Psychiatry related information on RAS

• SRA-13, a member of the SRA family of chemosensory receptors, negatively regulates RAS/MAPK signalling during vulval induction and the olfaction of volatile attractants [1].

High impact information on RAS

• Here we show that the let-7 family negatively regulates let-60/RAS [2].
• The 3'UTRs of the human RAS genes contain multiple LCSs, allowing let-7 to regulate RAS expression. let-7 expression is lower in lung tumors than in normal lung tissue, while RAS protein is significantly higher in lung tumors, providing a possible mechanism for let-7 in cancer [2].
• Inositol trisphosphate mediates a RAS-independent response to LET-23 receptor tyrosine kinase activation in C. elegans [3].
• We show that an inositol trisphosphate receptor can act as a RAS-independent, tissue-specific positive effector of LET-23 [3].
• Notch inhibition of RAS signaling through MAP kinase phosphatase LIP-1 during C. elegans vulval development [4].

Biological context of RAS

• These effects include genetic interactions that place tam-1 into a group called the class B synMuv genes (for a Synthetic Multivulva phenotype); this family plays a negative role in the regulation of RAS pathway activity in C. elegans [5].
• Vulval induction in Caenorhabditis elegans has helped define an evolutionarily conserved signal transduction pathway from receptor tyrosine kinases (RTKs) through the adaptor protein SEM-5 to RAS [6].
• Genetics of RAS signaling in C. elegans [7].
• RNA interference experiments suggest that SOS-1 participates in RAS-dependent signaling events downstream of LET-23 EGFR, EGL-15 FGFR and an unknown RTK [6].
• Here, we report that, in addition to its known function during mitosis, ECT-2 promotes the specification of the primary vulval cell fate by activating RAS/mitogen-activated protein kinase (MAPK) signalling before the end of the S-phase [8].

Anatomical context of RAS

• EGL-30 acts with muscle-expressed EGL-19 L-type voltage-gated calcium channels to promote vulva development, and acts downstream or parallel to LET-60 (RAS) [9].

Associations of RAS with chemical compounds

• Fine-tuning the RAS signaling pathway: Zn(2+) makes the difference [10].
• Here we describe the identification, cloning and genetic characterization of C.ELEGANS: SOS-1, a putative guanine nucleotide exchanger for LET-60 RAS [6].

Physical interactions of RAS

• The C. elegans G-protein-coupled receptor SRA-13 inhibits RAS/MAPK signalling during olfaction and vulval development [1].

Regulatory relationships of RAS

• The Caenorhabditis elegans homologue of the proto-oncogene ect-2 positively regulates RAS signalling during vulval development [8].

Other interactions of RAS

• An ark-1 mutation synergizes with mutations in other negative regulators of let-23, resulting in increased RAS signaling [11].
• Loss-of-function mutations in puf-8 cause ectopic vulval differentiation when combined with mutations in negative regulators of the EGFR/RAS/MAPK pathway and suppress the vulvaless phenotype caused by mutations that reduce EGFR/RAS/MAPK signalling [12].
• Genetic epistasis tests are consistent with models in which lin-39 acts downstream of the RAS pathway to regulate response to inductive signal [13].
• Our results raise the possibility that the transforming activity of the mammalian ect-2 oncogene could be due to hyperactivation of the RAS/MAPK pathway [8].

References