA repair protein XPA. The protein was also shown to inhibit the accumulation of cyclin D1, and thus induce cell cycle arrest. Several alternatively spliced transcript variants of this gene encoding distinct isoforms have been reported. [provided by RefSeq, May 2011]
GeneCards Summary for RASSF1 Gene
RASSF1 (Ras Association (RalGDS/AF-6) Domain Family Member 1) is a Protein Coding gene. Diseases associated with RASSF1 include intracranial primitive neuroectodermal tumor and monophasic synovial sarcoma. Among its related pathways are Ras signaling pathway and Pathways in cancer. GO annotations related to this gene include identical protein binding and protein N-terminus binding. An important paralog of this gene is RASSF3.
UniProtKB/Swiss-Prot for RASSF1 Gene
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.