High impact information on Rassf1

• No overtly altered cell cycle parameters or aberrations in centrosome number were detected in Rassf1A null fibroblasts [1].
• Rassf1A null embryonic fibroblasts displayed an increased sensitivity to microtubule depolymerizing agents [1].
• Thus, our results demonstrate that Rassf1A acts as a tumor suppressor gene [1].
• Irradiated Rassf1A null mice also showed increased tumor susceptibility, particularly to tumors associated with the gastrointestinal tract, compared with wild-type mice [1].
• Rassf1A null fibroblasts did not show increased sensitivity to microtubule poisons or DNA-damaging agents and showed no evidence of gross genomic instability, suggesting that cellular responses to genotoxins were unaffected [1].

Biological context of Rassf1

• Heterozygotes develop normally despite being haplo-insufficient for twelve genes including the candidate tumour suppressor gene Rassf1 [2].

Associations of Rassf1 with chemical compounds

• Additional mutation of tyrosine 992 to phenylalanine in the truncated receptor mutant (Dc-123F) further decreased the receptor internalization rate to a minimal level (ke = 0.07-0.10/min), equivalent to the ke measured for cells expressing kinase-negative receptor (A721) [3].
• Two mutants, F5, in which all five tyrosine autophosphorylation sites substituted by phenylalanine, and Dc 123F, in which four tyrosines were removed by deletion and the fifth (Tyr-992) was mutated into phenylalanine, phosphorylated eps8 and eps15 as efficiently as the wild-type receptor [4].

References