Gene Ontology annotation through association of InterPro records with GO terms
Gene Ontology annotation based on Enzyme Commission mapping
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot keyword mapping
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Systematic identification of protein complexes in Saccharomyces cerevisiae by mass spectrometry.
Subcellular localization of the yeast proteome.
Ras recruits mitotic exit regulator Lte1 to the bud cortex in budding yeast.
The Ras/cAMP-dependent protein kinase signaling pathway regulates an early step of the autophagy process in Saccharomyces cerevisiae.
Unipolar cell divisions in the yeast S. cerevisiae lead to filamentous growth: regulation by starvation and RAS.
Ras and the Rho effector Cla4 collaborate to target and anchor Lte1 at the bud cortex.
Increased phosphoglucomutase activity suppresses the galactose growth defect associated with elevated levels of Ras signaling in S. cerevisiae.
Global landscape of protein complexes in the yeast Saccharomyces cerevisiae.
The plasma membrane proteome of Saccharomyces cerevisiae and its response to the antifungal calcofluor.
Chemical inhibition of CaaX protease activity disrupts yeast Ras localization.
Feedback regulation of Ras2 guanine nucleotide exchange factor (Ras2-GEF) activity of Cdc25p by Cdc25p phosphorylation in the yeast Saccharomyces cerevisiae.
The membrane localization of Ras2p and the association between Cdc25p and Ras2-GTP are regulated by protein kinase A (PKA) in the yeast Saccharomyces cerevisiae.
The cAMP-dependent protein kinase signaling pathway is a key regulator of P body foci formation.
Localization of Ras signaling complex in budding yeast.
Live-cell imaging of endogenous Ras-GTP shows predominant Ras activation at the plasma membrane and in the nucleus in Saccharomyces cerevisiae.
Mapping the functional yeast ABC transporter interactome.
Quantitative variations of the mitochondrial proteome and phosphoproteome during fermentative and respiratory growth in Saccharomyces cerevisiae.
Isolation and characterization of temperature-sensitive mutations in the RAS2 and CYR1 genes of Saccharomyces cerevisiae.
One library to make them all: streamlining the creation of yeast libraries via a SWAp-Tag strategy.
A product of yeast RAS2 gene is a guanine nucleotide binding protein.
Biochemical characterization of yeast RAS2 mutants reveals a new region of ras protein involved in the interaction with GTPase-activating proteins.
Ras2 signals via the Cdc42/Ste20/mitogen-activated protein kinase module to induce filamentous growth in Saccharomyces cerevisiae.
Falcon deep research report on RAS2 (Saccharomyces cerevisiae)
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RAS2 (Ras2p) is a 322-residue Ras-family small GTPase that acts as a
molecular switch, cycling between an inactive GDP-bound state and an
active GTP-bound state under control of upstream GEFs and GAPs.
"Ras2p cycles between an **inactive GDP-bound** state and an **active GTP-bound** state. This GTPase cycle is central to Ras2p’s signaling role and is controlled by upstream regulators (GEFs and GAPs)."
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The primary biochemical function of RAS2 is activation of adenylate
cyclase (Cyr1/CDC35) to produce cAMP, which binds Bcy1 to activate the
PKA catalytic subunits Tpk1/2/3, defining the core Ras-cAMP-PKA pathway
that controls growth and metabolism.
"In budding yeast, both Ras1p and Ras2p act upstream of **adenylate cyclase (Cyr1/CDC35)** to stimulate **cAMP** production; cAMP then binds the regulatory subunit **Bcy1** to activate **PKA catalytic subunits Tpk1/2/3**, establishing the core **Ras–cAMP–PKA** pathway that controls growth and metabolism."
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RAS2-GTP levels are set by the GEF Cdc25 (required for glucose-induced
Ras-GTP increase) and the GAPs Ira1 and Ira2, which stimulate intrinsic
GTP hydrolysis and negatively regulate cAMP output.
"The primary Ras GEF **Cdc25** promotes GDP→GTP exchange on Ras proteins and is required for the **glucose-induced increase in Ras-GTP**; temperature-sensitive cdc25 mutants show reduced intracellular cAMP and reduced adenylate cyclase activity"
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RAS2 membrane targeting depends on CAAX processing: it is farnesylated
at Cys319 and palmitoylated at Cys318; farnesylation is required for
plasma membrane localization and effector recruitment, and loss of
palmitoylation (C318S) mislocalizes Ras2p to the cytoplasm.
"Ras2p is reported to be **farnesylated at Cys319** and **palmitoylated at Cys318**; **farnesylation** is required for efficient **plasma membrane localization** and effector recruitment, whereas loss of palmitoylation (C318S) mislocalizes Ras2p to the cytoplasm in the cited work."
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Activation of Cyr1 by RAS2 occurs at the plasma membrane, although RAS2
and its partners are also observed on endomembranes, contacting the ER
and accumulating at mitochondria under nutrient depletion, with nuclear
active Ras2 reported in invasive growth contexts.
"While Ras2p and its regulators/partners have been observed on **endomembranes**, the activation of Cyr1 by Ras2 that drives cAMP production is described as occurring at the **plasma membrane**."
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RAS2 is a dominant controller of glucose-responsive transcription,
accounting for nearly ~90% of the transcriptional changes observed upon
glucose addition.
"Ras2-driven Ras/cAMP/PKA signaling is described as accounting for **nearly ~90%** of the transcriptional changes observed upon glucose addition, placing Ras2 as a dominant controller of glucose-responsive transcriptional reprogramming."
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RAS1 and RAS2 double loss is lethal while single deletions are viable on
glucose; ras2Delta strains show defects in growth on nonfermentable
carbon sources.
"Yeast has two Ras genes (**RAS1** and **RAS2**). Loss of both is **lethal**, consistent with an essential requirement for Ras-dependent activation of the cAMP/PKA pathway, while single deletions are viable under standard glucose conditions."
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RAS2 influences filamentous/invasive growth and cell-fate decisions,
linking Ras2/cAMP/PKA signaling to differentiation outputs including
Flo8-linked programs.
"Ras2 influences filamentous/invasive growth and broader “cell fate” decisions; the corpus links Ras2/cAMP/PKA signaling to differentiation outputs (including Flo8-linked programs) and provides a localization-focused treatment of nuclear active Ras2 in invasive growth."
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RAS2 is best interpreted as a central nutrient-state integrator,
positioned at the interface between extracellular nutrient cues
(especially glucose) and broad intracellular programs for growth, stress
protection, and differentiation.
"Ras2p is best interpreted as a **central nutrient-state integrator**: upstream regulators (Cdc25; Ira1/2; additional modulators such as Gpb1/2) determine the fraction of Ras2p in the GTP-bound state, which is then transduced primarily by Cyr1 into cAMP dynamics and PKA activation."